2 in 1



1. I was sitting in one of my hectic clinics one day. Patients came in and out the room one by one. A mum was denying that her son was over-active when the fact showed clearly that the child was running up and about the room and his condition was getting worst and worst from the perspective of his class teacher.

2. What can I do to accelerate the turnover of patients? I scanned the file of my next patient. Here..there is some familiarity. I called the mum in. The boy was wearing the red shirt. Oh..similar with this patient. However, in striking contrast, the newly identified boy was full of order and looked like he was well compliant with my treatment.

3. I made much of this and suggested he must be taking medicine as prescribed. The mum nodded.

4. Well, can you tell her what happen to your son after taking medication, I seemed to suggest. They were looking at each other, unbelievable and hardly say anything for a moment.

5. The mum of the orderly boy started by describing how she gave the medication and to her astonishment, it’s work.

6. Well, then, I wonder, they just need facilitation. I facilitated the discussion to the point where a mum told the others that teachers won’t be able to handle hyperactive kids in the class. Imagine they have 30 more kids to look after. There is no teachers’ aid in Malaysian setting, either.

7. Finally, the former was influenced to start her kid on medication and that solved my biggest headache of the day.

8. Many parents are misinformed about the need to start medication on their hyperactive kids. To some extent, the internet is to be blamed. The benefit has to outweigh the risk before any medication has to be started. By and large, from my experience, at least 80% of children will respond to medication.

9. The only problem at the moment is that the child has to swallow the pill or otherwise the pill has to be crushed. No liquid preparation is available.

NSAIDs increase the risk of heart attack


1. A new international study finds that popular painkillers or anti-inflammatories know as NSAIDs can increase the risk of heart attack or stroke by a third, with some having a much stronger effect than others, and size of the dose also making a difference. However, experts urge patients worried about the findings not to give up on their NSAID medication and to speak to their doctor about their concerns.

2. Researchers from Hull York Medical School (HYMS), a joint venture between the Universities of Hull and York and the NHS in the UK and the Institute for Clinical Evaluative Sciences in Canada, systematically reviewed 51 large-scale studies of non-steroidal, anti-inflammatory drug (NSAID) conducted in Europe, USA, Canada and Australia. Their findings are published online this week the journal PLoS Medicine.

3. They found that patients with heart problems who used NSAIDs, including diclofenac and indomethacin, had a significantly higher risk of serious cardiovascular events such as heart attack and stroke compared to patients who did not.

4. Even in doses available over the counter without a doctor’s prescription, diclofenac could raise someone’s risk of heart attack or stroke, they said.

5. However, other common NSAIDs, including naproxen and low doses of ibuprofen do not appear to be linked to an increase in risk.

6. Lead researcher Dr. Patricia McGettigan from HYMS told the press that:

7. “NSAIDs provide pain relief for millions of patients with chronic inflammatory disorders. The cardiovascular risk is well described but often overlooked. In choosing which one of the many available NSAIDs to use, patients and doctors would benefit from the knowledge of the balance between benefit and harm for individual NSAIDs.”

8. Many people use NSAIDs in both over the counter and prescription form for pain relief and for their anti-inflammatory effects to treat conditions such as headaches, arthritis, back pain, gout, and the aches and fever of flu.

9. In 2010 in England alone, GPs wrote out nearly 17 million prescriptions for NSAIDs, that is one for every three people in the country. Of these, nearly 6 million, more than a third, were for diclofenac; 5 million were for ibuprofen and 3 million were for naproxen. All of these can also be bought without a prescription.

10. The researchers found that for the most commonly used NSAIDs, the highest risk was seen with diclofenac, which overall was linked to an increased risk of 40% for a cardiovascular event like a heart attack or stroke, compared with non-use.

11. This means that for a person with a 5% or more background risk of a cardiovascular event (typically someone with diabetes, a history of heart problems and high blood pressure), taking diclofenac would most likely increase that risk to over 7%, explained McGettigan:

12. “In other words, one in 50 such patients might suffer an avoidable heart attack. This is important information in making choices, particularly if there is a safer alternative,” she added.

13. In contrast, a healthy young person with an annual risk of heart attack or stroke of under 0.1% will experience a negligible increase in risk from taking any of the commonly used NSAIDs, said McGettigan.

14. The researchers found that the lowest risks were with naproxen and low doses of ibuprofen: they weren’t linked to increased cardiovascular risks. But, they did find when ibuprofen daily doses exceeded 1200 mg a day, it was linked to an 80% higher risk.

15. For diclofenac, the link was there at both high and low dose: with a near doubling of increased risk at the higher dose.

16. The safest NSAID, as far as the effect on cardiovascular risk is concerned, appears to be naproxen. Neither low nor high doses of this were linked to increased risk.

17. The researchers also looked at the newer types of NSAIDs, the Cox-2 selective; these are available only on prescription. They found these newer NSAIDs are also linked to raised cardiovascular risks.

18. For instance, Rofecoxib, which was taken off the market worldwide in September 2004 because of its cardiovascular risks, was linked to an increase in the risk of 45%.

19. Of the newer NSAIDs on the UK market, the researchers found that celecoxib was tied to an increase in risk at both low and high doses and etoricoxib appeared to raise risk more than celecoxib.

20. Indomethacin, an old NSAID that is still popular for the treatment of gout, was linked to a raised cardiovascular risk of 30%. The drug also has other side effects, which together with this new finding should make its clinical use even more questionable, said the researchers.

21. One of the drawbacks of NSAIDs is that they raise the risk of gastrointestinal ulcers, which can be reduced by taking anti-ulcer drugs like omeprazole. But you can’t do this for the cardiovascular risk, so this is another reason why it is important to have these comparisons to hand when giving patients advice, said McGettigan.

22. “New NSAIDs like celecoxib were developed to have a much lower risk of gastrointestinal ulcers compared with older drugs like ibuprofen, diclofenac, and naproxen. They achieved this, but as the review finds, they do not have lower cardiovascular risks,” she warned.

23. The British Heart Foundation (BHF) urged patients who are already taking NSAIDs and are worried by these findings not to simply give up on their medication.

24. “As with any medicine there are benefits and potential risks to taking painkillers,” said Doireann Maddock, Senior Cardiac Nurse at BHF, “You should always speak to your doctor first because the benefits may well outweigh the risks for you.”

25. She explained that we have known for some time that certain painkillers are risky for heart patients and the findings of this new study should not be ignored.

26. “But scientists and drug regulators will need to delve deeper before we draw any firm conclusions about these drugs and their side effects,” she said.

Written by Catharine Paddock PhD
Courtesy: Medical News Today

New Approach to Keeping Coronary Arteries Open After Angioplasties


1. Research at Loyola University Chicago Stritch School of Medicine could help lead to new ways to prevent coronary arteries from reclogging after balloon angioplasties.

2. The latest in a series of studies in this effort is published online ahead of print in Arteriosclerosis, Thrombosis and Vascular Biology, a journal of the American Heart Association. The senior author is Allen M. Samarel, MD, and the first author is Yevgeniya E. Koshman, Ph.D.

3. In an angioplasty, a tiny balloon is inflated to open a clogged coronary artery. Typically, a stent is deployed to prevent the artery from collapsing after the balloon is deflated.

4. The procedure itself irritates the interior walls of the artery. In response, smooth muscle cells migrate to the site and form scar tissue. In roughly one-third of cases, the artery reclogs and another angioplasty is needed.

5. Newer stents release drugs that prevent migration of muscle cells to the site. But these drugs have the unwanted effect of also stopping endothelial cells from moving to the site. Endothelial cells are needed to repair the irritation to the walls of the artery. (The angioplasty removes endothelial cells that line the inside walls of the artery. This increases the risk that clots will form, break loose and cause heart attacks and strokes. Consequently, patients must take anti-clotting medications for months after their angioplasties.)

6. The Loyola study points to a new strategy for preventing the unwanted migration of muscle cells while allowing the beneficial movement of endothelial cells. The study involved cell cultures as well as rats that had received balloon angioplasties in their carotid arteries.

7. Researchers focused on two proteins, known as FAK and FRNK. Both proteins are products of the same gene, but have opposite effects: FAK jump-starts the migration of muscle cells to the angioplasty site, while FRNK inhibits such migration. (FAK stands for focal adhesion kinase; FRNK stands for FAK-related nonkinase.)

8. Introducing FRNK early on in the course of an angioplasty could prevent the migration of artery-clogging muscle cells while allowing the movement of artery-repairing endothelial cells, Samarel said.

9. Earlier this year, Koshman presented an abstract of the study to the American Heart Association Arteriosclerosis, Thrombosis, and Vascular Biology 2011 Scientific Sessions, where it was judged among the top 10 percent of accepted abstracts.

10. Samarel is the William B. Knapp Professor of Medicine and Physiology and Koshman is a research associate at Loyola University Chicago Stritch School of Medicine. Other co-authors are Miensheng Chu, PhD.; Steven J. Engman, MD, PhD.; Taehoon Kim, MS; Rekha Iyengar, MBA; and Seth Robia, Ph.D.

11. The study was supported by the National Institutes of Health and Dr. Ralph and Marian Falk Medical Research Trust. During the course of the study, Koshman was an American Heart Association postdoctoral fellow and Engman was a heart association predoctoral fellow.

(Courtesy: Science Daily)

Tip on how to reduce stigma


1. People are very afraid of labeling. What more if it about labeling them as mental patients. How do I explain in order to minimize stigma?. This is just my way of doing things. You can follow if you like. The example below is how I go about normalizing the stigma about mood disorder.

Man is in fact an emotional creature. Everyone experiences happiness, sadness, fear, disgust and anger. These emotions help us to identify our place among our friends.

Emotions come and go like waves. They determine our state of mind. Everyone has ups and downs. Sometimes you feel sad and at other times you are happy. It’s very much like the waves in the South China Sea (because I am living near the South China Sea). These variation of mood is part of life. It is not unusual to feel sad in adversity.

But it is abnormal to feel sad for too long and to the extend that you cannot go to work (or to school).  When your emotional experiences are very intense, they can become like in a monsoon season.

If you descend to the depths, you are suffering from depression. If you ascend to the height you are suffering form mania. Both episodes when we total up is called bipolar disorder.

2. In most instances, my patients are happy to this kind of approach. Then you can proceed in explaining about drugs, side-effect and the important of compliance.

Categorical Brain


1. The human brain is adept at recognizing similar items and placing them into categories — for example, dog versus cat, or chair versus a table. In a new study, MIT neuroscientists have identified the brain activity that appears to control this skill.

2. The findings, published in the July 27 issue of the journal Neuron, suggest a potential explanation for why autistic children focus intently on details, but often seem unable to group things into broad categories, says Earl Miller, the Picower Professor of Neuroscience and senior author of the paper.

3. “We think what may happen in autism is the system may get out of balance … and as a result, the details overwhelm the category. Then you have a brain that’s not only too good at memorizing details, it can’t help but memorize the details,” says Miller, a principal investigator at the Picower Institute for Learning and Memory at MIT.

4. Miller and Picower postdoc Evan Antzoulatos focused their study on two brain regions, the prefrontal cortex and the striatum, which is part of a larger structure known as the basal ganglia. Both regions are known to be important for learning.

5. Until a few years ago, it was believed that the prefrontal cortex learns information quickly, then sends what it learns to the basal ganglia, which helps form habits, such as the ability to play a musical instrument. However, in 2005, Miller and colleagues showed that when monkeys learn simple tasks, their basal ganglia are more active early in the process, followed by a slower activation in the prefrontal cortex.

6. In other words, the striatum quickly learns the individual puzzle pieces, and the prefrontal cortex puts them together, Miller says. He and Antzoulatos theorized that the same pattern would be evident during category learning.

7. For the new Neuron study, Antzoulatos trained monkeys to assign patterns of dots into one of two categories. At first, the animals would see only two examples, or “exemplars,” from each category — a small enough number that they could memorize the category to which each belonged, without having to learn the general category traits.

8. After the animals learned the first two exemplars, the number would be doubled. Eventually, the number of exemplars became so great that it was impossible to memorize them, and the monkeys’ brains would start picking up on general traits that characterize each category.

9. As they did so, brain activity shifted from the striatum, a more primitive brain region, to the prefrontal cortex, which is responsible for high-level functions such as planning and decision making.

10. “What happens during category learning is the more primitive, faster basal ganglia can memorize the exemplars, but then it sends what it learns up to the prefrontal cortex. And the prefrontal cortex figures out what’s common among all the exemplars, among all the individuals, and extracts the essence,” Miller says.

11. Gregory Ashby, a professor of psychology at the University of California at Santa Barbara, says the new study represents the “clearest picture yet” of the striatum’s involvement in category learning. “We’ve known for quite a while that the striatum plays an important role in category learning, but it was not at all clear exactly what that role was,” he says.

12. In future studies, the MIT researchers hope to test their theory that autism results from an imbalance between the striatum and prefrontal cortex by interfering with the normal balance between the two brain regions and observing the results.

(Courtesy: Anne Trafton, MIT News Office)

Update on Heart Research


A conductive patch of carbon nanotubes can regenerate heart tissue growing in a dish, according to preliminary research from Brown University. The patch, made of tiny chains of carbon atoms that fold in on themselves, forming a tube, conducts electricity and mimics the rough surface of natural tissue. The more nanotubes the Brown researchers added to the patch, the more cells around it were able to regenerate.

During a heart attack, areas of the heart are deprived of oxygen, killing muscle and nerve cells used to keep the heart beating strongly and rhythmically. The tissue cannot regenerate on its own, which disrupts the heart’s rhythm, weakens it, and sometimes leads to a repeat heart attack. Tissue engineers around the globe are searching for ways to regenerate or repair this damaged tissue using different types of scaffolds and stem cells.

Thomas Webster, an associate professor of engineering and orthopedics at Brown and senior author of the study, says his work is distinctive because he examined not just the muscle cells that beat, but also the nerve cells that help them contract and the endothelial cells that line the blood vessels leading to and from the heart. The fact that the patch helped regenerate all three types of cells, which function interdependently in the heart, suggests the newly grown tissue is similar to normal heart tissue. The research was published today in Acta Biomaterialia.

In another development, a functioning strip of heart muscle has been created from mouse embryonic stem cells, thanks to the identification of a new type of cardiac stem cell. The research has not yet been repeated with human cells, but it lays a blueprint for how to generate heart muscle that could be used to repair damage from heart attacks and to test new drugs. The scientists, from Harvard University, are now working on isolating similar cardiac cells from lines of human stem cells.

Stem-cell therapy for heart disease has so far focused on trying to repair heart-attack damage with injections of patient-derived stem cells from bone marrow, but studies have yielded mixed results. Rather than using undifferentiated cells, “the push now is to try to obtain cardiac myocytes [heart muscle cells] from people and use them as patches that would be placed over damaged tissue in someone who has had a heart attack,” says Benoit Bruneau, a researcher at theGladstone Institute of Cardiovascular Disease, in San Francisco. “They made engineered cardiac tissue from embryonic stem cells. From a bioengineering point of view, that’s significant.”

Embryonic stem cells, which are capable of forming any type of tissue in the body, can spontaneously form clumps of beating heart cells when grown in a dish. But it has been difficult to isolate large numbers of these cells from the mix of tissue types that can develop from embryonic stem cells. A heart patch would require a huge number of these cells, perhaps billions, says Christine Mummery, a biologist at the Leiden University Medical Center, in the Netherlands.

The Harvard team, led by Kenneth Chien, director of the Massachusetts General Hospital Cardiovascular Research Center, in Boston, has made progress toward this goal, previously developing a method of isolating a master cardiac stem cell from embryonic stem cells and fetal tissue–one capable of producing all the cell types that make up the heart. In the most recent study, published today in the journalScience, Chien’s team developed a way to isolate particularly desirable progeny of this master stem cell, cells that produce only ventricular muscle cells, the type damaged in heart attacks. “If you want to create a cardiac patch, you want cells that will behave–that would line up nicely like they do in the heart,” says Bruneau.

Scientists genetically engineered mice to express two markers of different colors–one that marked the master cardiac stem cell, and the other that turns on when the cells start making muscle. They then isolated the 0.5 percent of cells in the developing mouse embryo that expressed both markers. In addition to making only ventricular muscle cells, these cells also have the ability to continue to reproduce, enabling the production of large volumes of cells. “This ability to divide and make muscle is something that normal heart cells do not have,” says Chien.
(Excerpt From MIT Journal)

The Benefit of Exercise


Exercise use to defeat stress. Human body is made to move. At the very least it is likely exercise reduces emotional discomfort. Exercise frees the mind from the stresses and strains of the day. It releases tension that built up, sometimes out of proportion. Going for exercise is as good and probably even better than having a rest. So when feeling anxious, better get out of the office and walk the tension away.

Exercise recharge the batteries after tension and stress have drained you of power and energy. It is as natural as breathing and it is the regular rhythmical action that drains away tension from our muscle and leaves us with a feeling of pleasant tiredness and calm, clear mind.

Exercise works because as we exercise, we become unconscious of our body and its movement, and we are just aware of the rhythm. We are born along in a total body-mind experience which make us whole.

That is why I will advise my patients whether they are suffering from psychological stress, neurotic disorder or even psychotic disorder to embark on exercise.

Bye.

Selecting a hypnotic, anyone?


Insomnias have various etiologies and recognition of these should enable initiation of an appropriate treatment. In all cases, behavioral and nutritional measures constitute an important component of treatment. However, when insomnia is poorly tolerated, with physical and/or psychological repercussions, recourse to a hypnotic is justified.

The choice of hypnotic should be a matter of careful thought and should take into account, besides the efficacy of the product on the various types of insomnia, its likely side-effects, differing in nature and importance according to the pharmacological class in particular. the residual effects of the hypnotic may have am adverse impact on day time vigilance and psychomotor performance or be associated with impairment of cognitive functions, thereby minimizing the benefits of the sleep recovered.

The emergence of rebound phenomena on treatment discontinuation i.e. an aggravation of insomnia such that this becomes more severe than the original disorder prompting prescription of the hypnotic, may take it difficult to stop the treatment and consequently lead to an undesirable prolongation of hypnotic use.

This phenomenon is more frequently observed with short-acting benzodiazepines. The likelihood of development of tolerance, necessitating a progressive increase in dose to maintain the same effect or of dependence must also be assessed.