HowStuffWorks - How Force, Power, Torque and Energy Work

If you've read many http://howstuffworks.com/ articles, you've seen a lot of terminology thrown around -- words such as mass, force, torque, work, power and energy. What do the-se words really mean, and are they interchangeable? Go to http://howstuffworks.com/ and find the answer.

Why Dichotomizing Variables is a Bad Idea

This is a nice review from the research perspective, but may be not so practicable without using dichotomized variable of a continuous variable. For example, the criteria of diabetes and hypertension diagnosis are based on dichotomized variables from continuous blood glucose level and blood pressure level.

_From Bob

        It is well recognized in the methodological literature that dichotomization of continuous variables introduces major problems in the analysis and interpretation of models derived in a data-dependent fashion. Nevertheless, dichotomization of continuous variables is widespread in clinical research. Problems include loss of information, reduction in power, uncertainty in defining the cutpoint, arriving at a biologically implausible step function as the estimate of a dose–response function, and the impossibility of detecting a non-monotonic dose–response relation. Uncertainty in how to select a ‘sensible’ cutpoint to group a continuous variable into two classes has led researchers to use either the median or an ‘optimal’ cutpoint. The latter approach gives a highly inflated type 1 error probability, together with biased parameter estimates and variances that are too small [9, 11]. Although some remedies for these diffculties have been developed [9, 21–23], none of the authors of these papers actually recommends the use of ‘optimal’ cutpoints with their proposed corrections. In general, the situation seems hardly to have improved since the advice in 1993 of Maxwell and Delaney [1] to avoid dichotomization, quoted at the beginning of this paper.

Instead of dichotomizing a continuous variable, we prefer to obtain a prognostic index by methodology which combines selection of variables with selection of functions for continuous variables [4, 26]. As stated in an editorial [2] in an epidemiological journal a decade ago, ‘these elegant approaches [fractional polynomials and splines] merit a larger role in epidemiology.’ Clinical researchers should in general avoid dichotomization at the model-building stage and adopt more powerful methods.

Royston, Patrick (2006) Statistics in Medicine 25:127-141

Please share this with your son.

Gentlemen,

Yes gentlemen, you are no longer the little Tiger Cubs we started out with 5 years ago.  Each of you have grown up into nice young men during that time. It has been my pleasure being first a Den Leader and then the Cubmaster for your years in the Pack.  Over these 5 years  have seen you boys grow not only in size but as a human beings.  I hope that Cub Scouts has been a positive experience for you.  For those that have decided to take a break from the Scouting program I hope that you will find your way back to it at some point.  Either in a few years as a Boy Scout or later as an adult with your son in Scouting.  The mission of the Boy Scouts is to instill values in young people and to help prepare them to make ethical choices during your lifetime.  These values can be found in the Scout Oath and Law.  Please remember the 12 point of the Scout Law and try to live your life based upon these 12 points, not only as a youth but also as an Adult.

It has been a pleasure working with you young gentlemen.

YIS

Mr. Alan  

In memory of Dr. John Denis McGarry

In memory of Dr. John Denis McGarry

Dr. Denis McGarry was a great teacher and sage. His lecture affects my way of thinking on diabetes. Unforgettable.

“In 1992, he published a famous paper in Science entitled “What if Minkowski Had Been Ageusic?” (1). In this paper he suggested that scientific concentration on abnormal glucose metabolism had masked the critical importance of abnormal fat metabolism, especially in type 2 diabetes. Subsequent to this paper there was a huge swing by investigators toward the key role of abnormal lipid metabolism in insulin resistance and lipotoxic damage to tissues as diverse as the heart and the β-cell of the pancreas.”

Please find the full article here.

K M Venkat Narayan: A case of well-intentioned public health reductionism?

K M Venkat Narayan: A case of well-intentioned public health
reductionism?

Very good comments.

http://blogs.bmj.com/bmj/2010/03/04/k-m-venkat-narayan-a-case-of-well-in
tentioned-public-health-reductionism/

Findings - When It Comes to Salt, No Rights or Wrongs. Yet. - NYTimes.com

 

This article may not  be scientifically proved, but I like the title and Effect E. By the way, I don’t like the comparison of smoking and salt, it makes salt such a evil substance like cigarette. We cannot abstain from salt. The question is how much and the answer is it depends…

FDA internal reports unhappy about rosiglitazone (Avandia)

Research Ties Diabetes Drug to Heart Woes

 

http://www.nytimes.com/2010/02/20/health/policy/20avandia.html

 

Does anyone know why Avandia increases the risk of CHD? Is because of efficiently lowing the glucose level (too low)? Or any other side-effects.

 

A Lasting Gift to Medicine That Wasn't Really a Gift

A Lasting Gift to Medicine That Wasn’t Really a Gift

 

 

http://www.nytimes.com/2010/02/02/health/02seco.html?th&emc=th

 

A cell line called HeLa (for Henrietta Lacks) was born. Those immortal cells soon became the workhorse of laboratories everywhere. HeLa cells were used to develop the first polio vaccine, they were launched into space for experiments in zero gravity and they helped produce drugs for numerous diseases, including Parkinson’s, leukemia and the flu. By now, literally tons of them have been produced.

Dr. Gey did not make money from the cells, but they were commercialized. Now they are bought and sold every day the world over, and they have generated millions in profits.

Ukrainian registry of type 2 dm shows U-shaped relation of BMI to mortality

Ukrainian registry of type 2 dm shows U-shaped relation of BMI to mortality
(Heart 2009;95:454-460. doi:10.1136/hrt.2008.150524)

Not too surprising, a common sense is that extreme, fundamental, or radical ends are not good. But one of the interesting figures (finding) is even obese population (≥45) had lower risk of death than low BMI population (<20 for all-cause death, and <21 for CVD death).

Manifest Destiny is an funny video related to the report of recent stable obesity rate.

This is a good omen. This means that we will see the diabetes prevalence going to reach the platform soon.
_____________________________________________
Obesity rate appears to be stabilizing.

ABC World News (1/13, story 8, 0:20, Stephanopoulos) reported, "New numbers today from the CDC show the rate of obesity stabilizing."
The New York Times (1/14, A20, Belluck) reports that "Americans, at least as a group, may have reached their peak of obesity." The good news is that "the numbers indicate that obesity rates have remained constant for at least five years among men and for closer to 10 years among women and children -- long enough for experts to say the percentage of very overweight people has leveled off." The bad news is that "nearly 34 percent of adults are obese, more than double the percentage 30 years ago," while "the share of obese children tripled during that time, to 17 percent," according to studies published online Jan. 13 in the Journal of the American Medical Association.
The first study "examined height and weight data in a nationally representative sample of 5,555 adult Americans collected in 2007 and 2008," the Los Angeles Times (1/14, Stein) reports. "In the sample, 33.8% of the subjects" were "obese." After comparing "those numbers...to ones collected from 1999 to 2006 in a similar sample," researchers found that "among women, obesity statistics remained fairly flat throughout the period encompassed by the two studies," while "obesity rates among men rose slightly during the decade, but leveled off in the later years."
In the second study of nearly 4,000 children ranging in age from two to 19, the Wall Street Journal (1/14, Dooren) reports, researchers found that 17% of the youngsters met the threshold for obesity and 32% could be deemed to be overweight, a pattern similar to what was seen a decade ago. For both studies, the Journal notes that the CDC researchers based their estimates on data derived from the most recent National Health and Nutrition Examination Surveys.
USA Today (1/14, Hellmich) reports that "William Dietz, director of the CDC's Division of Nutrition, Physical Activity and Obesity, says this may reflect that people are becoming aware of 'the adverse health consequences of obesity' and are adopting healthier habits." Still, when it comes to the impact of obesity on children, Cynthia L. Ogden, PhD, the author of both studies, is concerned, because "obese kids are at a greater risk of weight-related health problems such as high cholesterol, blood pressure, and diabetes, plus they are at a greater risk of becoming obese adults, she says."
Bloomberg News (1/14, Ostrow), the AP (1/14, Tanner), Reuters (1/14, Steenhuysen), Time (1/13, Kluger), HealthDay (1/13, Gordon), &&&WebMD (1/13, DeNoon), and &&&HeartWire (1/13, O'Riordan) also covered the story.

Why Genes Aren't Destiny
 An article from Time

A nice article for understanding the relation of disease and DNA and epigenetic markers

... Biologists offer this analogy as an explanation: if the genome is the hardware, then the epigenome is the software. "I can load Windows, if I want, on my Mac," says Joseph Ecker, a Salk Institute biologist and leading epigenetic scientist. "You're going to have the same chip in there, the same genome, but different software. And the outcome is a different cell type."...

High-Fructose Corn Syrup Linked to Obesity, Diabetes


High-fructose corn syrup (HFCS) is also known as corn syrup, isoglucose and fructose on package labels and has been undergoing scrutiny for the last several years. Back in the '80s, when the low-fat craze started, HFCS began to be added to everything as a relatively easy way to add flavor and moisture to lower-fat products. Seemed like a great idea at the time. Corn is in abundance in the United States, and corn syrup is cheap and easy to add to commercially prepared foods. Little did we know that this type of sugar is digested very differently, and unlike glucose, actually prevents you from feeling full even when you have eaten a lot. Here's how it works: You eat something with HFCS and the sugar goes to your liver for processing. There it gets broken down into smaller components and eventually gets broken down completely. This is how all sugars are managed by the body. The problem is HFCS uses a lot more of the cell's energy to breakdown and leaves the cell with less energy to properly metabolize other foods. In addition, the breakdown products of the process cause an increase in lipid levels and triglycerides in the blood and within the cell itself, causing the fat to fill the cell. HFCS metabolism increases circulating insulin levels significantly and results in insulin resistance (the precursor of adult onset diabetes and metabolic syndrome). Lastly, unlike glucose, HFCS byproducts in the blood send a message to the brain that you are still hungry and need to eat. The more you eat, the more you crave! Most other sugars get stored in the cell, not as fat but as a substance called glycogen that can be easily mobilized for energy when needed, unlike the lipid that is formed from HFCS that is hard to mobilize when needed. HFCS leads to fatty liver, high blood lipids and triglycerides, high blood insulin levels and a continued craving to eat even when the body doesn't need any more calories. This is a recipe for central body obesity, heart disease, diabetes and liver failure from fatty deposits. Interestingly, this is the exact outcome when alcohol is consumed (minus the buzz or drunken feeling). If you drink alcohol too much, you get a "beer belly" (central obesity), fatty liver, heart disease from high triglycerides and lipids, and type 2 diabetes. We wouldn't dream of giving our kids alcohol, but as it turns out, HFCS is metabolized in the exact same way with the same damage done, calorie for calorie. For most adults, some alcohol drinking is OK, but excessive use or abuse can lead to serious long-term physical consequences. The same is true for HFCS. By the way, even though fresh fruit contains fructose, because it is "packaged" with natural fiber, it is digested very differently and doesn't cause these changes. Whole, fresh fruit is healthy, but fruit juices, fruit roll-ups and fruit snacks are devoid of the fiber and therefore no better than candy. I encourage families to spend time reading labels and becoming aware of how ubiquitous this additive is. It is in store-bought bread, crackers, pop, cookies, some lunch meats, fruit juices, packaged chocolate milk, candy, all-natural fruit snacks and many other packaged foods. I am not suggesting you need to completely eliminate it from your life, but I encourage you to decrease the amount your family eats every day.

Dr. Molly O'Shea is a Troy pediatrician. Read Dr. Molly's blog, get answers to your questions and discuss children's health issues at detnews.com/drmolly.

Health News Review - Objective Ratings of Health and Medical Journalism
http://www.healthnewsreview.org/

NHS 2009 Annual Evidence Update on Diabetes and Complication

http://www.library.nhs.uk/Diabetes/ViewResource.aspx?resID=328114

This is the third year of review on diabetes issues.

Colorbrewer: Color Advice for Maps

Colorbrewer: Color Advice for Maps

http://colorbrewer2.org/

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

The metabolic abnormalities of type 2 diabetes can be reversed reproducibly by bariatric surgery. By quantifying the major pathophysiological abnormalities in insulin secretion and insulin action after surgery, the sequence of events leading to restoration of normal metabolism can be defined. Liver fat levels fall within days and normal hepatic insulin sensitivity is restored. Simultaneously, plasma glucose levels return towards normal. Insulin sensitivity of muscle remains abnormal, at least over the weeks and months after bariatric surgery. The effect of the surgery is explicable solely in terms of energy restriction. By combining this information with prospective observation of the changes immediately preceding the onset of type 2 diabetes, a clear picture emerges. Insulin resistance in muscle, caused by inherited and environmental factors, facilitates the development of fatty liver during positive energy balance. Once established, the increased insulin secretion required to maintain plasma glucose levels will further increase liver fat deposition. Fatty liver causes resistance to insulin suppression of hepatic glucose output as well as raised plasma triacylglycerol. Exposure of beta cells to increased levels of fatty acids, derived from circulating and locally deposited triacylglycerol, suppresses glucose-mediated insulin secretion. This is reversible initially, but eventually becomes permanent. The essential time sequence of the pathogenesis of type 2 diabetes is now evident. Muscle insulin resistance determines the rate at which fatty liver progresses, and ectopic fat deposition in liver and islet underlies the related dynamic defects of hepatic insulin resistance and beta cell dysfunction. These defects are capable of dramatic reversal under hypoenergetic feeding conditions, completely in early diabetes and to a worthwhile extent in more established disease.

Qian Xuesen, Tsien Hsue-shen

http://zh.wikipedia.org/wiki/%E9%92%B1%E5%AD%A6%E6%A3%AE
http://en.wikipedia.org/wiki/Tsien_Hsue-shen

Association of A1C and Fasting Plasma Glucose Levels With Diabetic Retinopathy Prevalence in the U.S. Population


... CONCLUSIONS The steepest increase in retinopathy prevalence occurs among individuals with A1C ≥5.5% and FPG ≥5.8 mmol/l. A1C discriminates prevalence of retinopathy better than FPG...

Diagnosis of diabetes using the oral glucose tolerance test

The prevalence of type 2 diabetes varies greatly by ethnic group within and across countries. The most reliable data on the prevalence of diabetes are based on two hour plasma glucose values after an oral glucose tolerance test,¹ which is currently the gold standard epidemiological and clinical diagnostic test for diabetes and impaired glucose tolerance. In Newcastle, England, on the basis of clinical evidence and oral glucose tolerance test results, about 20% of British South Asians had diabetes, compared with only 4% of white Europeans, after age adjustment in a sample of 25-74 year olds.² Might such observed differences in prevalence, at least in part, be artefacts of the diagnostic method?

In 1965, the World Health Organization expert committee drew attention to the "lack of suitable epidemiological information about glucose tolerance in various populations of various races and cultures in different countries"³ and highlighted the need for research in different populations. The call was repeated in 1980,¹ with special reference to the oral glucose tolerance test and the dose of glucose, with 75 g being recommended pending further investigations. The International Diabetes Federation in consultation with WHO and the American Diabetes Association (ADA) have raised similar concerns, particularly about the oral glucose tolerance test.^{4 5} With a 75 g dose, a venous plasma glucose value of 11.1 mmol/l or more is indicative of diabetes, as indicated by its association with complications such as retinopathy. A value of 7.8-11.0 mmol/l is indicative of impaired glucose tolerance. Yet these concerns have not been dealt with.
The prevalence of diabetes is increasing worldwide, and accurate testing is more important than ever. The best way to make a diagnosis has been debated for decades,^{1 3 4 5} and more guidance is imminent. In some ethnic groups, comparatively low fasting plasma glucose concentrations are seen in people who have two hour postload glucose values that are diagnostic for diabetes.⁶
In the light of these concerns it is vital to know whether the 75 g carbohydrate load is appropriate for all adults, regardless of ethnicity. Glucose tolerance is influenced by several factors—from genetics, to body build (height and weight), to diet and lifestyle. Differences in body composition and skeletal muscle mass are important determinants of postprandial glucose metabolism, and height measurement partly reflects such differences.
An independent inverse association with two hour plasma glucose after the oral glucose tolerance test has been repeatedly shown for height in diverse populations.^{7 8} In a study of the prevalence of type 2 diabetes in white Europeans, African-Caribbeans, and Pakistanis, height almost completely accounted for ethnic differences in two hour plasma glucose in multiple regression models. Pakistanis, in whom the prevalence was the greatest, were markedly shorter (by 2-5 cm) than people in other ethnic groups.⁷ The implications of these findings are that a uniform oral glucose load may not accurately assess glucose tolerance across populations,¹ and a high two hour plasma glucose after the oral glucose tolerance test may overdiagnose impaired glucose tolerance in some ethnic groups compared with white populations.
Other factors related to body composition that vary by ethnicity may also be important. Varying the glucose load, as is done in children, or adjusting the results according to ethnicity or height (or both), may improve measures of glucose tolerance. These general observations could have wider implications in explaining inequalities. Impaired fasting glucose is more prevalent in men, whereas impaired glucose tolerance is more prevalent in women.⁹ Women are generally shorter than men, so this difference could simply reflect height differences by sex.
Whereas height has been shown to have a marked association with two hour plasma glucose after the oral glucose tolerance test, fasting plasma glucose and glycated haemoglobin measurements vary very little with height or sex.^{8 10} We should consider whether the oral glucose tolerance test can be replaced with other measures, such as glycated haemoglobin, in everyday clinical practice. This was a topic of debate at this year’s ADA annual conference in New Orleans, and work is already under way to standardise the measurement of glycated haemoglobin. However, as with the oral glucose tolerance test, the validity of glycated haemoglobin needs to be shown across ethnic groups before it is accepted and implemented.
WHO’s warnings in 1965 about the validity of the oral glucose tolerance test across various populations were prescient and deserve continuing attention. The uniform size of the oral glucose load used in this test, even though body size and composition vary, may account for some of the variation in the prevalence of diabetes between men and women and different ethnic groups. Nonetheless, the excess of diabetes in South Asians is marked using other criteria, such as those based on fasting glucose used by the ADA.¹¹ The complications of diabetes, such as retinopathy and nephropathy, are also greater in South Asians.¹²
Clinicians must be confident that the key tests for diabetes or impaired glucose tolerance are accurate, because the consequences of these diagnoses are considerable and lifelong. Although a false positive result might lead to good advice about diet and exercise, it could also provoke anxiety and adoption of the sick role. A false negative result is potentially dangerous in view of the high levels of cardiovascular diseases and renal dysfunction in South Asians. We must always establish the validity of diagnostic tests across sexes, age groups, and ethnic groups. This still applies to the oral glucose tolerance test and its likely successor, the measurement of glycated haemoglobin.
Cite this as: BMJ 2009;339:b4354