role of media in election

a good way to do election coverage is to do an appraisal of what journalists have covered in the last five years in our area of coverage. Often the performance is as poor as political leaders. There are certain places they visit only during elections and, like politicians, forget them for the next five years. Now the five yearly rituals have come upon them once again and so Kishalay's route map has been drawn up. And so here's how it goes...

arm and the man

When the nation pays a tribute to the Kargil martyrs, all of us should review our attitude towards lesser known but equally valiant soldiers.

एक्शन of digoxin

[edit] Mechanism of action
The mechanism of action is not completely understood; however the current hypothesis is outlined below.
Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and decreases its function. This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na+/K+ pump leads to increased intracellular Na+ levels, which in turn slows down the extrusion of Ca2+ by the sodium-calcium exchanger that relies on the high Na+ gradient. This effect causes an increase in the length of Phase 4 and Phase 0 of the cardiac action potential, which when combined with the effects of digoxin on the parasympathetic nervous system, lead to a decrease in heart rate.[citation needed] Increased amounts of Ca2+ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This leads to increased contractility of the heart. This is a different mechanism from that of catecholamines.
Digoxin also increases vagal activity via its action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias (see below).

क्लीनिकल उसे

Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response, but beta- or calciumchannel- blockers should be the first choice[3] [4]. High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling.
The use of digoxin in heart problems during sinus rhythm was once standard, but is now controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and other effective treatments are now available. Digoxin is no longer the first choice for congestive heart failure, but can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment. It has fallen out of favor because it was proven to be ineffective at decreasing morbidity and mortality in congestive heart failure. It is shown to increase quality of life, however.
Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125 μg or 250 μg dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (such as digitoxin which although having a much longer elimination half-life of around 7 days, is mainly eliminated from the body via the liver, and thus not affected by changes in renal function).
Effective plasma levels are fairly well defined, 1-2.6 nmol/l. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled (see side effects below).
Researchers at Yale University looked at data from an earlier study to see if digoxin affected men and women differently. That study determined that digoxin, which has been used for centuries and makes the heart contract more forcefully, did not reduce deaths overall but did result in less hospitalization. Researcher Dr. Harlan Krumholz said they were surprised to find that women in the study who took digoxin died more frequently (33%) than women who took a placebo pill (29%). They calculated that digoxin increased the risk of death in women by 23%. There was no difference in the death rate for men in the study.
Digoxin is also used as a standard control substance to test for p-glycoprotein inhibition.

digoxin

Digoxin (INN) (pronounced /dɨˈdʒɒksɨn/[1]), also known as digitalis, is a purified cardiac glycoside extracted from the foxglove plant, Digitalis lanata.[2] Its corresponding aglycone is digoxigenin, and its acetyl derivative is acetyldigoxin. Digoxin is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication. Digoxin preparations are commonly marketed under the trade names Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/mL oral solution and 0.25 mg/mL or 0.5 mg/mL injectible solution. It is marketed by GlaxoSmithKline.

Cancerevo: Evolution and cancer
Studying cancer as an evolutionary disease. News and reviews about research on cancer and evolution from a theoretician's perspective.
Is there anything models can't do?
Date:
Monday, 06 Apr il 2009 - 00:15 UTC
I have to admit that I was thinking about posting something about coffee (it is still early in the morning here) and an article in The Economist mentions how coffee is being used to power cars. Apparently the same energy that can power people can power cars too, no idea whether that would be a sign that cars are becoming more human-like. Still, reassuringly for me, what the cars would use is not directly double espressos but the leftover grounds which would mean I could potentially feed my espresso cravings and fuel my car right with the same effort and cost.
Still, the topic of the day (or week to be a bit more realistic) is, as it was the previous time, something I read in Jerry Coyne’s book Why Evolution is true. The book describes the use of mathematical biology by Dan-Eric Nilsson and Susanne Pelger in a paper entitled A pessimistic estimate of the time required for an eye to evolve. In their model, a patch of cells capable (at least initially) of sensing light is allowed to evolve in a way in which only those mutations that increase the survival advantage were allowed to spread. Their conclusion is that, even in the worst case scenario, vision would nature evolve in only a few hundreds of thousands of years. As most evolutionary processes (unlike cancer) take lengths of time that are difficult for the human mind to fully grasp, a mathematical model can be a very useful tool to explain the evolutionary origin of one of the most sophisticated and, deceptively, engineered-like biological features.
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क्लीनिकल trial

In response to my last post, I wondered what Chris Scott's analysis of clinicaltrials.gov would say if he looked for fetal stem cells. He just told me he did the relevant search, and came up with nothing. In fact, one trial by StemCells that does use fetally derived cells does not say so in its clinical trial description. (See his post and several interesting comments at the link above.) Christopher Scott directs the program on stem cells and society at Stanford.
Scott has told me before that he is concerned that, because of enthusiasm for stem-cell research, clinicians may be including the term “stem cell” in clinical trials even if what’s being transplanted are poorly purified and characterized mixtures likely to contain stem cells. When I asked him about his recent analysis, he said he couldn't prove whether or not stem cells had been carefully purified or characterized. "It's just that the words "stem cell therapy" sounds sexier than "cell therapy" which is more accurate because most studies transplant populations of cells "enriched" for stem cells."
I suppose similar PR reasoning can explain the dearth of "fetal stem cells" in the database. A more charitable explanation would be that, of course, fetal stem cells is as poor a descriptor as is adult stem cells, since fetuses have already formed all their major organs. All the trials I know of using fetal cells use fetal neural cells. (But see my last post for more on that.)

स्टेम cells

Now we have the technology that can make a cloned child” reads the headline of the most-read article in the Independent right now. But the article does not actually break any news, nor does it use the common method of cloning; rather it discusses a well-understood implication of that recent reprogramming breakthroughs might yield yet another weird way of making a baby.If a technician wanted to do this, here’s how it would work: First, cells would be gathered from an existing human, probably through a skin biopsy. Second, these cells would be reprogrammed to an embryonic like state. (Current techniques to do this require engineered viruses to insert copies of genes into the reprogrammed cells. This makes the cells’ behavior less predictable and more prone to form tumours, but many scientists believe that new reprogramming techniques will soon be available that don’t require genetic modification.) Next, the reprogrammed cells would be merged with an early stage embryo, created by sperm fusing with egg in a laboratory dish. The “chimeric” embryo would be cultured for a few days and then implanted into a woman. If a baby was born, he or she would contain cells from two genetic individuals: the embryo and the human who supplied the cells. The baby would have three parents: two who gave the gametes for the embryo, one who gave the cells from a biopsy. (Such an individual would not be a clone. However, it is feasible that the chimeric embryo could be manipulated such that the original embryo only forms placenta and the reprogrammed cells form the body. This has been accomplished with mixtures mouse embryonic stem cells and mouse embryos, but not with mixtures of reprogrammed mouse cells and mouse embryos. )The results of some quick internet research suggests that using human iPS cells this way would not be allowed: In the UK, creating or using embryos outside the body requires a special license from the government, so I’d guess that permission would need to happen proactively. The US lacks legislation on reproductive cloning, though some individual states ban it. Australia distinguishes between research embryos (created through technical manipulation or by mixing genes from three or more people) and reproductive embryos (created through fusion of sperm and egg) and allows only reproductive embryos to used to create an embryo. A document dated to 2004 from Japan banned, among other things, the creation of chimeric human-human embryos for research.
Continue reading "Cloning by reprogramming?"