Medicine Questions & Answers

Medicine Questions & Answers

Can you miss a down follicle testing, 2 weeks after you took 2 puffs of marijuana. if you have not smoked within 5 yrs?
This is a follow up, to this question I asked a few days ago. and the answer is yes, because I did ! but you can bet that I will not put myself under that much…

Can you mix adderall and headache medication, resembling tylenol?
No…you can’t mix them. It is dangerous. It may cause drug interaction. Source(s): http://www.drug3k.com/drug/Adderall-11461.htm – Acetaminophen is not contraindicated with use of Adderall. Drugs such as SSRI’s MAOI’s, anti depressants and any drug that effects liver enzymes are not to be used and are contraindicated. –

Can you mix an expired drug for 8 and younger next to Advil?
My daughter is 12 and she took a Tylenol for kids that was 8 and younger and I was wondering if she could take an Advil after if the Tylenol didn’t work. Thank you! It depends on how long it’s be since you gave her the Tylenol….

Can you mix Benedryl near Sudafed?
I have a stuffy nose … all mucus is clear. I clutch sudafed but then I get a really bad stuffy snout. I take benedryl to dry that up but then I have a stuffy proboscis again. I tried zicam nasal swabs, claritin D nothing worked! HELP PLEASE can i take the two together??…

Can you mix prednisone next to powerfull or h.g.h?
i need to knoww.. prednisone is a steroid used to decrease inflammation we often treat individuals with pneumonia with prednisone to decrease the inflammation contained by their lungs. I don’t know what powerfull or h.g.h. is but i’m assuming they are to help increase your bulk. although prednisone is a seriod-…

Can you mix suboxone next to any benzo’s? For example 1mg suboxone SL and .5mg Clonazepam? Is that unsafe?
Do NOT do this. These drugs are contradictions to each other. Mixing the two has a potential for causing mortal respiratory depression. –

Can you mix Wellbutrin and alcohol?
You can but you shouldn’t. You will get drunk a lot faster and it will destroy your liver greatly quicker. Only drink in moderation. – You can….it didn’t bother me much but ymmv. I found wellbutrin really made me want to smoke and drink less. Bupropion (the generic name of wellbutrin) have lately been…

Can you narrate a mothers blood type if you know her childrens blood types?
My brother and I are both A neg, but neither of my parents know their blood types. You can guess Then again, the child’s bloodtype is also determined by the father’s gene. If the child has: Mother can be: A / A,AB,O B / …

Can you newly grasp brain stem destruction..or does it nick while to form and does a ct scan show it?
was wondering about this,any answers? The best imaging for brain death is nuclear imaging. – Usually brain stem departure is from trauma, but if you had a bleed there (like from a CVA or stroke) it could possibly form gradually…

Can you nick pills next to dairy products?
My grandmother always told me not to take any medicine next to milk because it doesn’t allow it to digest or something properly? I’ve always followed this rule just in suitcase it WAS true.. but I was wondering if this was just an “dated wives tale” or if there is actually scientific…

Can you nickname 10 adjectives medicinal plants within found within India?
tulsi neem eucaluptus clove babul pu rajmari bel ginger(it does have medicinal uses) garlic ” – Malabar Nut Hophead Bell Weed Crested Lepidagathis Nongmangkha Singkrang Gandarusa Sage Leaved Alangium Sessile Joyweed Himalayan Thorowax ;-) – neem tulsi babul shikakai rajmari hansraj bel pu satyanashi..[LOL..wot a name] gokhulakanta -…

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Can you obtain elevated on coladapins?
im not sure of the spelling but i think there muscle relaxers. they are round and yellow? can you attain high off of them? and by it being small and washed out and round can someone tell me the mg Yes I’m sure you can. My wife uses them and they hold things up…

Can you obtain remunerated if you donate.?
blood and semen? I think I saw it a few times but im not sure if you actually get salaried for it. If yes, how much (like per grams or something)? Thanks Not sure about semen…but donating blood is something expected to be given from the heart – therefore, you are not compensated…

Can you OD on xanax and what happen if you do?
also, in case you give your answer contained by bars and because im curious anyway, about how many milligrams of xanax are surrounded by one xanax bar? xanax comes in different milligram strengths. it depends on the prescription amount. you can overdose on it, and it will cause you…

Can you offer me INformation on LSD?
OK. well i am doing this research paper on the drug LSD. well i cant appear to find what the drug was medically used for? so please help! It was used surrounded by psychiatric analysis- given to the mentally ill for the purpose of therapy. Some doctors want it to be allowed for…

Can you over dose on advil?
ok so i have a friend who claims that he over dosed on advil, and im not quite sure if that is possible so pleaseee backing me? [[: it’s a non-steroidal anti-inflammatory – the only major side effects are GI upset and decrease renal function. As it does however decrease renal function it may…

Can you overdose & die on 20 Robitussin pills?
I don’t know if i should take these gel Robitussin pills for cough. I want it to trip. Sure, i’ve tooken 14 Dramamine pills before, but this is 20. I’ve never had this frequent, Is it safe? I don’t want to die. Help me? Here’s a hint – when an notion…

Can you overdose (die) from Codeine (Tylenol 3)? If so whats the avg vicious dose? and is it a stinging extermination?
not suicidal. just curious tylenol 3 contains acetominophen so taking largish does over long periods can “kill” your liver so you can die painfully or prematurely see knit http://www.medscape.com/viewarticle/5570… – The idiot who described it as a “painless death”?…

Can you overdose after taking three zolpidems, five hydrocodones, and two klonopins?
If you take three zolpidems, five hydrocodones, two klonopins, and three ritalin at the same time, can you overdose? My heart isn’t beating hasty, all I feel is very chill and for a time tired. Yikes, that’s a lot of drugs! Don’t be surprised if you acquire a…

Can you overdose beside headache pills?
Yes, make sure you read the directions on the back, they will warn you and say aloud the limit of how many you take. You probably won’t be for always injured if you accidentally take one extra headache pill. – You can overdose on anything. It depends on the particular drug that you are…

Can you overdose from snorting cocaine?
Definitely yes. And it’s not just overdose. The amount causing fatality varies widely from character to person. Cocaine may cause a heart attack, a fatal heart arrhythmia or a life-threatening seizure. You only have to read the word recently about pitchman Billy Mays, disc jockey DJ AM, and most classically, John Belushi who had…

Can you overdose next to Motrin?
not like im going to kill myself, but the ideal hit me when i took two of them. can you overdose on motrin and if so how much is to much, cuz i hold this fear of dying by overdose and i want to no so i dont more than that. It can wreak…

Can you overdose on 8 hydroco/ibu 7.5-200 pills?
meaning die 60mg of hydrocodone is a pretty high dose for people near no tolerance to opiates. Expect severe nausea and itching. If you experience very shallow breathing, call 911. 1600 mg of ibuprofen is also a high dose but not vicious. Expect moderate abdominal pain and a hangover. Keep in mind…

Can you overdose on a food?
Like too many cranberries? it really depends on the food, some kids end up over dosing on a pernickety plant seed, which they get high past its sell-by date of. – I think you can overdose on any type of food I notice that when I have not be eating a certain type of…

Can you overdose on anti-depressants?
Asking because I know that not all meds will kill you if u try to overdose. So will anti-depressants do it? Yes. You can over-dose on anything. Whether it will kill you, do permanent damage, or none, is another story. Just in the region of any over-dose will make you feel sick&miserable though. – yes…

Can you overdose on Aspirin?
how many pills does it take? Yes you can overdose on Aspirin. In reality thousands die each year from taking just one pill. – yes you can OD on Aspirin. As far as how several pills it takes, well that depend on you body mass. However I wouldn’t recommend ODing on Aspirin because what will…

Can you Overdose on benadryl?
Im not suicidal just wanting to know…. Just for future reference and if you can how plentiful? Na you merely sleep it off and wake up feeling moral. – I mull over you’ll probably end up with such a dry mouth that even water wouldn’t minister to. The is the way benadryl works is by…

Can you overdose on birth control pills? accidently unsurprisingly?
I would assume especially if you smoke…it can cause a heart attack or stroke. – Yeah, if you took a whole bunch then you would go and get a dangerous amount of hormones. I don’t know what would happen though but I definitely wouldn’t want to find out. – no -…

Can you overdose on dope?
? no…u might be able to suffocate yourself someway – You can overdose on ANYTHING you ingest, including water (see http://en.wikipedia.org/wiki/KDND#Hold_Y… – no. no, you cannot. – As the old saying go, you know WHY they call it dope… Source(s): NJ RN – IF YOU EVER HEARD A LOT OF YOUNG PEOPLE TALKING ABOUT GETTING…

Can you overdose on herion taken vocally?
doing research for school thanks yes – Yes. You can die from it, I know a few people that have. – A person can overdose on any drug, if taken surrounded by excess. Heroin is in a calss of drugs known as opioid agonists. Typically they all do duplicate thing, which is bind…

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Cardiac markers new and old

Cardiac markers new and old

Introduction

Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream.

They are:

A: specific.

1.     Cardiac troponin I and cardiac troponin T

2.     Creatine kinase-MB isoenzyme (CK-MB).

B: Non specific.

Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury.

1.C-reactive protein

2.B-type natriuretic peptide

3.Copeptin

4.lactate dehydrogenase

5.Aspartatetransferase

6.myoglobin

7.ischemia modified albumin.

8.Glycogen phosphorylase isoenzyme BB.

9.Adiponectin.

10.Adrenomedullin.

A: specific.

1.Cardiac troponin I and cardiac troponin T .

The troponins are part of the actomyosin contractile apparatus of muscle cells. Structurally unique forms of troponin T and troponin I are found in cardiac tissue, enabling the development of immunoassays, which recognise only the cardiac forms of these two proteins. In most clinicalsituations both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) seem to offer similarly useful clinical information.

When a cardiac myocyte dies, CK-MB passes rapidly from the cytoplasm into the circulation and is cleared. In contrast, most of the troponin within the myocyte is found in the structural elements of the cell, so when necrosis occurs there is a steady leaching of troponin into the circulation. Consequently, troponin remains in the circulation for several days after a cardiac event.

Despite extended searching, there is currently no evidence that the cardiac troponins may be produced by tissues other than myocardium. However, the presence of cardiac troponin, while indicating that cardiac injury has occurred, provides no information as to the mechanism of injury. Cardiac troponin concentrations may rise in conditions unrelated to ischaemic damage such as pericarditis, trauma and sepsis. Such rises provide no information about the likelihood of future ischaemic cardiac disease.

When associated with coronary artery ischaemia even low concentrations of cardiac troponin predict an adverse outcome. This is regardless of whether the other WHO criteria for the formal diagnosis of myocardial infarction are met. The pathophysiological mechanism for these acute coronary syndromes is the presence of an unstable coronary plaque, with release of micro-emboli causing focal myocardial necrosis with release of cardiac troponin. The increased mortality is a reflection of a large thrombus separating from the unstable plaque.This improved understanding of the mechanism of the acute coronary syndrome, has led to a proposal to redefine myocardial infarction, using the presence of a cardiac biochemical marker, with some evidence of coronary artery ischaemia, as the central diagnostic criterion.

False positive troponin.

1.Cardiac troponins in patients with renal failure

A small proportion of patients with renal failure undergoing dialysis have detectable concentrations of cTnT. This finding was originally thought to be a false positive test, but careful analysis has shown that these patients do have a worse cardiac prognosis. When one considers that approximately 20% of patients on dialysis die each year and that cardiac disease is the commonest cause of mortality, this result is not unexpected. Although there is some increase in cTnI in dialysis patients, this appears to be one area where cTnT is more informative.

2.Problems with assays for cardiac troponin I

Cardiac troponin I is prone to modification in the circulation. It may be phosphorylated and oxidised and can exist as a complex with either cTnT or cardiac troponin C. This has some clinical relevance, because the different antibodies used in commercial assays may recognise these different molecular forms to varying extents. A major problem with cTnI assays is that the different assays are calibrated with different standards. The same blood sample may give quite different apparent concentrations in different assays. If it is accepted that the presence of any cardiac troponin in the presence of coronary artery ischaemia indicates a worse prognosis, then the absolute concentration is less important.

2.Creatine kinase-MB isoenzyme (CK-MB) .

Creatine kinase (CK) and more particularly its isoenzyme CK-MB still have a formal place in defining myocardial infarction. However the current definition is not a particularly useful one because studies have shown that, as currently defined, patients with myocardial infarction and unstable angina have similar outcomes.

Interpretation of CK-MB is problematic, with both false positives and false negatives occurring. While CK-MB is relatively cardiac-specific, even healthy people may have low concentrations of this isoenzyme in their blood. People with chronic myopathies may have high concentrations of CK-MB because it is produced by regenerating skeletal muscle. A high concentration of CK-MB may therefore be unrelated to cardiac disease (false positive).

The half-life of CK-MB in the circulation is relatively short (approximately 12 hours). Samples collected many hours after an infarction may have both a low absolute concentration of CK-MB and a low ratio of CK-MB to total CK (due to the longer half-life of the major isoenzyme, CK-MM). This can give a false negative result.

Some specialists believe that it is no longer appropriate to use CK-MB in the diagnosis of myocardial infarction. It may be more helpful for investigating possible reinfarction, where its short half-life may be useful compared to the longer time that cardiac troponins spend in the circulation.

B:non specific.

1.C-reactive protein

C-reactive protein (CRP) is an acute phase reactant produced by the liver in response to cytokine release during inflammation. It has long been used in clinical practice to follow systemic inflammation, especially bacterial infection. More recently, epidemiological evidence has shown that basal levels of CRP, in the absence of apparent inflammatory disease (so-called hs-CRP) may be informative in predicting future myocardial or cerebrovascular events.

The value of hs-CRP appears to relate to activity in the atherosclerotic plaque. Amongst the cellular elements of the atherosclerotic plaque are inflammatory cells, which, by releasing interleukin-6, cause secretion of CRP into the circulation. In the Physicians’ Health Study, when people in the highest quartile of CRP values were compared to people with the lowest quartile of CRP values, they had a relative risk of future myocardial infarction of 1.9. In the Women’s Health Study the relative risk was 4.4.

There are a number of problems in using CRP measurements to predict the likelihood of future cardiovascular events. These are both biological and analytical.

Biological variability in basal CRP concentration is considerable. Even mild, subclinical infections can cause significant increases in CRP concentration that are unrelated to cardiovascular disease. For this reason, no measurements should be made within two weeks of any infection. Even with this precaution, CRP concentrations may vary markedly. Several studies have investigated the variability of the CRP concentration in blood collected repeatedly from individuals over periods of weeks to months. The standard deviation for each individual varies from 30% to 63% of the mean value.Thus it might be highly misleading to contemplate using a single measurement to guide possible therapy. It has been proposed that two separate measurements should be made on each individual, while they are quite well, and at intervals of more than a week apart. The lowest value is then used to determine which quartile the person is in. Even this approach may be insufficient to correct for the variability.

There are outstanding laboratory problems with use of hs-CRP. Not all assays produce identical results. No laboratory has the resources to determine its own reference ranges, so transportability of results between assays is obviously of great importance in defining the concentrations that relate to the different quartiles of basal CRP concentration. At the present time it appears undesirable to attempt to use hs-CRP in individual risk stratification.

2 .B-type natriuretic peptide

The cardiac natriuretic peptide family of neuro-endocrine hormones has a complex physiological role in modulating blood volume and pressure. This involves natriuresis and diuresis as well as antagonism to the angiotensin-renin system. These peptides are also antimitotic and may modulate cardiac hypertrophy. In the presence of left ventricular dysfunction, with worsening cardiac failure, the concentration of plasma B-type natriuretic peptide (BNP) increases in proportion to the New York Heart Association’s (NYHA) classification of severity. However, there are a number of other pathophysiological states in which BNP may be elevated, such as hypertension and cardiac hypertrophy, pulmonary hypertension and renal disease. The most appropriate use of this marker remains to be defined.

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As with cTnI, several different assays for BNP or its associated peptides (e.g. NT-proBNP) have been used in the published studies. As these assays are not yet standardised, numerical values from one assay cannot be compared quantitatively with those from another.

B-Type Natriuretic Peptide: Prognostic in Heart Failure?
Many patients hospitalized with acute exacerbations of heartfailure are cared for by primary care physicians after discharge.Although some patients avoid rehospitalization within the next6 months, others are prone to multiple hospital admissions.Recently, BNP determinations have shown the potential to bea good prognostic marker for morbidity and mortality in patientswith heart failure, including predicting future cardiac eventin patients with acute exacerbations

One prospective study found that an initial BNP concentrationof 480 pg/mL had a sensitivity of 68%, specificity of 88%, andan accuracy of 85% of predicting a congestive heart failureendpoint (death, hospital admissions, and repeated emergencydepartment visits) after a 6-month follow-up period after hospitaldischarge. Patients with BNP levels greater than 480 pg/mLhad a 51%, 6-month cumulative probability of a heart failureevent (35% of these patients had death from heart failure astheir event), whereas BNP levels of less than 250 pg/mL hada much better prognosis, with only a 2.5% cumulative probabilityof a heart failure event. The authors reported that increasedBNP levels were associated with progressively worse prognosis.

Another well-designed study compared BNP levels with the patient’sheart failure survival score (HFSS), a recognized and acceptedtool in determining a patient’s prognosis. Patientswere classified into three different prognostic groups basedon the HFSS score: low risk, medium risk, or high risk. Therewere significant differences in each group. The mean BNP concentrationfor the low-risk group was 95.7 ± 11.2 pg/mL, for themedium-risk group was 244.4 ± 33.4 pg/mL, and for thehigh-risk group was 419.9 ± 55.5 pg/mL. More importantly,the authors were able to show that higher BNP levels were associatedwith a change in cardiovascular functional class with time.The initial BNP level in patients who improved during the ensuing12 months had a BNP concentration of 42.4 ± 8.6 pg/mL,those who remained stable had a BNP level of 102.2 ±16.1 pg/mL, and those who deteriorated during the ensuing 12months had a BNP level of 256.9 ± 28.5 pg/mL.

B-Type Natriuretic Peptide and Therapeutic Monitoring of Heart Failure
Primary care physicians have the task of managing patients withcongestive heart failure. An important aspect of patient managementis the ability to monitor the therapeutic efficacy of the patient’spharmacological regimen. BNP levels have been found to followventricular function in response to medical management.

One study evaluated left ventricular volume and mass, includingneurohormone levels, in patients with mild to moderate nonischemiccongestive heart failure before and after 4 months of treatmentwith spironolactone or placebo. Patients who received a fixed25-mg dose of spironolactone had a change in their mean BNPconcentration from 200 ± 66 pg/mL at baseline to 89.7± 27 pg/mL at 4 months (P< .01), whereas the controlgroup showed no significant change.

Another study managed to show that BNP-guided treatment of heartfailure reduced total cardiovascular events and delayed timeto first event compared with intensive clinically guided treatment.The BNP concentration decreased 79 pmol/L in the BNP-guidedgroup compared with 3 pmol/L in the clinically-guided group.More importantly, the primary combined clinical endpoint (cardiovasculardeath, hospital admission, and outpatient heart failure) wassignificantly reduced in the BNP-guided group (P< .02).This significance increased when covariates were accounted for(baseline left ventricular ejection fraction, baseline BNP,and medication dosages, New York Heart Association heart failureclass, and systolic blood pressure) in the regression model(P< .001). The authors suggested that BNP-guided treatmentrepresents a preventive strategy targeting more intensive pharmacotherapyand follow-up for patients with elevated circulating BNP levelswho are at high risk of cardiovascular events.

Although both studies describe an important use of BNP, thesmall study sizes should raise caution when applying these findingsto clinical practice

3.Copeptin

Approximately 15 million patients present to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) every year. The vast majority (70 to 80%) of them finally prove not to have AMI. However, due to a delayed increase of circulating levels of Troponin it takes up to six hours before it can be measured. Therefore serial blood sampling is recommended by the European Guidelines. Study results indicate that by testing for both markers, along with an Electrocardiogram (ECG) and the clinical findings, approximately two-thirds of the patients would not need to wait those six hours in the ED for the second Troponin test. This may obviate the need for prolonged monitoring and serial blood sampling in the majority of patients.

“In the very situation of a patient presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) the clinician quickly needs to know whether the person is in real danger or not. Ruling out AMI in this setting is an urgent and unmet need. The use of Copeptin together with Troponin can accelerate the rule out of AMI and thus improves patient management in the ED immensely. Two thirds of these patients may be ruled out with the first blood draw and most of them probably could leave the ED very soon,” explained Dr. Tobias Reichlin from the Department of Internal Medicine at the University Hospital, Basel, Switzerland. While the concentration of Troponin rises four to six hours after the event of an AMI, concentrations of the new Copeptin biomarker are highest right after the onset of symptoms and then begin to drop. This difference makes the use of the combination of the two extremely promising.

The study was conducted in the University Hospital of Basel, Switzerland. In 487 consecutive patients presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI), the research team measured levels of copeptin at presentation, using a novel sandwich immunoluminetric assay in a blinded fashion. The final diagnosis was adjudicated by two independent cardiologists using all available data.

The adjudicated final diagnosis was Acute Myocardial Infarction (AMI) in 81 patients (17%). Copeptin levels were significantly higher in AMI patients compared with those in patients having other diagnoses (median 20,8pmol/l vs. 6,0 pmol/l, p<0,001). The combination of Troponin and Copeptin at initial presentation resulted in an area under the receiver-operating characteristic curve of 0,97 (95% confidence interval: 0,95 to 0,98), which was significantly higher than the 0,86 (95% confidence interval: 0,80 to 0,92) for Troponin alone (p<0,001). A Copeptin level < 14 pmol/l in combination with a Troponin ? 0,01 µg/l correctly ruled out AMI with a sensitivity of 98,8% and a negative predictive value of 99,7%.

Copeptin, the C-terminal part of the vasopressin prohormone, is a marker of acute endogenous stress. Arginine vasopressin (AVP) is a key hormone in the human body. Despite the clinical relevance of AVP in maintaining fluid balance and vascular tone, measurement of mature AVP is difficult and subject to preanalytical errors. Recently, Copeptin, a 39-amino acid glycopeptide that comprises the C-terminal part of the AVP precursor (CT-proAVP), was found to be a stable and sensitive surrogate marker for AVP release, analogous to C-peptide for insulin. Copeptin measurement has been shown to be useful in various clinical indications, including the diagnosis of diabetes insipidus and the monitoring of sepsis and cardiovascular diseases.

Copeptin is scheduled for fall introduction on the European market and joins a series of excellent BRAHMS biomarkers for cardiovascular diseases. The study results were already presented in a Late Breaking Clinical Trial Session at the ACC-Meeting in March. It marks the third time in just a few months that BRAHMS, with a new cardiac marker, succeeded in joining a Late Breaking Clinical Trial Session at a major cardiology congress.

The BRAHMS Aktiengesellschaft conducts researches, develops, produces and markets innovative diagnostic biomarkers. It is one of the three largest biotechnology companies in Germany. The company sells its products in more than 65 countries via its own subsidiary companies and sales organizations as well as laboratory systems from its own production and globally operating licensees. The headquarter of BRAHMS is at Hennigsdorf / Berlin, where about 220 out of 400 of the world wide employees of the company are posted.

4.lactate dehydrogenase

Peak in  72 hours

Lactate dehydrogenase catalyses the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. LDH levels are also high in tissue breakdown or hemolysis. It can mean cancer, meningitis, encephalitis, or HIV. this usually back to normal 10–14 days.

5.Aspartate transaminase

(AST) This was the first used.It is not specific for heart damage, and it is also one of the liver function tests.

6.Myoglobin.

Rinsing in 2 hours.

Myoglobin is used less than the other markers. Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis.

7.Ischemia-modified albumin.

(IMA) low specificity IMA can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB test has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required.

8.Glycogen phosphorylaseisoenzyme BB

High sensitivity and specificity early after chest pain.Glycogenphosphorylaseisoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue. Because of the blood-brain barrier GP-BB can be seen as heart muscle specifc. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the “new cardiac markers” which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1-3 hours after process of ischemia.

9.Adiponectin.

ADIPONECTIN IS AN adipocyte-derived protein that has gainedconsiderable interest due to its positive effects on insulinsensitivity , atherosclerosis , and inflammation , hereby linking adipose tissue with the cornerstones of themetabolic syndrome.

There is substantial experimental and clinical evidence thatadiponectin protects the vascular endothelium against the processesleading to atherosclerosis. Experimentally, adiponectinknockout animals show an increased neointimal formation aftervascular injury as compared with wild-type littermates ,whereas adiponectin-deficient mice infected with an adenovirusoverexpressing mouse adiponectin showed a normal vascular responseto injury . Furthermore, in the ApoE-deficient mouse, a modelof accelerated atherosclerosis, breeding with adiponectin transgenicmice inhibited the progression of atherosclerosis despite anunaltered glucose and lipid metabolism, suggesting that adiponectinpossessed direct antiatherogenicactions .

In keeping with the experimental support for a vasoprotectiveeffect of adiponectin, several clinical investigations basedon cross-sectional study cohorts have reported on reduced circulatingadiponectin levels in patients with verified coronary heartdisease (CHD). However, some studies have not beenable to demonstrate an association between low levels of adiponectinand an increased risk for CHD , and others have shown thatthe relationship becomes insignificant after adjustment forhigh-density lipoprotein (HDL) cholesterol . On theother hand, nested case control studies have shown that healthysubjects with adiponectin levels within the upper 20% rangehave a 2-fold reduced risk for myocardial infarction  anda 7-fold reduced risk for progression of coronary artery calcification. We are not aware of studies describing the relationshipbetween adiponectin and the risk for CHD in population-basedcohorts.

Insulin resistance is a major risk factor for the developmentof atherosclerosis , and it also affects plasma levelsof adiponectin, which become gradually decreased with increasinginsulin resistance . Although adiponectin exerts potentinsulin-sensitizing actions in experimental in vivo models, it remains to be clarified whether the inverse associationbetween adiponectin and insulin sensitivity is a cause-effectrelationship. Thus, it could be speculated that the observedrelationship between adiponectin and the risk for CHD simplyreflects changes in insulin sensitivity. Based on these considerations,we found it of interest to study the risk for CHD and its relationshipwith plasma adiponectin and measures of insulin sensitivityin a population-based cohort of healthy 70-yr-old men followedfor more than 10 yr.

10.Adrenomedullin.

Adrenomedullinis a 52-amino acid peptide originally isolatedfrom pheochromocytoma cells. It has been detected in arange of tissues, including the heart, vasculature, kidney,adrenal medulla, lung, and brain. In experimental heartfailure, adrenomedullin expression is increased and peptidelevels rise, and administered peptide has powerful vasodilatoreffects, increases cardiac output and is natriuretic.Plasma concentrations are in the low picomolar range in healthyindividuals, but they increase in those with hypertension andcongestive heart failure (CHF) in proportion to the severityof the disease. In heart failure, plasma adrenomedullinis inversely related to left ventricular ejection fraction (LVEF)and is positively associated with left ventricular (LV) end-diastolicpressure. At least two reports have indicated that plasmaadrenomedullin levels act as an indicator of prognosis afteracute MI.

There are no published data relating plasma concentrations ofeither N-BNP or adrenomedullin to cardiovascular prognosis inpatients with established ischemic LV dysfunction. We hypothesizedthat plasma levels of either or both peptides would have independentprognostic utility in such patients and also assist in predictingany benefit from treatment with carvedilol. We report the resultsfrom 297 patients with ischemic LV impairment who were randomlyassigned to treatment with carvedilol or placebo for CHF

 

 

 

 

 

 

Kinetics of cardiac markers in myocardial infarction with or without reperfusion treatment.

 

 

 

References

1. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined – a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am CollCardiol 2000;36:959-69.

2. Schroeder JS, Lamb IH, Hu M. Do patients in whom myocardial infarction has been ruled out have a better prognosis after hospitalization than those surviving infarction? N Engl J Med 1980;303:1-5.

3. Hamm CW, Braunwald E. A classification of unstable angina revisited. Circulation 2000;102:118-22.

4. Pennell JP. Optimizing medical management of patients with pre-end-stage renal disease. Am J Med 2001;111:559-68.

5. Chen HH, Burnett JC Jr. The natriuretic peptides in heart failure: diagnostic and therapeutic potentials. ProcAssoc Am Physicians 1999;111:406-16.

6. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001;103:1813-8.

7. Campbell B, Badrick T, Flatman R, Kanowski D. Limited clinical utility of high-sensitivity plasma C-reactive protein assays. Ann ClinBiochem 2002;39:85-8. BRAHMS Aktiengesellschaft

http://www.innovations-report.com/html/reports/life_sciences/cardiac_marker_copeptin_accelerates_diagnosis_acute_135172.html

9.http://en.wikipedia.org/wiki/Reference_ranges_for_blood_tests#Cardiac_tests.for cardiac markers refrencereanges.

10.http://content.onlinejacc.org/cgi/content/full/37/7/1781.foradrenomedullin.

 

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Stem cell and cell reprogramming as regenerative medicine

Stem cell and cell reprogramming as regenerative medicine

Stem cell therapy and stem cell research have been a hotly debated topic over recent years. Most of us may have general understanding of the controversy, but we may be unaware of the specific issues surrounding stem cell therapy and its research. A trial on a patient with severe spinal injuries is the first to test a treatment that has huge potential to cure disease and disability. But it also highly controversial and considered unethical among many Christian and pro-life groups. Research in the stem cell field grew out of findings by Canadian scientists E.A McCulloch and James E. Till in the1960s (1,2).

Three types of mammalian stem cells are as follows:

Embryonic stem cells are isolated from the inner cell mass of blastocysts. A blastocyst is an early stage embryo- approximately four to five days old in humans and crossing of 50-150 cells. Embryonic stem cells are pluipotent and give rise during development to all derivatives of the three primary germ layers: ectoderm, endoderm and mesoderm, In other words, they can develop into each of the more than 200 cell types of the adult body when given sufficient necessary stimulation for a specific cell type. They do not contribute to the extra-embryonic membranes or the placenta (3).

Adult stem cells that are found in adult tissues. The term adult stem cell refers to any cell which is found in developed organism that has two properties: the ability to divide and create another cell like itself and also divide and create a cell more differentiated than itself. Pluripotent adult stem cells are rare and generally small in number of tissues including umbilical cord blood (3).

Fetal stem cells are primitive cell types found in the organs of fetuses. The classification of fetal stem cells remains unclear and this type of stem cell is currently often grouped into adult stem cell (3).

Potency specifies the differentiation potential (the potential to differentiate into different cell types) of the stem cell. Totipotent or omnipotent stem cells can differentiate into embryonic and extraembryonic cell types. Such cells can construct a complete, viable organism. These cells are produced from the fusion of an egg and sperm cell. Cells produced by the first few divisions of the fertilized egg are also totipotent. Pluripotent stem cells are the descendants of totipotent cells and can differentiate into nearly all cells, i.e. cells derived from any of the germ layers. . Multipotent stem cells are partially differentiated, so that they can form a restricted number of tissue types. Multipotent stem cells can be found in the fetus, in numerous adult tissues and umbilical cord blood. The stem cells can become any tissue in the body, excluding placenta. Pluripotent embryonic stem cells originate as inner mass cells within blastocyst . Only the morula’s cells are totipotent, able to become all tissues and a placenta (3).

Stem cells and progenitor cells in adult organisms act as repair system for the body, replenishing specialized cells, but also maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.  Human stem cell research is both a controversial as well as a cutting-edge technology. Medical researchers believe that stem cell therapy has the potential to dramatically change the treatment of human disease. A number of adult stem cell therapies already exist, particularly bone marrow transplants that are used to treat leukemia. On one hand it promises to revolutionize medicine while on the other hand it raises a host of ethical issues. A stem cell is capable of developing into other types of cells, like kidney cells, liver cells, heart cells, etc. Stem cells circulate and function to replace dysfunctional cells, naturally maintaining optimal health.

There are many advantages and disadvantages to stem cell therapy and research.

Advantages:

It provides medical benefits in the fields of therapeutic cloning and regenerative medicine.
It provides great potential for discovering treatments and cures to a plethora of diseases including Parkinson’s disease, schizophrenia, Alzheimer’s disease, Cancer, spinal cord injuries, diabetes and many more.
Limbs and organs could be grown in a lab from stem cells and then used in transplants or to help treat illnesses.
It will help scientists to learn about human growth and cell development.
Scientists and doctors will be able to test millions of potential drugs and medicine, without the use of animals or human testers. This necessitates a process of simulating the effect the drug has on a specific population of cells. This would tell if the drug is useful or has any problems.
Stem cell research also benefits the study of developmental stages that cannot be studied directly in a human embryo, which sometimes are linked with major clinical consequences such as birth defects, pregnancy loss and infertility. A more comprehensive understanding of normal development will ultimately allow the prevention or treatment of abnormal human development.
It holds the key to reversing the effects of aging and prolonging our lives. Stem cell research has already found many treatments that help slow the aging process, and a bonus of further stem cell research is a possible ‘cure’ for aging altogether.
The usage of adult stem cells to treat disease is that a patient’s own cells could be used to treat a patient. Risks would be quite reduced because patients’ bodies would not reject their own cells.
An advantage of using embryonic stem cells is that they can develop into any cell types of the body, and may then be more versatile than adult stem cells.

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Disadvantages:

The use of embryonic stem cells for research involves the destruction of blastocysts formed from laboratory-fertilized human eggs. For those people who believe that life begins at conception, the blastocyst is a human life and to destroy it is immoral and unacceptable.
 Like any other new technology, it is also completely unknown what the long term effects of such an interference with nature could materialize.
Embryonic stem cells may not be the solution for all ailments.
According to a new research stem cell therapy was used on heart disease          patients. It was found that it can make their coronary arteries become narrower.
A disadvantage of most adult stem cells is that they are pre-specialized, for instance, blood stem cells make only blood, and brain stem cells make only brain cells.
A disadvantage of embryonic stem cells is that they are derived from embryos that are not a patient’s own and the patient’s body may reject them.

The results of the procedure, carried out by privately funded US company Geron, will be awaited eagerly around the by doctors and scientists working in regenerative medicines. If a success, it could be the catalyst to open up stem treatments from nerve damage, to Alzheimer’s disease to diabetes. Professor Chris Mason, an expert in regenerative medicine at University College of London, said it marked the dawn of the ‘stem cell age’. He also stated that this pivotal clinical trial is a major morale boost for scientists, clinicians and most of all patients by finally commencing the transformation of stem cells from a scientific curiosity into advanced health care.

Millions of embryonic stem cells, which come from human embryos left over from fertility treatments, are injected into the damaged area. The hope is that they will travel to the site of the damaged tissue and help the tissue regenerate. Thomas  Okarma, chief executive of Geron, said that it is a milestone for the field of human embryonic stem cell-based therapies.

Embryonic stem cells are master cells found in human embryos, which give rise to more than 200 specialized types of tissue in the adult body, and can be grown into any kind of tissue to replace cells damaged by injury or disease. Use of embryonic stem cells is controversial because they must be harvested from human embryos that are destroyed in the process. This has raised moral objection from those who believe that embryos have the same right as humans and see the treatment as unethical. At long last researchers have proved that they can make human embryonic stem cells (hESCs) without destroying embryos. This may got round some moral objections to embryo research, but more importantly it has brought to light a substance that should help cell stem cell researchers improve their craft (4). That substance is laminin – a protein found in the basement membranes underlying layers of skin. It made all the difference to work by Lanza and his team at Advanced Cell Technology, a company in Worcester, Massachusetts, who reported creating hESCs from human embryos without destroying them. Lanza proved that hESCs could be generated from blastomeres, but none of the embryos he took them from survived. Also, just 2 per cent of his blastomeres generated hESCs, so large numbers of embryos were needed. But when laminin was added to the dishes in which the embryos were grown, the majority of them survived the removal of blastomere, and 20 to 50 per cent of the blastomeres went on to generate hESCs- about the same success rare as when taking hESCs directly from embryos. Laminine appears to stop newly extracted blastomeres from turning into useless trophectoderm cells from which placenta originates, and instead encourages them to turn into hESCs.

New techniques circumvent a road block to the production of embryonic stem cell-like lines from adult tissue. Such reprogrammed cell lines should be much safer to use for therapy. Shinya Yamanaka’s amazing discovery (5) that cells from differentiated tissues can be reprogrammed into induced pluripotent stem (iPS) cells- cells that can potentially differentiate into any cell type- has transformed research in stem- cell biology and regenerative medicine. Transgenic expression of just four defined transcription factors (c-Myc, Klf4, Oct4 and Sox2) is sufficient to reprogram somatic cells to a pluripotent state  virus-free integration of reprogramming genes, followed by their removal. Woltjen et al (6) and Kaji et al (7) combined powerful technologies, developed independently, to overcome many of the difficulties others encountered in attempting virus-free reprogramming. These groups also made use of the virally derived 2A- peptide sequence to create multi-protein expression vectors incorporating all of the reprogramming genes. Instead of retroviruses or plasmids, however, they used the piggyback transposon/transposase gene-delivery system. This vector can easily integrate into the genome. But more importantly, the integrated DNA can also be removed from the genome- through transient expression of the transposase enzyme- in a highly efficient and seamless fashion, leaving no trace of the integration in the genome of the iPS cells. The use of the 2A peptide is crucial, not just because it allows delivery of all of the required reprogramming genes in a single construct, but also because it makes complete excision of the foreign constructs much easier (6,7)

Vierbuchen et al (8) maintain the pace of this research by describing a potential innovation for generating disease-specific and patient-specific tissues of the central nervous system (CNS) that does not rely on stem cells. The route to possible regenerative-medicine-based treatment of CNS disorders such as epilepsy, stroke and Parkinson’s disease may have taken another unexpected turn. They reported that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. Starting  from a pool of 19 candidate genes, they (8) identified a combination of only three factors, AscI1, Brn2 and Myt1I, that suffice to rapidly and efficiently convert mouse embryonic and postnatal fibroblasts into functional neurons in vitro. These induced neuronal (iN) cells express multiple neuron-specific proteins, generate action potentials and form functional synapses.

As is the case for embryo-derived stem cells, application of reprogrammed human induced pluripotent stem cells is limited by our understanding of lineage specification. Here Bhatia (9) demonstrated the ability to generate progenitors and mature cells of the haematopoietic fate directly from human dermal fibroblasts without establishing pluripotency. Ectopic expression of OCT4 (also called POU5F1)-activated hematopoietic transcription factors, together with specific cytokine treatment, allowed generation of cells expressing the pan-leukocyte marker CD45. These unique fibroblast-derived cells gave rise to granulocytic, monocytic, megakaryocytic and erythroid lineages, and demonstrated in vivo engraftment capacity. They (9) noted that adult haematopoietic programs are activated, consistent with bypassing the pluripotent state to generate blood fate: this is distinct from hematopoiesis involving pluripotent stem cells, where embryonic programs are activated. These findings demonstrated restoration of multipotency from human fibroblasts, and suggested an alternative approach to cellular  reprogramming for autologous cell-replacement therapies that avoids complications associated with the use of human pluripotent stem cells.

Scientists have coaxed adult human skin into producing blood, a breakthrough that could offer an alternative source of the vital fluid to cancer patients or those undergoing surgery.  What’s more, the procedure is simple- there is no need to first convert the skin cells (which actually deliver the different types of cells), a step that is essential to other such processes (9).

The scientists- led by Mickie Bhatia, director of McMaster’s Stem Cell and Cancer Research Institute at the Michael G. DeGroote School of Medicine, and main author of the study- found that a protein called OCT4 can reprogramme skin stem cells obtained from a patch of human skin into blood without resorting to any intermediary steps. They further refined the process by adding several other growth factors, which improve the efficiency (9). Normally, blood is produced in the bone marrow. For scientific and therapeutic applications, in recent times, blood cells have also been harvested from preserved umbilical cords and placentas. This has given rise to whole new industry that works towards preserving cord blood for future use. Bhatia hopes that clinical trials will begin in 2012.

The most efficient stem cells are embryonic stem cells which, as the name suggests, are derived from human embryos. Apart from ethical issues, there are biological concerns that the cells might be rejected when transplanted into an adult and also that their source is limited.  Truly, the controversy over cell reprogramming research will continue to rage furiously. We hope there is some novel scientific innovation of human cell reprogramming in the future, it could be quickly applied to the creation of disease-specific cells for disease modeling and regenerative drug discovery, and to understanding the genetic and epigenetic mechanisms that determine the cell fate.

References:

Becker A.J, McCulloch E.A, Till J.E, Nature, 197:452-454 (1963).
Siminovitch L, McCulloch E.A, Till J.E, J.Cell.Comp.Physiol, 62: 327-336 (1963).

http://en.wikipedia.org/wiki/Stem_cell_research

Coghlan. A . NewScientist, 19th January, 2008
Takahashi, K and Yamanaka, S. Cell, 126:663-676(2006).
Woltjen, K et al. Nature, 458: 766-770 (2009).
Kaji, K et al. Nature, 458: 771-775 (2009).
Vierbuchen, T et al. Nature, 463: 1035-1041 (2010).
Szabo, E. et al. Nature, 468: 521-526 (2010).

I was born in Kolkata, Qualified Ph.D on 1989 from Calcutta University (Spl. Endocrinology), acquired research experience of more than 22 years with publications of around 29 papers in various national / international journals , acquired teaching experience of more than 15 years, acquired experience of writing biology text book under ISC course which is currently under Cambridge press (Kolkata) for publication. Awarded Sangit Prabhakar and Prayag Sangit Samiti in Indian Classical music.  Awarded certificate of appreciation – Celebrations of the centenary of Ramkrishna Mission & of Swamy Vivekananda’s historic return from west in 1897 as well as of 66th foundation day of the pratisthan.  Ramakrishna Mission Seva Pratisthan (Kol-India), expressed its participation of my contribution to the success of the seminar in 1997. 

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Acne Vulgaris

Acne Vulgaris

Terminology

Different types of Acne Vulgaris: A: Cystic acne on the face, B: Subsiding tropical acne of trunk, C: Extensive acne on chest and shoulders.

The term acne comes from a corruption of the Greek (acne in the sense of a skin eruption) in the writings of Atius Amidenus. Used by itself, the term “acne” refers to the presence of pustules and papules. The most common form of acne is known as “acne vulgaris”, meaning “common acne”. Many teenagers get this type of acne. Use of the term “acne vulgaris” implies the presence of comedones.

The term “acne rosacea” is a synonym for rosacea, however some individuals may have almost no acne comedones associated with their rosacea and prefer therefore the term rosacea. Chloracne is associated with exposure to polyhalogenated compounds.

Causes of acne

Acne develops as a result of blockages in follicles. Hyperkeratinization and formation of a plug of keratin and sebum (a microcomedo) is the earliest change. Enlargement of sebaceous glands and an increase in sebum production occur with increased androgen (DHEA-S) production at adrenarche. The microcomedo may enlarge to form an open comedone (blackhead) or closed comedone (whitehead). Whiteheads are the direct result of sebaceous glands becoming clogged with sebum, a naturally occurring oil, and dead skin cells. In these conditions the naturally occurring largely commensal bacteria Propionibacterium acnes can cause inflammation, leading to inflammatory lesions (papules, infected pustules, or nodules) in the dermis around the microcomedo or comedone, which results in redness and may result in scarring or hyperpigmentation.

Primary causes

A 16 year-old teenager with acne on his cheek.

Acne is known to be partly hereditary, but no particular genetic cause has been identified. Acne is not contagious or infectious. Several factors are known to be linked to acne:

Family/Genetic history. The tendency to develop acne runs in families. For example, school-age boys with acne often have other members in their family with acne as well. A family history of acne is associated with an earlier occurrence of acne and an increased number of retentional acne lesions.

Hormonal activity, such as menstrual cycles and puberty. During puberty, an increase in male sex hormones called androgens cause the follicular glands to grow larger and make more sebum.

Inflammation, skin irritation or scratching of any sort will activate inflammation.

Stress. While the connection between acne and stress has been debated, scientific research indicates that “increased acne severity” is “significantly associated with increased stress levels.” The National Institutes of Health (USA) list stress as a factor that “can cause an acne flare.” A study of adolescents in Singapore “observed a statistically significant positive correlation [] between stress levels and severity of acne.”

Hyperactive sebaceous glands, secondary to the three hormone sources above.

Bacteria in the pores. Propionibacterium acnes (P. acnes) is the anaerobic bacterium that causes acne. In-vitro resistance of P. acnes to commonly used antibiotics has been increasing.

Use of anabolic steroids.

Exposure to certain chemical compounds. Chloracne is particularly linked to toxic exposure to dioxins, namely Chlorinated dioxins.[citation needed]

Acne on an arm.

Several hormones have been linked to acne: the androgens testosterone, dihydrotestosterone (DHT) and dehydroepiandrosterone sulfate (DHEAS), as well as insulin-like growth factor 1 (IGF-I).

Development of acne vulgaris in later years is uncommon, although this is the age group for Rosacea which may have similar appearances. True acne vulgaris in adult women may be a feature of an underlying condition such as pregnancy and disorders such as polycystic ovary syndrome or the rare Cushing’s syndrome. Menopause-associated acne occurs as production of the natural anti-acne ovarian hormone estradiol fails at menopause. The lack of estradiol also causes thinning hair, hot flashes, thin skin, wrinkles, vaginal dryness, and predisposes to osteopenia and osteoporosis as well as triggering acne (known as acne climacterica in this situation).

Diet

Chocolate

The popular belief that chocolate intake, in and of itself, is a cause of acne is not supported by scientific studies. As discussed below, various studies point not to chocolate, but to the high glycemic nature of certain foods containing simple carbohydrates as a cause of acne. Chocolate itself has a low glycemic index.

Milk

Recently, three epidemiological studies from the same group of scientists found an association between acne and consumption of partially skimmed milk, instant breakfast drink, sherbet, cottage cheese, and cream cheese. The researchers hypothesize that the association may be caused by hormones (such as several sex hormones and bovine insulin-like growth factor 1 (IGF-1)) or even iodine present in cow milk.

Carbohydrates

The long-held belief that there is no link between diets high in refined sugars and processed foods, and acne, has recently been challenged. The previous belief was based on earlier studies (some using chocolate and Coca-Cola) that were methodologically flawed. The recent low glycemic-load hypothesis postulates that rapidly digested carbohydrate foods (such as soft drinks, sweets, white bread) produce an overload in blood glucose (hyperglycemia) that stimulates the secretion of insulin, which in turn triggers the release of IGF-1. IGF-1 has direct effects on the pilosebaceous unit (and insulin at high concentrations can also bind to the IGF-1 receptor) and has been shown to stimulate hyperkeratosis and epidermal hyperplasia. These events facilitate acne formation. Sugar consumption might also influence the activity of androgens via a decrease in sex hormone-binding globulin concentration.

In support of this hypothesis, a randomized controlled trial of a low glycemic-load diet improved acne and reduced weight, androgen activity and levels of insulin-like growth factor binding protein-1. High IGF-1 levels and mild insulin resistance (which causes higher levels of insulin) had previously been observed in patients with acne. High levels of insulin and acne are also both features of polycystic ovarian syndrome.

According to this hypothesis, the absence of acne in some non-Westernized societies could be explained by the low glycemic index of these cultures’ diets. It is possible that genetic reasons account for there being no acne in these populations, although similar populations (such as South American Indians or Pacific Islanders) do develop acne. Note also that the populations studied consumed no milk or other dairy products.

Further research is necessary to establish whether a reduced consumption of high-glycemic foods, or treatment that results in increased insulin sensitivity (like metformin) can significantly alleviate acne, though consumption of high-glycemic foods should in any case be kept to a minimum, for general health reasons. Avoidance of “junk food” with its high fat and sugar content is also recommended.

Vitamins A and E

Studies have shown that newly diagnosed acne patients tend to have lower levels of vitamin A circulating in their bloodstream than those who are acne free. In addition people with severe acne also tend to have lower blood levels of vitamin E.

Hygiene

Acne is not caused by dirt. This misconception probably comes from the fact that blackheads look like dirt stuck in the openings of pores. The black color is not dirt but simply oxidized keratin. In fact, the blockages of keratin that cause acne occur deep within the narrow follicle channel, where it is impossible to wash them away. These plugs are formed by the failure of the cells lining, the duct, to separate and flow to the surface in the sebum created there by the body. Built-up oil of the skin can block the passages of these pores, so standard washing of the face could wash off old oil and help unblock the pores.

Treatments

Available treatments

There are many products available for the treatment of acne, many of which are without any scientifically proven effects. Generally speaking, successful treatments show little improvement within the first two weeks, instead taking a period of approximately three months to improve and start flattening out.[citation needed] Many treatments that promise big improvements within two weeks are likely to be largely disappointing.[citation needed] However, short bursts of cortisone can give very quick results, and other treatments can rapidly improve some active spots, but usually not all active spots.[citation needed]

Modes of improvement are not necessarily fully understood but in general treatments are believed to work in at least 4 different ways (with many of the best treatments providing multiple simultaneous effects):

normalising shedding into the pore to prevent blockage

killing Propionibacterium acnes

anti-inflammatory effects

hormonal manipulation

A combination of treatments can greatly reduce the amount and severity of acne in many cases. Those treatments that are most effective tend to have greater potential for side effects and need a greater degree of monitoring, so a step-wise approach is often taken. Many people consult with doctors when deciding which treatments to use, especially when considering using any treatments in combination. There are a number of treatments that have been proven effective:

Benzoyl peroxide cream.

Hygiene

Proper washing and skin care can help to remove bacteria and oils which cause acne. Some anecdotal reports indicate placing a clean towel over one’s pillow each night can help prevent contaminating the pillow with the bacteria that causes acne, and reintroducing it to the face. Additionally, cleaning the hands before touching the affected area can prevent transmission of the bacteria from one part of the body to another.[citation needed]

Topical bactericidals

Widely available OTC bactericidal products containing benzoyl peroxide may be used in mild to moderate acne. The gel or cream containing benzoyl peroxide is applied, twice daily, into the pores over the affected region. Bar soaps or washes may also be used and vary from 2% to 10% in strength. In addition to its therapeutic effect as a keratolytic (a chemical that dissolves the keratin plugging the pores) benzoyl peroxide also prevents new lesions by killing P. acnes. In one study, roughly 70% of participants using a 10% benzoyl peroxide solution experienced a reduction in acne lesions after six weeks. Unlike antibiotics, benzoyl peroxide has the advantage of being a strong oxidizer and thus does not appear to generate bacterial resistance. However, it routinely causes dryness, local irritation and redness. A sensible regimen may include the daily use of low-concentration (2.5%) benzoyl peroxide preparations, combined with suitable non-comedogenic moisturisers to help avoid overdrying the skin.

Care must be taken when using benzoyl peroxide, as it can very easily bleach any fabric or hair it comes in contact with.

Other antibacterials that have been used include triclosan, or chlorhexidine gluconate. Though these treatments are often less effective, they also have fewer side-effects.

Products containing azeleic acid are also used in the treatment of P. acnes. It is available in the United States as a 20% concentration and does not generate bacterial resistance.

Prescription-strength benzoyl peroxide preparations do not necessarily differ with regard to the maximum concentration of the active ingredient (10%), but the drug is made available dissolved in a vehicle that more deeply penetrates the pores of the skin.

Topical antibiotics

Externally applied antibiotics such as erythromycin, clindamycin or tetracycline kill the bacteria that are harbored in the blocked follicles. While topical use of antibiotics is equally as effective as oral use, this method avoids possible side effects including upset stomach and drug interactions (e.g. it will not affect use of the oral contraceptive pill), but may prove inefficient to apply over larger areas than just the face alone.

Oral antibiotics

Oral antibiotics used to treat acne include erythromycin or one of the tetracycline antibiotics (tetracycline, the better absorbed oxytetracycline, or one of the once daily doxycycline, minocycline, or lymecycline). Trimethoprim is also sometimes used (off-label use in UK). However, reducing the P. acnes bacteria will not, in itself, do anything to reduce the oil secretion and abnormal cell behaviour that is the initial cause of the blocked follicles. Additionally the antibiotics are becoming less and less useful as resistant P. acnes are becoming more common. Acne may return soon after the end of treatmentays later in the case of topical applications, and weeks later in the case of oral antibiotics. Furthermore, side effects of tetracycline antibiotics can include yellowing of the teeth and an imbalance of gut flora, so are only recommended after topical products have been ruled out.

It has been found that sub-antimicrobial doses of antibiotics such as minocycline also improve acne. It is believed that minocycline’s anti-inflammatory effect also prevents acne.

Hormonal treatments

In females, acne can be improved with hormonal treatments. The common combined estrogen/progestogen methods of hormonal contraception have some effect, but the antiandrogen, Cyproterone, in combination with an oestrogen (Diane 35) is particularly effective at reducing androgenic hormone levels. Diane-35 is not available in the USA, but a newer oral contraceptive containing the progestin drospirenone is now available with fewer side effects than Diane 35 / Dianette. Both can be used where blood tests show abnormally high levels of androgens, but are effective even when this is not the case. Along with this, treatment with low dose spironolactone can have anti-androgenetic properties, especially in patients with polycystic ovarian syndrome.

If a pimple is large and/or does not seem to be affected by other treatments, a dermatologist may administer an injection of cortisone directly into it, which will usually reduce redness and inflammation almost immediately. This has the effect of flattening the pimple, thereby making it easier to cover up with makeup, and can also aid in the healing process. Side effects are minimal, but may include a temporary whitening of the skin around the injection point; and occasionally a small depression forms, which may persist, although often fills eventually. This method also carries a much smaller risk of scarring than surgical removal.

Topical retinoids

A group of medications for normalizing the follicle cell lifecycle are topical retinoids such as tretinoin (brand name Retin-A), adapalene (brand name Differin), and tazarotene (brand name Tazorac). Like isotretinoin, they are related to vitamin A, but they are administered as topicals and generally have much milder side effects. They can, however, cause significant irritation of the skin. The retinoids appear to influence the cell creation and death lifecycle of cells in the follicle lining. This helps prevent the hyperkeratinization of these cells that can create a blockage. Retinol, a form of vitamin A, has similar but milder effects and is used in many over-the-counter moisturizers and other topical products. Effective topical retinoids have been in use over 30 years but are available only on prescription so are not as widely used as the other topical treatments. Topical retinoids often cause an initial flare up of acne and facial flushing.

Oral retinoids

Main article: isotretinoin

A daily oral intake of vitamin A derivative isotretinoin (marketed as Accutane, Amnesteem, Sotret, Claravis, Clarus) over a period of 46 months can cause long-term resolution or reduction of acne. It is believed that isotretinoin works primarily by reducing the secretion of oils from the glands, however some studies suggest that it affects other acne-related factors as well. Isotretinoin has been shown to be very effective in treating severe acne and can either improve or clear well over 80% of patients. The drug has a much longer effect than anti-bacterial treatments and will often cure acne for good. The treatment requires close medical supervision by a dermatologist because the drug has many known side effects (many of which can be severe). About 25% of patients may relapse after one treatment. In those cases, a second treatment for another 46 months may be indicated to obtain desired results. It is often recommended that one lets a few months pass between the two treatments, because the condition can actually improve somewhat in the time after stopping the treatment and waiting a few months also gives the body a chance to recover. Occasionally a third or even a fourth course is used, but the benefits are often less substantial. The most common side effects are dry skin and occasional nosebleeds (secondary to dry nasal mucosa). Oral retinoids also often cause an initial flare up of acne within a month or so, which can be severe. There are reports that the drug has damaged the liver of patients. For this reason, it is recommended that patients have blood samples taken and examined before and during treatment. In some cases, treatment is terminated or reduced due to elevated liver enzymes in the blood, which might be related to liver damage. Others claim that the reports of permanent damage to the liver are unsubstantiated, and routine testing is considered unnecessary by some dermatologists. Blood triglycerides also need to be monitored. However, routine testing are part of the official guidelines for the use of the drug in many countries. Some press reports suggest that isotretinoin may cause depression but as of September 2005 there is no agreement in the medical literature as to the risk. The drug also causes birth defects if women become pregnant while taking it or take it while pregnant. For this reason, female patients are required to use two separate forms of birth control or vow abstinence while on the drug. Because of this, the drug is supposed to be given to females as a last resort after milder treatments have proven insufficient. Restrictive rules (see iPledge program) for use were put into force in the USA beginning in March 2006 to prevent misuse, causing occasioned widespread editorial comment.

Sulfur

Sulfur has an inhibitory effect on the growth of Propionibacterium acnes and, when combined with sodium sulfacetamide (5% and 10%, respectively) has been shown to reduce acne with only mild side effects.

Dermabrasion

Dermabrasion is a cosmetic medical procedure in which the surface of the skin is removed by abrasion (sanding). It is used to remove sun-damaged skin and to remove or lessen scars and dark spots on the skin. The procedure is very painful and usually requires a general anaesthetic or “twilight anaesthesia”, in which the patient is still partly conscious Afterward, the skin is very red and raw-looking, and it takes several months for the skin to regrow and heal. Dermabrasion is useful for scar removal when the scar is raised above the surrounding skin, but is less effective with sunken scars.

In the past, dermabrasion was done using a small, sterilized, electric sander. In the past decade, it has become more common to use a CO2 or Er:YAG laser. Laser dermabrasion is much easier to control, much easier to gauge, and is practically bloodless compared to classic dermabrasion.

Microdermabrasion comes from the above mentioned technique dermabrasion. Microdermabrasion is a more natural skin care that is a gentler, less invasive technology for doing an exfoliation on the skin. The goal of the microdermabrasion is to eliminate the superficial layer of the skin called the epidermis. If the surface of the abraded skin is touched, a roughness of the skin will be noticed. The roughness is keratinocytes, which are better hydrated than the surface corneocytes. Keratinocytes appear in the basal layer from the proliferation of keratinocyte stem cells. They are pushed up through the cells of the epidermis, experiencing gradual specialization until they reach the stratum corneum where they form a layer of dead, flattened, strongly keratinized cells called squamous cells. This layer creates an efficient barrier to the entry of foreign matter and infectious elements into the body and reduces moisture loss. Keratinocytes are shed and restored continuously from the stratum corneum.

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The time of transit from basal layer to shedding is generally one month. Corneocytes are cells derived from keratinocytes in the late stages of terminal specialization of squamous epithelia. The microdermabrasion is done to eliminate some of the corneocytes. These cells are responsible for the impermeability of the skin. The minimizing or elimination of scars, skin lesions, blotchiness and stretch marks from the skin can be an easy process with the use of skin exfoliation. The result depends on how well the procedure known as “skin remodeling” works. Results are optimal and fewer treatments are needed with more recent and/or superficial scars. Still, microdermabrasion can be used on scars that showed up during puberty or many years later.

Phototherapy

‘Blue’ and red light

Light exposure has long been used as a short term treatment for acne. Recently, visible light has been successfully employed to treat mild to moderate acne (phototherapy or deep penetrating light therapy) – in particular intense violet light (405-420 nm) generated by purpose-built fluorescent lighting, dichroic bulbs, LEDs or lasers. Used twice weekly, this has been shown to reduce the number of acne lesions by about 64% and is even more effective when applied daily. The mechanism appears to be that a porphyrin (Coproporphyrin III) produced within P. acnes generates free radicals when irradiated by 420 nm and shorter wavelengths of light. Particularly when applied over several days, these free radicals ultimately kill the bacteria. Since porphyrins are not otherwise present in skin, and no UV light is employed, it appears to be safe, and has been licensed by the U.S. FDA.

The treatment apparently works even better if used with a mixture of the violet light and red visible light (660 nanometer) resulting in a 76% reduction of lesions after three months of daily treatment for 80% of the patients; and overall clearance was similar or better than benzoyl peroxide. Unlike most of the other treatments few if any negative side effects are typically experienced, and the development of bacterial resistance to the treatment seems very unlikely. After treatment, clearance can be longer lived than is typical with topical or oral antibiotic treatments; several months is not uncommon. The equipment or treatment, however, is relatively new and reasonably expensive to buy initially, although the total cost of ownership can be similar to many other treatment methods (such as the total cost of benzoyl peroxide, moisturizer, washes) over a couple of years of use.

Photodynamic therapy

In addition, basic science and clinical work by dermatologists Yoram Harth and Alan Shalita and others has produced evidence that intense blue/violet light (405-425 nanometer) can decrease the number of inflammatory acne lesion by 60-70% in four weeks of therapy, particularly when the P. acnes is pretreated with delta-aminolevulinic acid (ALA), which increases the production of porphyrins. However this photodynamic therapy is controversial and apparently not published in a peer reviewed journal. A phase II trial, while it showed improvement occurred, failed to show improved response compared to the blue/violet light alone.

Surgery

For patients with cystic acne, boils can be drained through surgical lancing.

Subcision

Subcision is a process used to treat deep rolling scars left behind by acne or other skin diseases. Essentially the process involves separating the skin tissue in the affected area from the deeper scar tissue. This allows the blood to pool under the affected area, eventually causing the deep rolling scar to level off with the rest of the skin area. Once the skin has leveled, treatments such as laser resurfacing, microdermabrasion or chemical peels can be used to smooth out the scarred tissue.

Laser treatment

Laser surgery has been in use for some time to reduce the scars left behind by acne, but research has been done on lasers for prevention of acne formation itself. The laser is used to produce one of the following effects:

to burn away the follicle sac from which the hair grows

to burn away the sebaceous gland which produces the oil

to induce formation of oxygen in the bacteria, killing them

Since lasers and intense pulsed light sources cause thermal damage to the skin, there are concerns that laser or intense pulsed light treatments for acne will induce hyperpigmented macules (spots) or cause long-term dryness of the skin.

In the United States, the FDA has approved several companies, such as Candela Corp., to use a cosmetic laser for the treatment of acne. However, efficacy studies have used very small sample sizes (fewer than 100 subjects) for periods of six months or less, and have shown contradictory results. Also, laser treatment being relatively new, protocols remain subject to experimentation and revision, and treatment can be quite expensive. Also, some Smoothbeam laser devices had to be recalled due to coolant failure, which resulted in painful burn injuries to patients.

Less widely used treatments

Aloe vera: there are treatments for acne mentioned in Ayurveda using herbs such as Aloe vera, Neem, Haldi (Turmeric) and Papaya. There is limited evidence from medical studies on these products. Products from Rubia cordifolia, Curcuma longa (commonly known as Turmeric), Hemidesmus indicus (known as ananthamoola or anantmula), and Azadirachta indica (Neem) have been shown to have anti-inflammatory effects, but not aloe vera.

Azelaic acid (brand names Azelex, Finevin and Skinoren) is suitable for mild, comedonal acne.

Calendula used in suspension is used as an anti-inflammatory agent.

Cortisone injection into spots, also cortisone pills are sometimes used.

Comedo extraction

Hydrogen Peroxide oxidizes acne which kills bacteria.

Heat: local heating may be used to kill the bacteria in a developing pimple and so speed healing.

Naproxen or ibuprofen are used for some moderate acne for their anti-inflammatory effect.

Nicotinamide, (Vitamin B3) used topically in the form of a gel, has been shown in a 1995 study to be of comparable efficacy to topical clindamycin topical antibiotic used for comparison. Topical nicotinamide is available both on prescription and over-the-counter. The property of topical nicotinamide’s benefit in treating acne seems to be its anti-inflammatory nature. It is also purported to result in increased synthesis of collagen, keratin, involucrin and flaggrin and may also according to a cosmetic company be useful for reducing skin hyperpigmentation (acne scars), increased skin moisture and reducing fine wrinkles.

Pantothenic acid, (high dosage Vitamin B5)

Rofecoxib was shown to improve premenstrual acne vulgaris in a placebo controlled study.

Tea tree oil (melaleuca oil) dissolved in a carrier (5% strength) has been used with some success, where it is comparable to benzoyl peroxide but without excessive drying, kills P. acnes, and has been shown to be an effective anti-inflammatory in skin infections.

Zinc: Orally administered zinc gluconate has been shown to be effective in the treatment of inflammatory acne, although less so than tetracyclines.

Detoxification is a common method used by alternative medicine practitioners for the treatment of acne, although there have been no studies to prove its success. Detoxification is the process of cleansing the body of toxins purportedly caused by the environment, pharmaceutical drugs, food, and cosmetics.

History of some acne treatments

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The history of acne reaches back to the dawn of recorded history. In Ancient Egypt, it is recorded that several pharaohs were acne sufferers. From Ancient Greece comes the English word ‘acne’ (meaning ‘point’ or ‘peak’). Acne treatments are also of considerable antiquity:

Ancient Rome: bathing in hot, and often sulfurous, mineral water was one of the few available acne treatments. One of the earliest texts to mention skin problems is De Medicina by the Roman writer Celsus.

1800s: Nineteenth century dermatologists used sulphur in the treatment of acne. It was believed to dry the skin.

1920s: Benzoyl Peroxide is used

1930s: Laxatives were used as a cure for what were known as ‘chastity pimples’. Radiation also was used.

1950s: When antibiotics became available, it was discovered that they had beneficial effects on acne. They were taken orally to begin with. Much of the benefit was not from killing bacteria but from the anti-inflammatory effects of tetracycline and its relatives. Topical antibiotics became available later.

1960s: Low Radiation treatments are widely used.

1970s: Tretinoin (original Trade Name Retin A) was found effective for acne. This preceded the development of oral isotretinoin (sold as Accutane and Roaccutane) in 1980.

1980s: Accutane is introduced in the United States, and later found to be a teratogen, highly likely to cause birth defects if taken during pregnancy. In the United States more than 2,000 women became pregnant while taking the drug between 1982 and 2003, with most pregnancies ending in abortion or miscarriage. About 160 babies with birth defects were born.

1990s: Laser treatment introduced

2000s: Blue/red light therapy

Future treatments

A vaccine against inflammatory acne has been tested successfully in mice, but it is not certain that it would work similarly in humans.

A 2007 microbiology article reporting the first genome sequencing of a Propionibacterium acnes bacteriophage (PA6) said this “should greatly enhance the development of a potential bacteriophage therapy to treat acne and therefore overcome the significant problems associated with long-term antibiotic therapy and bacterial resistance.”

Talarozole, a retinoic acid metabolism blocking agent, is currently under investigation for acne therapy in combination with tretinoin.[citation needed]

Preferred treatments by types of acne vulgaris

Comedonal (non-inflammatory) acne: local treatment with azelaic acid, salicylic acid, topical retinoids, benzoyl peroxide.

Mild papulo-pustular (inflammatory) acne: benzoyl peroxide or topical retinoids, topical antibiotics (such as erythromycin).

Moderate inflammatory acne: benzoyl peroxide or topical retinoids combined with oral antibiotics (tetracyclines). Isotretinoin is an option.

Severe inflammatory acne, nodular acne, acne resistant to the above treatments: isotretinoin also known as Accutane, can be prescribed by a doctor, or contraceptive pills with cyproterone for females with virilization or drospirenone.

Acne scars

Acne often leaves small scars where the skin gets a “volcanic” shape.

Physical acne scars are often referred to as “Icepick” scars. This is because the scars tend to cause an indentation in the skin’s surface. There are a range of treatments available. Although quite rare, the medical condition Atrophia Maculosa Varioliformis Cutis also results in “acne like” depressed scars on the face.

Ice pick scars: Deep pits, that are the most common and a classic sign of acne scarring.

Box car scars: Angular scars that usually occur on the temple and cheeks, and can be either superficial or deep, these are similar to chickenpox scars.

Rolling scars: Scars that give the skin a wave-like appearance.

Hypertrophic scars: Thickened, or keloid scars.

Pigmentation

Pigmented scars is a slightly misleading term as it suggests a change in the skin’s pigmentation and that they are true scars; however, neither is true. Pigmented scars are usually the result of nodular or cystic acne (the painful ‘bumps’ lying under the skin). They often leave behind an inflamed red mark. Often, the pigmentation scars can be avoided simply by avoiding aggravation of the nodule or cyst. When sufferers try to ‘pop’ cysts or nodules, pigmentation scarring becomes significantly worse[citation needed], and may even bruise the affected area. Pigmentation scars nearly always fade with time taking between three months to two years to do so, although rarely can persist.

On the other hand, some peoplearticularly those with naturally tanned skino develop brown hyperpigmentation scars due to increased production of the pigment melanin. These too typically fade over time.

Grading scale

There are multiple grading scales for grading the severity of acne vulgaris, three of these being: Leeds acne grading technique: Counts and categorises lesions into inflammatory and non-inflammatory (ranges from 0-10.0). ‘Cook’s acne grading scale: Uses photographs to grade severity from 0 to 8 (0 being the least severe and 8 being the most severe). Pillsbury scale: Simply classifies the severity of the acne from 1 (least severe) to 4 (most severe).

See also

Blackhead

Keratosis pilaris

Rosacea

Chloracne

Liamitus

List of cutaneous conditions

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^ Procter & Gamble. “Niacinamide Research” (PDF). http://www.pgdermatology.com/images/learning_library/anti_aging/PG-Niancinamide-FINAL-090105.pdf. 

^ Leung, Lit-Hung (December 1998). “Pantothenic Acid in the Treatment of Acne Vulgaris Medical Hypothesis” , originally printed in Journal of Orthomolecular Medicine 12(2).

^ Tehrani R, Dharmalingam M (1 November 2004). “Management of premenstrual acne with Cox-2 inhibitors: A placebo controlled study”. Indian J Dermatol Venereol Leprol [serial online] 70 (6): 345348. ISSN 0378-6323. PMID 17642660. http://www.ijdvl.com/text.asp?2004/70/6/345/13475. Retrieved 2007-06-23. 

^ Koh KJ, Pearce AL, Marshman G, Finlay-Jones JJ, Hart PH (December 2002). “Tea tree oil reduces histamine-induced skin inflammation”. Br. J. Dermatol. 147 (6): 12127. doi:10.1046/j.1365-2133.2002.05034.x. ISSN 0007-0963. PMID 12452873. 

^ Khalil Z, Pearce AL, Satkunanathan N, Storer E, Finlay-Jones JJ, Hart PH (October 2004). “Regulation of wheal and flare by tea tree oil: complementary human and rodent studies”. J. Invest. Dermatol. 123 (4): 68390. doi:10.1111/j.0022-202X.2004.23407.x. ISSN 0022-202X. PMID 15373773. http://www.nature.com/jid/journal/v123/n4/full/5602507a.html. 

^ Dreno B, Amblard P, Agache P, Sirot S, Litoux P (1989). “Low doses of zinc gluconate for inflammatory acne” (Free full text). Acta Derm Venereol 69 (6): 5413. ISSN 0001-5555. PMID 2575335. http://www.nlm.nih.gov/medlineplus/acne.html. 

^ Dreno B, Moyse D, Alirezai M, Amblard P, Auffret N, Beylot C, Bodokh I, Chivot M, Daniel F, Humbert P, Meynadier J, Poli F (2001). “Multicenter randomized comparative double-blind controlled clinical trial of the safety and efficacy of zinc gluconate versus minocycline hydrochloride in the treatment of inflammatory acne vulgaris”. Dermatology 203 (2): 13540. doi:10.1159/000051728. ISSN 1018-8665. PMID 11586012. 

^ “Tretinoin (retinoic acid) in acne” (Free full text). The Medical letter on drugs and therapeutics 15 (1): 3. January 1973. ISSN 0025-732X. PMID 4265099. http://www.nlm.nih.gov/medlineplus/acne.html. 

^ Jones H, Blanc D, Cunliffe WJ (November 1980). “13-cis retinoic acid and acne”. Lancet 2 (8203): 10489. doi:10.1016/S0140-6736(80)92273-4. ISSN 0140-6736. PMID 6107678. 

^ Brard A, Azoulay L, Koren G, Blais L, Perreault S, Oraichi D (February 2007). “Isotretinoin, pregnancies, abortions and birth defects: a population-based perspective”. British Journal of Clinical Pharmacology 63 (2): 196205. doi:10.1111/j.1365-2125.2006.02837.x. PMID 17214828. 

^ Holmes SC, Bankowska U, Mackie RM (March 1998). “The prescription of isotretinoin to women: is every precaution taken?”. The British Journal of Dermatology 138 (3): 4505. doi:10.1046/j.1365-2133.1998.02123.x. PMID 9580798. 

^ Kim J (October 2008). “Acne vaccines: therapeutic option for the treatment of acne vulgaris?”. The Journal of Investigative Dermatology 128 (10): 23534. doi:10.1038/jid.2008.221. PMID 18787542. 

^ Farrar MD, Howson KM, Bojar RA, et al. (June 2007). “Genome sequence and analysis of a Propionibacterium acnes bacteriophage”. Journal of Bacteriology 189 (11): 41617. doi:10.1128/JB.00106-07. PMID 17400737. 

^ Leeds, Cook’s and Pillsbury scales obtained from here

Further reading

Review articles and guidelines

Webster GF (August 2002). “Acne vulgaris”. BMJ 325 (7362): 4759. doi:10.1136/bmj.325.7362.475. PMID 12202330. 

Gollnick H, Cunliffe W, Berson D, et al. (July 2003). “Management of acne: a report from a Global Alliance to Improve Outcomes in Acne”. Journal of the American Academy of Dermatology 49 (1 Suppl): S137. doi:10.1067/mjd.2003.618. PMID 12833004. 

Feldman S, Careccia RE, Barham KL, Hancox J (May 2004). “Diagnosis and treatment of acne”. American Family Physician 69 (9): 212330. PMID 15152959. 

Haider A, Shaw JC (August 2004). “Treatment of acne vulgaris”. JAMA 292 (6): 72635. doi:10.1001/jama.292.6.726. PMID 15304471. 

Katsambas, A; Cunliffe, W (2004). “Commentary: Acne and its treatment”. Clinics in Dermatology 22: 359. doi:10.1016/j.clindermatol.2004.03.003. 

James WD (April 2005). “Clinical practice. Acne”. The New England Journal of Medicine 352 (14): 146372. doi:10.1056/NEJMcp033487. PMID 15814882. 

“Drugs for acne, rosacea and psoriasis”. Treatment Guidelines from the Medical Letter 3 (35): 4956. July 2005. PMID 15961971. http://www.medicalletter.org/scripts/articlefind.cgi?issue=35&page=49. 

Sinclair W, Jordaan HF (November 2005). “Acne guideline 2005 update”. South African Medical Journal 95 (11 Pt 2): 88192. PMID 16344888. http://blues.sabinet.co.za/WebZ/Authorize?sessionid=0:autho=pubmed:password=pubmed2004&/AdvancedQuery?&format=F&next=images/ejour/m_samj/m_samj_v95_n11_a21.pdf. 

Zaenglein AL, Thiboutot DM (September 2006). “Expert committee recommendations for acne management”. Pediatrics 118 (3): 118899. doi:10.1542/peds.2005-2022. PMID 16951015. 

Purdy S, de Berker D (November 2006). “Acne”. BMJ 333 (7575): 94953. doi:10.1136/bmj.38987.606701.80. PMID 17082546. 

Strauss JS, Krowchuk DP, Leyden JJ, et al. (April 2007). “Guidelines of care for acne vulgaris management”. Journal of the American Academy of Dermatology 56 (4): 65163. doi:10.1016/j.jaad.2006.08.048. PMID 17276540. 

Reference books and chapters

Plewig, Gerd; Kligman, Albert M. (2000). Acne and rosacea (3rd ed.). New York: Springer-Verlag. ISBN 3-540-66751-2. 

Cunliffe, William J.; Gollnick, Harald P. M. (2001). Acne : diagnosis and management. London: Martin Dunitz. ISBN 1-85317-206-5. 

Thiboutot, Diane M.; Strauss, John S. (2003). “Diseases of the sebaceous glands”. in Burns, Tony; Breathnach, Stephen; Cox, Neil; Griffiths, Christopher. Fitzpatrick’s dermatology in general medicine (6th ed.). New York: McGraw-Hill. pp. 67287. ISBN 0-07-138076-0. 

Zaenglein, Andrea L.; Thiboutot, Diane M. (2003). “Acne vulgaris”. in Bolognia, Jean L.; Jorizzo, Joseph L.; Rapini, Ronald P. (eds.). Dermatology. London: Mosby. pp. 53144. ISBN 0-32302-4092. 

Habif, Thomas P. (2004). “Acne, rosacea, and related disorders”. Clinical dermatology : a color guide to diagnosis and therapy (4th ed.). Edinburgh: Mosby. pp. 162208. ISBN 0-323-01319-8. 

Simpson, Nicholas B.; Cunliffe, William J. (2004). “Disorders of the sebaceous glands”. in Burns, Tony; Breathnach, Stephen; Cox, Neil; Griffiths, Christopher. Rook’s textbook of dermatology (7th ed.). Malden, Mass.: Blackwell Science. pp. 43.175. ISBN 0-632-06429-3. 

James, William D.; Berger, Timothy G.; Elston, Dirk M. (2006). “Acne”. Andrews’ diseases of the skin: clinical dermatology (10th ed.). Philadelphia: Saunders Elsevier. pp. 23150. ISBN 0-7216-2921-0. 

External links

Wikimedia Commons has media related to: Acne

Acne vulgaris: more than skin deep (on the psychological effects of acne)

Acne photo library at Dermnet

Acne from the U.S. National Library of Medicine

Story on Acne from the Better Health Channel

“AcneNet”. American Academy of Dermatology. http://www.skincarephysicians.com/acnenet.  – Dermatologist-reviewed information about acne.

Q&A about Acne, from the National Institutes of Health.

v  d  e

Acne-treating agents (D10)

Antibacterial

Azelaic acid  Benzoyl peroxide  Blue light therapy  Tea tree oil

Keratolytic

Glycolic acid  Salicylic acid  Sulfur  Benzoyl peroxide

Anti-inflammatory

Aspirin  Ibuprofen  Red light therapy

Antibiotics

Clindamycin  Dapsone  Erythromycin  Sulfacetamide  Minocycline  Tetracyclines

Hormonal

Antiandrogens  Contraceptives

Retinoids

Adapalene  Isotretinoin  Tazarotene  Tretinoin

Combinations

ZIANA  Duac  BenzaClin  PLEXION  Epiduo

v  d  e

Diseases of the skin and appendages by morphology

Growths

Epidermal

wart  callus  seborrheic keratosis  acrochordon  molluscum contagiosum  actinic keratosis  squamous cell carcinoma  basal cell carcinoma  merkel cell carcinoma  nevus sebaceous  trichoepithelioma

Pigmented

Freckles  lentigo  melasma  nevus  melanoma

Dermal and

subcutaneous

epidermal inclusion cyst  hemangioma  dermatofibroma  keloid  lipoma  neurofibroma  xanthoma  Kaposi’s sarcoma  infantile digital fibromatosis  granular cell tumor  leiomyoma  lymphangioma circumscriptum  myxoid cyst

Rashes

With

epidermal

involvement

Eczematous

contact dermatitis  atopic dermatitis  seborrheic dermatitis  stasis dermatitis  lichen simplex chronicus  Darier’s disease  glucagonoma syndrome  langerhans cell histiocytosis  lichen sclerosus  pemphigus foliaceus  Wiskott-Aldrich syndrome  Zinc deficiency

Scaling

psoriasis  tinea (corporis  cruris  pedis  manuum  faciei)  pityriasis rosea  secondary syphillis  mycosis fungoides  systemic lupus erythematosus  pityriasis rubra pilaris  parapsoriasis  ichthyosis

Blistering

herpes simplex  herpes zoster  varicella  bullous impetigo  acute contact dermatitis  pemphigus vulgaris  bullous pemphigoid  dermatitis herpetiformis  porphyria cutanea tarda  epidermolysis bullosa simplex

Papular

scabies  insect bite reactions  lichen planus  miliaria  keratosis pilaris  lichen spinulosus  transient acantholytic dermatosis  lichen nitidus  pityriasis lichenoides et varioliformis acuta

Pustular

acne vulgaris  acne rosacea  folliculitis  impetigo  candidiasis  gonococcemia  dermatophyte  coccidioidomycosis  subcorneal pustular dermatosis

Hypopigmented

tinea versicolor  vitiligo  pityriasis alba  postinflammatory hyperpigmentation  tuberous sclerosis  idiopathic guttate hypomelanosis  leprosy  hypopigmented mycosis fungoides

Without

epidermal

involvement

Red

Blanchable

Erythema

Generalized

drug eruptions  viral exanthems  toxic erythema  systemic lupus erythematosus

Localized

cellulitis  abscess  boil  erythema nodosum  carcinoid syndrome  fixed drug eruption

Specialized

urticaria  erythema (multiforme  migrans  gyratum repens  annulare centrifugum  ab igne)

Nonblanchable

Purpura

Macular

thrombocytopenic purpura  actinic purpura

Papular

disseminated intravascular coagulation  vasculitis

Indurated

scleroderma/morphea  granuloma annulare  lichen sclerosis et atrophicus  necrobiosis lipoidica

Miscellaneous

disorders

Ulcers

Hair

telogen effluvium  androgenic alopecia  trichotillomania  alopecia areata  systemic lupus erythematosus  tinea capitis  loose anagen syndrome  lichen planopilaris  folliculitis decalvans  acne keloidalis nuchae

Nail

onychomycosis  psoriasis  paronychia  ingrown nail

Mucous

membrane

aphthous stomatitis  oral candidiasis  lichen planus  leukoplakia  pemphigus vulgaris  mucous membrane pemphigoid  cicatricial pemphigoid  herpesvirus  coxsackievirus  syphilis  systemic histoplasmosis  squamous cell carcinoma

v  d  e

Disorders of skin appendages (L60-75, 700-709)

Nail

thickness: Onychogryphosis  Onychauxis

color: Beau’s lines  Yellow nail syndrome  Leukonychia  Azure Lunula

shape: Koilonychia  Clubbing

other: Ingrown nail  Anonychia

Hair

Hair loss

Alopecia areata (Alopecia totalis, Alopecia universalis, Ophiasis)

Androgenic alopecia  Hypotrichosis  Telogen effluvium  Traction alopecia  Lichen planopilaris  Trichorrhexis nodosa

Hypertrichosis

Hirsutism

Acne/rosacea

Acneiform eruption (Acne vulgaris, Chloracne, Blackhead)  Rosacea (Perioral dermatitis, Rhinophyma)

Follicular cysts

Epidermoid cyst  Trichilemmal cyst  Sebaceous cyst  Steatocystoma multiplex

Inflammation

Pseudofolliculitis barbae  Hidradenitis suppurativa  Folliculitis

Sweat glands

eccrine (Miliaria, Anhidrosis)  apocrine (Body odor, Chromhidrosis, Fox-Fordyce disease)

skin appendage navs: anat, noncongen/congen/neoplasia, symptoms+signs/eponymous, proc

link title

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I am an expert from China Auto Suppliers, usually analyzes all kind of industries situation, such as used canon gl1 , panasonic lumix dmc l1k.

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Advances in Glaucoma Medication

Advances in Glaucoma Medication

Article by Alex Ray









A new glaucoma medication with a different mechanism of action than current ophthalmic medications is entering clinical trials. The new glaucoma drug, still known as OPA6566, is an adenosine A2a receptor agonist. It works by activating the adenosine A2a receptor to stimulate fluid drainage from the eye through the trabecular meshwork (a spongy tissue near the front of the eye). As the fluid drains, eye pressure lowers. Like other glaucoma medication, OPA6566 is administered as eye drops.

The latest glaucoma treatment is a result of a partnership between Seattle biotechnical company Acucela and Tokyo-based Otsuka Pharmaceutical Co. “We believe the demand for better glaucoma treatments is great; and we are excited to advance this compound to the clinical stage just one year after signing our agreement with Otsuka Pharmaceutical,” said Dr. Ryo Kubota, PhD, Acucela Inc’s CEO. “Today’s announcement is in line with our strategy to develop leading-edge therapies for blinding eye diseases.”

OPA6566 is intended to treat open angle glaucoma (the most common form of the disease). Glaucoma is a chronic eye disease resulting from high intraocular (within the eyeball) pressure. Untreated glaucoma can cause blindness, starting with the peripheral vision. An estimated 60.5 million people across the world suffer from glaucoma – the second leading cause of blindness worldwide – and that number is expected to rise to 80 million by 2010.

Prostaglandin analogues (hormone-like substances) like latanoprost ophthalmic solution (brand name Xalatan), are the current leading glaucoma treatment. Latanoprost drops also work by increasing fluid drainage from the eye, but through a different pathway (between eye muscle bundles). The upcoming clinical trial should help establish which glaucoma eye drops mechanism of action is most effective.

At the same time as OPA6566 is being developed, researchers in Singapore are also working to build a better ophthalmic eye drop. The researchers are concerned that existing drops – while an effective first line glaucoma treatment – don’t have a sustained enough action, and are associated with poor patient compliance and possible ocular allergies from repeated use.

To combat these shortcomings, they incorporated the commonly prescribed glaucoma medication latanoprost (Xalatan) into something called large unilamellar vesicles, a type of liposome. Liposomes are often used to convey drugs, enzymes and other substances to targeted cells or organs.

They then compared this sustained release liposome version of latanoprost against conventional latanoprost eye drops in rabbits. The sustained release latanoprost was delivered in two ways – as a daily topical ophthalmic eye drop, and by subconjunctival (beneath the conjunctiva – a thin, transparent tissue that covers the outer surface of the eye) injection.

Both treatment methods resulted in a reduction of intraocular eye pressure (IOP) comparable to that achieved with traditional latanoprost eye drops. But the lowered IOP from a single subconjunctival injection lasted for up to 50 days, with no ill effects such as inflammation or toxicity.

“The outcomes from our studies report positive and significant benefits over the commercial eye drop formulation,” wrote the researchers, “Subconjunctival injection of liposomes to provide sustained delivery of ocular drugs may prove to be a suitably attractive alternative to current topical eyedrops.”



About the Author

Alex Ray is a regular contributor to the online glaucoma resource latanoprost.ca. She advises glaucoma patients to compare generic latanoprost and name brand Xalatan prices at the online Canadian pharmacy BigMountainDrugs.com before they buy Xalatan.










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Stop Losing Your Hair! This is How

Stop Losing Your Hair! This is How

“A hair on the head is worth two on the brush.” – Irish Proverb

As you might know, I always like to share my lessons learned, experience and insights to help others succeed. So here are my hair tips!

Yes, I also was suffering from losing my hair and getting a bit bald… Runs in the family and getting older and a busy lifestyle took their toll on my scalp as well… Based on various discussions I had on how to prevent or even stop losing your hair…, I can hereby reveal the secret ingredients you’ll need to stop losing and even start growing the hair on your scalp again!

On the advise of several friends of mine (two are GP’s) I started taking Propecia pills and using a special hair gain lotion. The result is that I now dare to reference this process as it is also working for me: I stopped losing hair and I started gaining more hair!!! After 3 months I do not have empty/thin hair area’s on my scalp anymore!

What is it and how does it work?
1. Propecia or Proscar (Finasteride, MSD) pills (for men only) are the only once-a-day pill for the treatment of certain types of male pattern baldness (androgenetic alopecia). Finasteride acts in the body to significantly lower levels of dihydrotestosterone (DHT) by inhibiting the type 2 5 Alpha Reductase enzyme which is responsible for the conversion of testosterone into DHT. High amounts of DHT contribute to prostate enlargement as well as hair loss in individuals with a genetic pre-disposition to it.

For all information on Finasteride, please see the Wikipedia entry: http://en.wikipedia.org/wiki/Finasteride

2. Minoxidil Topical Application lotion: Minoxidil is used to stimulate hair growth and to slow balding. It opens up the hair veins and enables hair growth. In combination with Finasteride it has the highest effect. It is most effective for men whose hair loss is recent. Unfortunately Minoxidil has no effect on receding hairlines.

Why use both?
A clinical study has shown that a combination therapy of Minoxidil and Finasteride (Propecia or Proscar) shows great promise in the treatment of hair loss. It may potentially become the main stay therapy in this condition. Please see: http://www.regrowth.com/hairloss-remedy/remox/promox-study.cfm

How and how often to take?
1. You take one Propecia (1mg) or one Proscar (1.25mg or 1mg) pill once a day. Preferably take on an empty stomach (officially Propecia and Proscar can be taken with or without food) with a glass of grapefruit juice. Grapefruit juice contains substances which inhibit certain digestive enzymes that break down Finasteride thus boosting (more or less doubling) your bloodsteam uptake of the drug. Important: because grapefruit juice boosts the uptake, make sure do not take any other medication besides the Finasteride! Otherwise just use water.
2. Every morning and every evening you drop 1ml of Minoxidil Topical lotion on your dry scalp and just lightly rub it in. It’s that simple and easy!

How long to take it?
The advise for a long lasting result is to take both for at least 12 months.

What are the risks/side effects?
Risks and side effects will differ per person, so always make sure you consult your GP, doctor or another qualified medical specialist first.
My own experience with side effects:
1. My GP told me that when taking Finasteride pills there is a risk of getting a lower libido and decreased sex lust…. Fortunately, so far that did not happen to me. I’ve not experienced any negative side effects. OK, just one: some hair started growing on my chest…

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2. Minoxidil Topical lotion may cause side effects like: scalp itching, dryness, scaling, flaking, irritation, or burning. If it happens than most often in the early stage after start of using the lotion. Personally I have not experienced any negative side effects so far.

What does it cost?
1. Monthly doses of Propecia (Finasteride, MSD) pills is approx. . Cost-conscious customers usually buy Proscar® (Finasteride, MSD) and cut the 5mg tablet into fourths (1.25mg) or even fifths (1mg) therefore getting all the benefits of Propecia at a dramatically reduced pricetag. If you cut Proscar into fourths ( 1.25mg ) you only need 3 boxes to save your hair for the entire year! Compare that to 12 boxes of Propecia and you will realise that Proscar is the cheapest way to save your hair and your save your bank balance. For more info, please see: http://hairloss.cyberatlantis.com/proscar.php
2. If you manage to buy the lotion online or at a discount pharmacy the price per box with 3 to 5 bottles of 60ml will vary between 9 and 9. It just depends on what kind of brand/packaging it has…..I shopped around and found a package with 5 bottles (enough for 5 months) for 9. The average cost per month for 1 60ml bottle of lotion will be approx. .

How to get it?
1. Propecia or Proscar pills can be obtained with a prescription from your GP. For Propecia pills, please ask your GP for repeat prescription of at least 6x or 12x (1 per month).
2. Minoxidil Topical Application lotion can be obtained at most drugstores (again; my advise is to shop around for the best price. It could save you – per package!). The Minoxidil Topical lotion I’m using is Hair A-Gain.

Other tips?
Yes, these three tips are proven ones as well (at least for me):
1. Stop using fancy shampoo’s. Just use baby shampoo! The best you can use is the Johnson & Johnson: ‘Johnson’s baby shampoo plus conditioner’ (red/pink bottle). It is scientifically proven to be less harmful to your hair.
2. Stop washing your hair every day. Just wash your hair bi-daily, which will be less harmful to your scalp and your hair.
3. Stop using gel, spray or foam to model your hair. Start using men’s hair wax, hair paste, or hair creme to model your hair. The difference is that gel, spray’s and foams will often affect your scalp and can also negatively impact the quality of your hair. Wax or hair creme will “sit” on your hair and will not touch your scalp, nor impact the hair veins or quality of the hair.

“Experience is a comb that is given to you, when you have already lost you hair.” – Giorgos Zambetas

I hope my experience helps you as well, as it works well for me!

Thanks, warm regards & success,

Patrick Driessen

© Patrick W. Driessen. All rights reserved.

Patrick Driessen is a visionary, entrepreneurial and intuitive executive leader, author, executive coach, mentor and inspirational speaker with a passion to help other people succeed! His stories are most often thought provoking, inspirational and motivational!

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Nursing Care for Patients Receiving tPA (tissue plasminogen activator) for Acute Limb Ischemia

Nursing Care for Patients Receiving tPA (tissue plasminogen activator) for Acute Limb Ischemia

 

Nursing Care for Patients Receiving Thrombolytic Therapy for Acute Limb Ischemia

By Jaaska L. Cather, RN, BSN, MSN

Jaaska@live.com

Staff Nurse (Clinical RN – Four)

 The Winchester Medical Center Cardiovascular Interventional Unit, Winchester, VA

 

                As the acuity of patients increase, more and more critical patients are now being cared for in step-down units and telemetry floors. The focus of this paper is to address the nursing assessments and interventions necessary to care for patients undergoing thrombolytic (specifically tissue plasminogen activator, aka tPA) therapy for acute limb ischemia.

It is estimated that peripheral vascular disease (PVD) occurs at a rate of 14 per 100,000 per year in the United States (1). Acute limb ischemia occurs when there is a lack of blood flow to a limb. It is usually as a result of an embolism or thrombosis of an artery in those with underlying PVD (1).

The formation of blood clots lies at the basis of a number of serious diseases. By breaking down the clot, the disease process can be arrested, or the complications reduced. While other anticoagulants such as heparin decrease the “growth” of a clot, thrombolytic agents actively reduce the size of the clot (1).

Thrombolysis is the breakdown (lysis) of blood clots (1). It is commonly referred to as clot busting for this reason. It works by stimulating fibrinolysis by plasmin through infusion of tissue plasminogen activator (tPA), the protein that normally activates plasmin.

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Most thrombolytic agents work by activating the enzyme plasminogen which clears the cross-linked fibrin mesh, which is the foundation or backbone of the clot (1). This makes the clot soluble and subject to further proteolysis by other enzymes, and restores blood flow through the occluded artery or arteries involved (1)

Thrombolytic drugs are administered together with a continuous infusion of unfractionated or low molecular weight heparin.  It is IMPERATIVE that the two medications are administered simultaneously. If Heparin is not administered concomitantly with tPA, clot formation could occur within the infusion catheter or sheath, and result in an increase in thrombosis, and most seriously could result in loss of limb!

The doseage is individually formulated by the physician based on the patient, co-morbidities, and the site being lysed. It is administered intravenous or intra-arterial. Lab work that needs to be assessed before thrombolytic therapy begins and every six hours during the duration of therapy are fibrinogen levels, PTT, H&H. Nursing assessment should include frequent vital signs, neurovascular status assessments, peripheral vascular assessments, groin management, strict bedrest of the patient, assessment of puncture sites for bleeding, and avoidance of IM injections.

Contraindications and precautions of thrombolytic therapy include but are not limited to:aneurysm, arteriovenous malformation, bleeding, brain tumor, coagulopathy, head trauma, HTN, intracranial bleeding, intracranial mass, surgery, trauma, renal failure, pregnancy (2).

            The most common adverse reaction is bleeding (Intracranial, gastrointestinal, retroperitoneal, and pericardial) (2). Other adverse reactions which may occur are: angioedema, bradycardia, coma, ecchymosis, fever,  hematoma, hematuria, hemoptysis, hypotension,  infection,   nausea, PVC’s,  purpura, seizures, stroke, thrombosis,  ventricular tachycardia, and  vomiting (2).

            If any of these reactions should occur the physician should be notified STAT, and the thrombolytic infusion will most likely be discontinued. Hemodynamic and cardiopulmonary support should be provided to stabilize the patient’s condition.

 

 

References

“Tissue Plasminogen Activator” retrieved from the world wibe web at Wikipedia.com @http.//en.wikipedia.org/wiki/Tissue_plasminogen_activator on August 6, 2010.
Nursing 2010 Drug Handbook (2010). Lippincott, Williams & Willcons. Philadelphia.

I have been a Registered Nurse since 1991. I have a Bachelor’s and Master’s degree in Nursing. My specialty is invasive cardiology.

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Improve Scalp Health and Hair Growth

Improve Scalp Health and Hair Growth

Article by Dianne M. Buxton









Hair thinning, whether genetically aggravated, pregnancy aggravated, fever aggravated or whatever! aggravated – let’s not mention getting OLD! is a frustrating situation. I was researching this topic when I came across a hair brush that is a low level laser tool, for hair regeneration. In fact there are several kinds. They seem to be growing in popularity for scalp health and hair regrowth treatments.

From Wikipedia:

“Credit for the development of laser theory is generally given to Albert Einstein. In his theory “Zur Quantum Theories der Strahlung”, published in 1916, he first used the name stimulated emission.

The word LASER is an accronym for Light Amplification by Stimulated Emission of Radiation.

In 1967 a few years after the first working laser was invented, Endre Mester in Semmelweis University Budapest, Hungary wanted to find out if laser light could cause cancer. He took some mice, shaved the hair off their backs, divided them into two groups and gave a laser treatment with a low-powered ruby laser to one group. They did not get cancer and to his surprise the shaved hair grew back more quickly on the treated group than the untreated group. That was how “laser biostimulation” was discovered.[2]“

From the BioFlex site, describing laser therapy in general:

“Once inside the cell, the photons comprising the laser beam can trigger many cellular changes such as the production of enzymes, protein substances vital for innumerable bio-chemical actions. Laser light also stimulates the cells’ mitochondria. Mitochondria are tiny biochemical engines that produce enzymes essential for cell function.

In short, low-level laser therapy appears to heal at a cellular level. It’s like shining a ray of sunlight directly on injured cells inside the body and stimulating the cells to return to normal function.”

From the MedX site, describing laser therapy in general:

“When the photons of light penetrate the skin and underlying tissue, they are absorbed by the cell, and converted into biological energy, thereby the cell membrane permeability is altered, and this triggers a cascade of cellular events including:”…(I have shortened this passage somewhat):

***Stimulation of respiratory chain (in the cell) by the energy of the laser***Increased DNA and RNA synthesis by the energy of the laser

***Increased levels of beta endorphins and serotonin by the light energy of the laser

***Enhanced collagen synthesis by the laser

***Accelerated tissue repair by the laser

***Increased local microcirculation by the laser”

From Wikipedia “There appear to be no safety concerns in its application for therapy in people or animals….”. Bear in mind, that no laser beam of any kind should ever be directed toward your eyes.

(It is recommended to use a sulfate-free shampoo with the laser brush. Tahitian Noni International has an entire line of sulfate-free hair products. Plus the benefit of the noni juice too.)

The several brands that I read about report a 3%-7% return rate for the laser brush and comb tools. This is an encouraging figure, I think. It seems you can find a 20 week up to one year refund time.

The laser brush from Verseo offers a full refund up to a year from purchase, if results are not to your satisfaction. An attractive zero risk factor! There is more information on their unit here.

If any of you try one of these devices, please let me know what results you get.



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Fat intake and Prostate cancer!

Fat intake and Prostate cancer!

Article by Yfish







Prostate Cancer is a leading cancer threat to men in United States. And now, there are studies showing that a high fat intake can have a direct correlation to the risk of prostate cancer.

According to wikipedia, Prostate Cancer is “a disease in which cancer develops in the prostate, a gland in the male reproductive system. It occurs when cells of the prostate mutate and begin to multiply out of control. These cells may spread (metastasize) from the prostate to other parts of the body, especially the bones and lymph nodes. Prostate cancer may cause pain, difficulty in urinating, erectile dysfunction and other symptoms.

Rates of prostate cancer vary widely across the world. Although the rates vary widely between countries, it is least common in South and East Asia, more common in Europe, and most common in the United States.

Prostate cancer develops most frequently in men over fifty. This cancer can occur only in men, as the prostate is exclusively of the male reproductive tract. It is one of the most common types of cancer in men. However, many men who develop prostate cancer never have symptoms, undergo no therapy, and eventually die of other causes.”

The article from Newschief.com suggests that fat makes up about 35% of calories in American diet, while it’s only about 15% in Japanese diet. This is probably a known fact to most American, as some of our daily lunch or dinner usually contain of fried food or fatty meat. It is exceptionally difficult for a lot of working people who simply go get fast food as daily lunch items.

There are of course things we can start to do. A high vegetables intake during the week can help lower the risk of prostate cancer, among which broccoli and cabbage are the best good to help protecting against the men threat. Also, tomatoes contain high level of antioxidant called lycopene – bright red carotenoid pigment and phytochemical that some preliminary research has suggested an inverse correlation between lycopene (consumption of tomato) and risk of cancer (which the kind of research is yet to get approved from FDA). One thing that anyone can prove is, however, a good amount of vegetables servings would be good to help reduce bad enzymes in our fragile body.

So, next time when you have to dine out, try to incorporate some tomatoes, broccoli or cabbage in your meal. Or, the best of all, try to reduce the amount of fat intake in your diet!

References:http://www.newschief.com/article/20081109/NEWS/811090351/1011/LIVING02?Title=Prostate_cancer_affected_by_amount_of_fat_in_diethttp://en.wikipedia.org/wiki/Prostate_cancerhttp://en.wikipedia.org/wiki/Lycopene



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Interest in finance, health and music. http://ysfinanceroom.blogspot.com/ http://health-food-room.blogspot.com/ http://ysmusicroom.blogspot.com/

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Improve Scalp Health and Hair Growth

Improve Scalp Health and Hair Growth

Article by Dianne M. Buxton







Hair thinning, whether genetically aggravated, pregnancy aggravated, fever aggravated or whatever! aggravated – let’s not mention getting OLD! is a frustrating situation. I was researching this topic when I came across a hair brush that is a low level laser tool, for hair regeneration. In fact there are several kinds. They seem to be growing in popularity for scalp health and hair regrowth treatments.

From Wikipedia:

“Credit for the development of laser theory is generally given to Albert Einstein. In his theory “Zur Quantum Theories der Strahlung”, published in 1916, he first used the name stimulated emission.

The word LASER is an accronym for Light Amplification by Stimulated Emission of Radiation.

In 1967 a few years after the first working laser was invented, Endre Mester in Semmelweis University Budapest, Hungary wanted to find out if laser light could cause cancer. He took some mice, shaved the hair off their backs, divided them into two groups and gave a laser treatment with a low-powered ruby laser to one group. They did not get cancer and to his surprise the shaved hair grew back more quickly on the treated group than the untreated group. That was how “laser biostimulation” was discovered.[2]“

From the BioFlex site, describing laser therapy in general:

“Once inside the cell, the photons comprising the laser beam can trigger many cellular changes such as the production of enzymes, protein substances vital for innumerable bio-chemical actions. Laser light also stimulates the cells’ mitochondria. Mitochondria are tiny biochemical engines that produce enzymes essential for cell function.

In short, low-level laser therapy appears to heal at a cellular level. It’s like shining a ray of sunlight directly on injured cells inside the body and stimulating the cells to return to normal function.”

From the MedX site, describing laser therapy in general:

“When the photons of light penetrate the skin and underlying tissue, they are absorbed by the cell, and converted into biological energy, thereby the cell membrane permeability is altered, and this triggers a cascade of cellular events including:”…(I have shortened this passage somewhat):

***Stimulation of respiratory chain (in the cell) by the energy of the laser***Increased DNA and RNA synthesis by the energy of the laser

***Increased levels of beta endorphins and serotonin by the light energy of the laser

***Enhanced collagen synthesis by the laser

***Accelerated tissue repair by the laser

***Increased local microcirculation by the laser”

From Wikipedia “There appear to be no safety concerns in its application for therapy in people or animals….”. Bear in mind, that no laser beam of any kind should ever be directed toward your eyes.

(It is recommended to use a sulfate-free shampoo with the laser brush. Tahitian Noni International has an entire line of sulfate-free hair products. Plus the benefit of the noni juice too.)

The several brands that I read about report a 3%-7% return rate for the laser brush and comb tools. This is an encouraging figure, I think. It seems you can find a 20 week up to one year refund time.

The laser brush from Verseo offers a full refund up to a year from purchase, if results are not to your satisfaction. An attractive zero risk factor! There is more information on their unit here.

If any of you try one of these devices, please let me know what results you get.



About the Author

If you find these ideas useful, you can find out more about them here.

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