Sleep And Your Heart

Here is a question for all of us during this Christmas season: Have we been sleeping enough? Should we be making a resolution for the new year to have sufficient sleep (and for those who sleep too much - not to sleep more than 9 hours)?

Who would have thought that how we sleep would turn out to be a coronary artery risk factor every bit as important as smoking or high blood pressure? But that's how it is shaping up. Getting a good night’s sleep prevents coronary artery calcification - the accumulation of calcified plaques in the coronary arteries, a predictor of future heart disease.

A recent study in the Journal of the American Medical Association is making the sleep-heart connection impossible to ignore. Although this is not a brand new discovery, they have demonstrated, with stronger evidence, that as hours of sleep drop toward five or fewer from the eight hours most humans seem to need, the chance of developing coronary disease in young middle-aged men and women grows in close proportion. The JAMA study used a relatively new low-dose CT scanning technique to detect calcium buildup in arteries long before patients have the slightest inkling any plaque is there. Recent studies have found that sleep duration is related with risk factors for coronary artery calcification including glucose regulation, blood pressure, sex, age, education, and body mass index.


To determine whether sleep duration and quality are associated with incidence of calcification, researchers from the University of Chicago followed 495 healthy individuals, aged between 35 and 47 years, for 5 years. The participants completed sleep questionnaires regularly.

Accelerating hardening of the arteries in those skimping on sleep is consistent with many prior observations. For example, people afflicted with chronic loud snoring, a sleep disrupter known particularly to men, experience more heart attacks and higher blood pressure than those who sleep like a baby. And a 10-year study involving 72 thousand middle-aged femal nurses found that those who slept for five or fewer hours a night had a greater chance of suffering heart attacks than similar women who managed a good eight hours of sleep. (Prudence in all things: Getting too much sleep wasn't the best either—with those exceeding nine hours bumping up their heart risk.)

Sure, these studies do not prove causality, but they do offer rather hefty circumstantial evidence of sleep's powers. And for ages, lay instincts have held that sleep is a health potion, with lore ranging from the belief that slumber heals weary bones, to early to bed making one healthy and wise, to sleep being the best face-lift.

The rather novel and surprising strong correlation between sleep deprivation and early coronary artery calcification is compelling enough to change behavior now. After all, the medical intervention is a prescription for more sleep, a therapy that's a pleasure to behold, costs nothing, and comes without side effects. Maybe it's time also to make a seven-to-eight-hour sleep night a serious public-health goal for all in 2009.

More details from the study:

• Ihe incidence of calcification in the heart arteries ranged from 6 percent among the participants who slept more than 7 hours per night, to 11 percent among those who slept between 5 and 7 hours nightly, and 27 percent in those who slept less than 5 hours.


• After adjusting for other factors that might influence the results, such as age, sex, race, education and smoking, one hour more of sleep per night decreased the estimated odds of calcification by 33 percent.

Pfizer to drop development of drugs for hyperlipidemia, atherosclerosis, and heart failure

This comes as a shocker to me since Pfizer is the main powerhouse of CV drug development. Their drug, Lipitor, is almost a household name, especially for families with members being treated for high cholesterol. It is a pity that all the experts in their team will have to go separate ways. However, I believe that it will not be long before this vacuum is quickly filled by companies waiting in the sidelines to make their forray into this market segment.

Pfizer to drop development of drugs for hyperlipidemia, atherosclerosis, and heart failure
October 2, 2008
New York, NY - Pfizer is getting out of the cholesterol-lowering game to focus on what it perceives to be more lucrative diseases, according to an internal memo obtained by Forbes [1]. And for the most part, the chosen "disease areas" don't include the heart.
In the memo, Martin Mackay, president of Pfizer Global Research & Development (R&D), informed his staff that the company plans to "exit" the fields of atherosclerosis/hyperlipidemia, heart failure, obesity, and peripheral arterial disease.
Instead, the company, whose cholesterol-lowering drug atorvastatin (Lipitor) is the world's top-selling drug, says it is turning its attention and R&D dollars to cancer, diabetes, Alzheimer's, pain remedies, and mental health as its "higher-priority areas."
The news comes in the wake of the flop of Pfizer's hoped-for new flagship, torcetrapib, a CETP inhibitor that was widely predicted to be the company's next blockbuster drug. While CV drugs have been the major moneymakers for Pfizer in recent years, those days are drawing to a close. In addition to Lipitor, which will lose patent protection in 2011, Pfizer's other major player in the CV drug arena is Norvasc (amlodipine), which came off patent in 2007.
Among the lower-priority "disease areas" where the company says it will continue working are thrombosis and transplant, the memo notes.
Contacted by heartwire, a handful of leaders for some of the major Pfizer-sponsored trials in cardiovascular disease over the past decade declined to comment on the company's announcement or speculate on what it might mean to the field of CV drug development—with one exception. Dr John Kastelein (Academic Medical Center, Amsterdam, the Netherlands), who was an investigator in the Pfizer-sponsored ASAP, TNT, and IDEAL trials, called Pfizer "a real powerhouse" in the CV drug arena.
"I kind of knew this was coming, but when you see it in print, it still hits hard," he told heartwire. "I think this is very, very significant both for the company itself and for the whole field of CV drug development. Pfizer had truly excellent people in the development arm of their company for CV and metabolic drugs, and they've contributed to this whole notion that you need more robust LDL lowering and that that's better than mild LDL lowering, which has become one of the axioms of CV prevention. And if they're stepping out now, that not only signifies their own problems, but it also signifies the problems in CV drug development, and how incredibly difficult and costly it has become to bring new drugs forward. And that's not good for patients."
Kastelein predicts that drug companies, having "lost faith" somewhat in HDL-raising therapies, will need to look more closely at anti-inflammatory drugs in the setting of coronary artery disease. "But there, the problem is, if you have no biomarkers whatsoever to do even dose-finding studies, you need to move from relatively small phase 2 trials to incredibly large, hard-outcome studies, which is taking quite a risk," he said. And that, at least for Pfizer, is too much risk.
"Everyone, not just Pfizer, is realizing that the days of the really big blockbuster drugs are over. And what is going to replace that are drugs in a class that are 10 times or 100 times more difficult to develop, so the risks are much higher. And these days, after Avandia and ezetimibe, everything is about safety. This means the FDA is forced, by public and colleague pressure, to demand even larger databases before drugs are going to market, which is of course making it more expensive. It's a cycle that's very hard to break."
Calls to Pfizer were not returned before this story was published.

Advantages of using sunflower oil, corn oil, canola oil, soybean oil, and olive oil

In the latest issue of the American Journal of Clinical Nutrition, it is reported that the consumption of partially hydrogenated vegetable oils (PHVO) [click to see what is meant by this], which contain high levels of trans-fat, has raised the level of inflammation in middle-eastern women. Inflammation leads to formation of artery blockages, which in turn, leads to heart disease and stroke.

So the take home point is: use non-hydrogenated vegetable oils! Examples of which are sunflower oil, corn oil, canola oil, soybean oil, and olive oil.

The abstract of the full-text article is given below. I have explained some terms in [brackets] for the sake of lay persons reading this.

American Journal of Clinical Nutrition, Vol. 88, No. 4, 913-921, October 2008

ORIGINAL RESEARCH COMMUNICATION
Home use of vegetable oils, markers of systemic inflammation, and endothelial dysfunction among women
Ahmad Esmaillzadeh and Leila Azadbakht

Department of Nutrition, School of Public Health, and the Food Security and Nutrition Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Background: Most knowledge about adverse health effects of trans fats was mainly derived from studies done in Western populations of European or American origins; few data are available in the understudied region of the Middle East.

Objective: We assessed the association between consumption of partially hydrogenated vegetable oils (PHVOs) [containing trans fat] and non-HVOs and circulating concentrations of inflammatory markers among Tehrani women aged 40–60 y.

Design: Usual dietary intakes were assessed with a food-frequency questionnaire among 486 apparently healthy women. PHVOs (commonly used for cooking in Iran) were considered as PHVOs category. Sunflower oil, corn oil, canola oil, soybean oil, and olive oil were defined as non-HVOs. Anthropometric measurements [eg body weight, height, blood pressure] were done, and fasting blood samples were taken to measure inflammatory markers [molecules in the blood that indicate the level of inflammation, eg CRP, TNF etc as listed by authors below].

Results: The energy-adjusted daily intakes (mean ± SD) of PHVOs and non-HVOs were 23 ± 11 and 22 ± 10 g/d, respectively. After control for potential confounders, women in the highest quintile of PHVO intake had higher plasma concentrations of C-reactive protein (CRP; percentage difference from lowest quintile: 45%; P for trend: <0.01), tumor necrosis factor- (TNF-; 66%; P for trend: <0.01), interleukin-6 (72%; P for trend: <0.05), and soluble intercellular adhesion molecule-1 (sICAM-1; 22%; P for trend: <0.01) than did women in the lowest quintile. In contrast, higher consumption of non-HVOs was associated with lower circulating concentrations of CRP (percentage difference between top and bottom quintiles: –23%; P for trend: 0.05), TNF- (–29%; P for trend: <0.01), serum amyloid A (–24%; P for trend: <0.01), and sICAM-1 (–19%; P for trend:<0.05). Adjustment for body mass index, fasting plasma glucose, and lipid profiles slightly attenuated the associations in some cases.

Conclusions: Higher intakes of PHVOs are associated with elevated concentrations of inflammatory biomarkers, whereas higher intakes of non-HVOs are associated with lower plasma concentrations of these biomarkers.

Take a genetic test first before you take your weight-loss drugs?

ScienceDaily (Oct. 2, 2008) — Obese patients with a specific genetic make-up lose more weight when taking the weight loss drug sibutramine and undergoing behavioral therapy compared to those without this genetic make-up, reports a new study in Gastroenterology, the official journal of the American Gastroenterological Association (AGA) Institute.

The obesity epidemic continues to be an increasingly global problem: an estimated 1.6 billion adults worldwide are overweight (body mass index [BMI]>25) and 400 million are obese (BMI>30). In addition, the incidences of diabetes and other debilitating diseases attributable to obesity continue to rise.


Genes Influence Effectiveness Of Weight-loss Drug
While there are numerous options for the treatment of obesity, this study examined sibutramine, a medication approved for the long-term treatment of obesity. The drug creates a feeling of fullness, prevents decline in metabolic rate associated with low calorie diets and causes weight loss, especially when combined with behavioral therapy. However, weight loss with the drug is highly variable. Therefore, a research team at the Mayo Clinic assessed the influence of specific markers of candidate genes controlling serotonergic and adrenergic mechanisms (α2A-receptor, 5-HTTLPR and GNβ3) on weight loss/body composition in response to sibutramine or placebo.

"We found significantly lower values for weight, BMI and proportion of body fat in patients taking sibutramine. The candidate gene variations provided useful markers of enhanced response to the drug," said Michael Camilleri, MD, AGAF, of the Mayo Clinic and lead author of the study. "Gene variations may help select obese patients who are more likely to experience improved outcome with this treatment. Since the different markers were present in almost 50 percent of patients, inclusion of screening for these genetic markers before prescribing the medication may even be cost-effective from a public health perspective."

In this randomized, double-blind, pharmacogenetic study, Dr. Camilleri and colleagues evaluated behavioral therapy and sibutramine (10 or 15 mg daily) or placebo for 12 weeks in 181 overweight or obese participants. They measured body weight, BMI, body composition, gastric emptying and genetic variation.

Study results showed that sibutramine at both doses, given in combination with behavioral therapy, caused significant weight loss (p = 0.009). The drug resulted in lower values for weight, BMI and proportion of body fat compared to placebo (p<0.01, p<0.001 and p=0.05, respectively). Weight loss at four weeks was a predictor of weight loss achieved at 12 weeks.
There was a statistically significant gene-by-dose interaction for GNβ3 genotype. This gene determines the function of G proteins, which are involved in translating the message from surface receptors that bind the transmitters serotonin and norepinephrine (e.g. of cells controlling appetite). Those surface receptors are indirectly influenced by sibutramine, which blocks the reuptake of the two transmitters. For each candidate gene, treatment effects were observed at 12 weeks (p<0.017) for all specific genotype variants. The research showed gene pairs (e.g. for GNβ3and α2A-receptor) resulted in greater sibutramine treatment effects on weight (both p<0.002). However, there was no evidence of synergism between combinations of two genotypes on the response to sibutramine therapy compared to the effect on weight loss associated with individual genotypes.
"Our results suggest the genetic make-up of patients could predispose their responsiveness to a drug. This could have important implications for the future of personalized molecular-based or individualized medicine," added Dr. Camilleri. As new and exciting research like this study continues into the causes, prevention and treatments for obesity, the role played by the GI tract is becoming more defined. This understanding has the potential to lead to novel endoscopic, pharmacological and nutritional therapies for obesity as well as changes in policies and societal practices related to obesity.

More Pics of Breckenridge

We had sometime in between conference sessions to go hiking.

The first thing we saw was what looked like a mini Indian tepee.

Climbing up the ski slope with the thin air at nearly 3000m made each step a breathless endeavour. But the view was breathtaking!

Some struggled real hard...

But these 2 immunologists were discussing immunology (what else?) on their way up despite having to gasp for air between words...

It rained, but only for a while.

Perseverance in action...

The visual treat was just fabulous higher up

The walk down was beautiful too.

Psyllium – The Natural Way To Reduce Your Cholesterol Levels

It is great to be back in sunny Singapore after a fruitful trip to Breckenridge!

Today, I would like to share a little about this wonder fiber that nature has provided for us, especially for those who need to control their high cholesterol. Our laboratory has independently conducted experiments to test the cholesterol-lowering effects of psyllium and I am therefore very convinced of its effects (read our paper if you want the details).

Benefits of Dietary Fiber

It has been known for a long time that a high intake of fiber in our daily diet is good for health. A high-fibre diet is associated with reduced risks of heart disease, colon cancer and obesity [1]. The health benefits of consuming large amount of dietary fiber were first suggested more than 30 years ago [2]. Since then, evidences of the link between dietary fiber and heart disease have accumulated from population studies [3-6] and clinical trials [7-8]. There are two main types of dietary fiber - soluble and insoluble. Insoluble fiber has not been shown to exhibit a consistent cholesterol-lowering effect. In contrast, consuming a high-fiber diet containing viscous soluble fiber is known to significantly lower the total and low-density lipoprotein (LDL) cholesterol levels, which is the bad cholesterols in the blood [9-11]. What is Psyllium? Psyllium is pronounced "sil-ee-um" (the "P" is silent). It is derived from Plantago ovato, or plantain plants, and is grown mainly in India, Spain and France. The outer part of the psyllium seed, called the husk, is the portion that has the cholesterol-lowering property. Psyllium husk is easily available in health food stores. It can be consumed by adding into fruit juice or any drink, or added into breads, cereals, and pasta. Some cereal products are enriched with psyllium.

Psyllium Husk

What you are more likely to see when you buy a packet/bottle of psyllium husk

Cholesterol-lowering properties of psyllium
Let us try to understand how the lowering of the cholesterol can be achieved. Very simply put, this can be brought about by either causing the body to get rid of more cholesterol or to make less of it. It appears that psyllium works through the former, that is, it helps the body to get rid of more cholesterol through the formation of bile acid [12], which is excreted out along with the stool. This process accounts for 40–50% of the daily elimination of cholesterol [13,14]. The liver is the main site of bile acid formation.

Among the various forms of viscous soluble fibers, psyllium husk appears to be the most effective in lowering cholesterol levels [15,16] and has the least adverse side effects.17 The effect of psyllium husks on fasting plasma cholesterol has been evaluated in individuals with high-cholesterol, obesity, or diabetes [18-19]. In general, these studies show that psyllium husk consumption could bring about a 5% reduction in total cholesterol and 7–8% reduction in LDL cholesterol, which were sustainable in the long term [20, 21].

How much of psyllium should I consume to lower my cholesterol and for how long?
Clinical trials have shown that typically, about 10g per day (over 2-3 doses) for about 2 months is sufficient to achieve a cholesterol-lowering effect.


Reference List
1. D. Kritchevsky and C. Bonifield, Dietary fiber in health and disease, Plenum Press, New York (1997).

2. D.P. Burkitt and H.S. Trowell, Refined carbohydrate foods and disease: some implications of dietary fibre, Academic Press, London (1975).

3. K.T. Khaw and E. Barrett-Connor, Dietary fiber and reduced ischemic heart disease mortality rates in men and women: a 12-year prospective study, Am J Epidemiol 126 (1987), pp. 1093–1102.

4. C.G. Humble, A.M. Malarcher and H.A. Tyroler, Dietary fiber and coronary heart disease in middle-aged hypercholesterolemic men, Am J Prev Med 9 (1993), pp. 197–202.

5. D. Kromhout, E.B. Bosschieter and C. de Lezenne Coulander, Dietary fibre and 10-year mortality from coronary heart disease, cancer, and all causes. The Zutphen study, Lancet 2 (1982), pp. 518–522.

6. A. Wolk, J.E. Manson, M.J. Stampfer, G.A. Colditz, F.B. Hu and F.E. Speizer et al., Long-term intake of dietary fiber and decreased risk of coronary heart disease among women, JAMA 281 (1999), pp. 1998–2004.

7. I. Hjermann, K. Velve Byre, I. Holme and P. Leren, Effect of diet and smoking intervention on the incidence of coronary heart disease Report from the Oslo Study Group of a randomised trial in healthy men, Lancet 2 (1981), pp. 1303–1310.

8. A.C. Arntzenius, D. Kromhout, J.D. Barth, A.V. Bruschke and B. Buis et al., Diet, lipoproteins, and the progression of coronary atherosclerosis The Leiden Intervention Trial, N Engl J Med 312 (1985), pp. 805–811. M.L. Burr, A.M. Fehily, J.F. Gilbert, S. Rogers, R.M. Holliday and P.M. Sweetnam et al., Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: Diet And Reinfarction Trial (DART), Lancet 2 (1989), pp. 757–761.

9. D.J. Jenkins, T.M. Wolever, A.R. Leeds, M.A. Gassull, P. Haisman and J. Dilawari et al., Dietary fibres, fibre analogues, and glucose tolerance: importance of viscosity, Br Med J 1 (1978), pp. 1392–1394.

10. S.R. Glore, D. Van Treeck, A.W. Knehans and M. Guild, Soluble fiber and serum lipids: a literature review, J Am Diet Assoc 94 (1994), pp. 425–436.

11. D.J. Jenkins, C.W. Kendall, M. Axelsen, L.S. Augustin and V. Vuksan, Viscous and nonviscous fibres, nonabsorbable and low glycaemic index carbohydrates, blood lipids and coronary heart disease, Curr Opin Lipidol 11 (2000), pp. 49–56.

12. C.C. Schwartz, M. Berman, Z.R. Vlahcevic and L. Swell, Multicompartmental analysis of cholesterol metabolism in man, J Clin Invest 70 (1982), pp. 863–876.

13. D.M. Heuman, Z.R. Vlahcevic, M.L. Bailey and P.B. Hylemon, Regulation of bile acid synthesis. 11 Effect of bile acid feeding on enzymes regulating hepatic cholesterol and bile acid synthesis in the rat, Hepatology 8 (1988), pp. 892–897.

14. Z.R. Vlahcevic, D.M. Heuman and P.B. Hylemon, Regulation of bile acid synthesis, Hepatology 13 (1991), pp. 590–600.

15. P. Bell, K.J. Hectorn, H. Reynolds and D.B. Hunninghake, Cholesterol lowering effects of soluble-fiber cereals as part of a prudent diet for patients with mild to moderate hypercholesterolemia, Am J Clin Nutr 52 (1990), pp. 1020–1026.

16. J.W. Anderson, A.E. Jones and S. Riddell-Mason, Ten different dietary fibers have significantly different effects on plasma and liver lipids of cholesterol-fed rats, J Nutr 124 (1994), pp. 78–83.

17. J.W. Anderson, D.A. Deakins, T.L. Floore, B.M. Smith and S.E. Whitis, Dietary fiber and coronary heart disease, Crit Rev Food Sci Nutr 29 (1990), pp. 95–147.

18. A.C. Frati-Munari, J.A. Fernandez-Harp, M. Becerril, A. Chavez-Negrete and M. Banales-Ham, Decrease in plasma lipids, glycemia and body weight by Plantago psyllium in obese and diabetic patients, Arch Invest Med 14 (1983), pp. 259–268.

19. L.P. Bell, K. Hectorne, H. Reynolds, T.K. Balm and D.B. Hunninghake, Cholesterol-lowering effects of psyllium hydrophilic mucilloid Adjunct therapy to a prudent diet for patients with mild to moderate hypercholesterolemia, JAMA 261 (1989), pp. 3419–3423 .

20. J.W. Anderson, L.D. Allgood, A. Lawrence, L.A. Altringer, G.R. Jerdack and D.A. Hengehold et al., Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials, Am J Clin Nutr 71 (2000), pp. 472–479.

21. J.W. Anderson, M.H. Davidson, L. Blonde, W.V. Brown, W.J. Howard and H. Ginsberg et al., Long-term cholesterol-lowering effects of Psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia, Am J Clin Nutr 71 (2000), pp. 1433–1438.

ANRIL, Chromosome 9p21 and Coronary Artery Disease

I had just attended a talk by Dr Ruth McPherson on the topic of “Genetic Insights into Coronary Artery Disease”. She spoke about her genomewide association study (GWAS) which she had recently published in Science. For a quick review of the recent developments in GWAS of CAD, you can refer to my editorial in the European Heart Journal.

GWAS have consistently pointed to chromosome 9p21 and its robust association with CAD. Several replication studies have confirmed this fact. Approximately 25% of Caucasians carry 2 copies of the risk allele and have a 1.5 fold higher risk for CAD. The increased risk associated with this allele is independent of all known CAD risk factors. Thus the identification of region suggests that a novel biological pathway may be involved in atherosclerosis.

The 9p21 locus overlaps a newly annotated antisense noncoding RNA in the INK4 locus splice variant (ANRIL or DQ485453). ANRIL spans 126.3kb and overlaps at its 5’end with CDKN2B (p15INK4b). It consists of 19 exons, of which the first 12 exons are conserved whereas exons 13-19 are subjected to alternative splicing.

It would be exciting to see how the investigations of the 9p21 region would unfold in the near future!

Breckenridge

After more 24 hours of flying and in transit, I have finally arrived in Breckenridge, a small highland town in Colorado, USA to attend the Keystone Symposium on Metabolism and Cardiovascular Risk . It was a pity that I had arrived late in the evening and was unable to see sceneries of the mountains on the way here. Nevertheless, I had some time this morning to take a walk around The Great Divide, the lodge where I am staying. A picture is worth a thousand words. So here are the pics!

Aerial shot while on flight from San Francisco to Denver.

Can anyone tell me what are those disc-like vegetation in the midst of the desert? I saw a few clusters of these.

Sky view of Colorado

Breckenridge
Breckenridge

My research interests

I have two major research focuses

I. Genetics of Coronary Artery Disease

This aspect of my research involves studying genes related to coronary artery disease (CAD). It includes genetic epidemiological studies of how genes influence plasma risk factors such as lipid levels and blood coagulation factors, as well as clinical outcome such as atherosclerosis.

In the process of studying the genes, we have also built up a sizable database of about 3000 CAD and healthy individuals with information on more than 32 genotypes, environmental risk factors and family/medical histories. We have capitalized on this by developing an algorithm with the help of statisticians to predict CAD risk. The algorithm has since been patented and we are now validating it with more test cases.

The ultimate aim of our research is to be able to assess an individual’s risk of heart disease through family history, biochemical factors and genetic tests, especially for the neonates, so that preventive measures can be implemented early in life in order to delay the occurrence of CAD significantly or prevent it from occurring altogether.

Recently, we have also conducted some studies in the mouse and human cell line models to elucidate molecular mechanisms involved in dietary and acute phase protein responses.

II. Development of Lab-on-a-Chip Devices for biomedical applications

Another aspect of my research is in the development of biochips or “Lab-on-a-Chip” (LOC) devices for use in molecular diagnostics. LOC basically serves to miniaturize all the functions of regular bench-top equipments in the laboratory onto a chip no larger than the size of a credit card. We have successfully developed silicon biochips that can automatically extract nucleic acids (DNA or RNA) from blood. In essence, at the push of a button, blood goes into the chip and out comes pure DNA or RNA for carrying out genetic testing after about 1 hour. This breakthrough was made possible by combining the expertise from a highly dynamic team of engineers and biologists. There are three key advantages of LOC over conventional methods. These include i) Portability - the ability to be used at point-of-care or anywhere without the need to send samples to the laboratory, ii) Full Automation - does not require skilled operator, iii) Small Reaction Volume - thereby reducing reagent cost. Coupled with another of our invention, the microPCR for DNA amplification and other commercially available portable detection systems, the full capability of the LOC could be realized. We believe there is tremendous potential of our invention in shaping the way genetic tests are going to be carried out in the near future in diverse fields such as clinical, veterinary, forensic and medicine; agriculture; animal husbandry and biodefence.

Hello World!

Hi!

I have just started this site. Please give me some time as I begin to load in contents and post my blogs.

Will be back soon!

CK