Monday, October 22, 2012
Thursday, May 31, 2012
“Private colleges charge a capitation fee of 40 – 50 Lacs for MBBS, you should have also produced some evidence of such practice. Like you call a victim in all your episodes, why not here? And do the same story Engineering, Architecture, Law and MBA colleges, do you think they are clean? Why target doctors alone?"
“One of your guest (Dr. Gulhati) said that doctors ask for 30% commission from Pharma companies to write their drugs. That is baseless, over-the-roof and sensationalizin g the matter. That is as true as “Most Leading actors ask newcomers to sleep with them”
“You compared the numbers of Licenses cancelled in England and in India. I must say your team is quite resourceful and please collect and compare following details also – a.Number of doctors beaten on duty by goons from various political outfits.”
“You said that the most brilliant students who take up medicine, should take it only for service to mankind, they should go to other fields if they want to earn. Why? Are we living in imperialism? Are doctors not allowed to earn and spend a good life? “
“For every 10 doctors who are doing wrong, there are more than 1000 healers. You owe us an apology!!!”
Tuesday, March 27, 2012
The vague answer would be ‘immunity’. At least that’s how I’ve always shut my brother up when he’s feeling inquisitive. But it’s always nice to understand ambiguities. Immunity is not a switch that can be at ‘good’ or ‘bad’ but a complex system governed by millions of pathways, enzymes, anatomical and external factors.
Researchers from a whole bunch of Universities and labs in the US and UK published an article in Nature on the 25th of March that might just have made a breakthrough of sorts in bringing some certainty into the hugely murky world of personalized medicine. Scientists from the Sanger Institute in Britain claim to have discovered the “crucial first line of defense” against the flu.
What they had to work with
In 2009 the journal Cell published a paper that established a protein called IFITM3 as having a crucial role in restricting viral replication, proving to be particularly hindrant to influenza, dengue and the West Nile virus. IFITM3 does this by inducing an immune agent called Interferon to prevent viruses from emptying their poison into cells, and consequently barring replication of the viral DNA in their host. See this for details.
However the study published in Cell was only demonstrated in-vitro, meaning in lab conditions. Usually an observed result only gains enough credibility to be applied once it is sufficiently replicated within a living system, or in-vivo.
It pays to play mice
The recent study from Nature have taken the IFITM3 study to the next level and proved that the IFITM3 does indeed play a highly significant role in determining how severely a flu virus affects its host. They did this by using one of the most efficient strategies to determine the functions of a gene/protein in a body. This involves deducing the role of substance ‘X’ in subject ‘Y’, for example, simply by observing the effect of Y in the absence of X. Since human subjects are not an option, the most commonly used animal model is Mus musculus or the house mouse(The mouse DNA is almost 85% similar to ours). Usually when the function of a gene, or its product -- a protein is to be determined, scientists genetically engineer mice with that particular gene absent or inactive so as to observe the effects. These mice are called knockout mice.
So these researchers used knockout mice which had an inactive IFITM3 gene and infected them with a low-pathogenicity (relatively mild) flu virus. They did the same for wild-type mice (normal variety) as well to compare the effects. They found out that the knockout mice suffered a great deal more than it’s wild cousins. The wild-type mice was tested and found to have increasing levels of the IFITM3 protein following infection, compared to the knockout mice which were unable to produce the protein. Similar results were seen when these two groups of mice were infected with the H1N1 virus which was recently responsible for the swine-flu pandemic.
From mouse to man
After collecting sufficient evidence of the protective role of IFITM3 in mice, the scientists proceeded to test their theory on human beings. How they did this is by examining influenza-ridden patients who have had to be hospitalized.
Now all human beings have the IFITM3 gene; the main differences lie within the gene itself. We’re all different from each other despite being more than 99% genetically similar. A large chunk of that variation is due to something called SNP’s or Single Nucleotide Polymorphisms.
SNP into it
Picture two chains of colour beads, each about 1200 beads long. The two chains are almost exactly identical except for example the 500th bead which is red in one chain but blue in the other. This would now be called rs500 (rs stands for reference SNP). And snp500 has two variants or alleles ie. R (red) and B (blue). In this analogy, the chain = IFITM3 gene, a bead = a nucleotide. Our cells are diploid, meaning we have two sets of each gene. So a person can either be RR (both red), BB (both blue) or RB (one of each). Of course in reality, our DNA is made of not color beads but nucleotides named A (adenine), G(guanine), C(cytosine) and T(thymine).
Sometimes the type of SNP, or the variant that you have on a particular gene will markedly affect the kind of protein that gene produces. One particular variant (‘CC’) of an SNP called rs12252 on the IFITM3 gene, results in the formation of a shortened version of the usual IFITM3 protein. This ‘CC’ variant of this SNP is much less prevalent than the more popular ‘TT’ and ‘TC’. Now if the IFITM3-flu virus hypothesis is true, the shorter protein produced in people with ‘CC’ in their IFITM3 gene will not be enough to resist the flu virus, and such a person would be more likely to have a severe attack than a person who is able to produce the usual protein.
They tested the hypothesis by selecting patients from various hospitals who were struck with severe influenza and testing their DNA to detect whether they were TT, TC, or the rogue CC. Then they compared this distribution to the normal frequency of these alleles in the population and concluded that the faulty variant CC is indeed more prevalent in severe flu patients than it is in normal circumstances.
Frankly my dear, should I give a damn?
This not only favours the hypothesis that the IFITM3 protein does indeed play a role in the progress of the flu, but also gives us a potentially useful way to predict a person’s susceptibility to a killer flu.
This also can explain why during the swine flu pandemic for example the virus was deadly for some and barely perturbed others.
With more confirmation, perhaps there could be a day when people can take informed decisions on whether or not he/she should take extra precautions like vaccines against the disease.
Even more in the future is the possibility of developing a drug that is similar to the IFITM3 protein so that it can curb the flu virus the same way.
But hold your horses…
There’s still a lot more to be done. The number of patients studied was only fifty three, hardly a large enough sample. The researchers themselves emphasise on the need for these results to be replicated in larger studies to hold good.
Another fact to keep in mind is that a living body is too complex for simple cause-effect relationships. Though the role of IFITM3 stands out, it is not the only gene that plays a role in our overall susceptibility to the disease. Other genetic and environment factors too interfere.
Wednesday, March 21, 2012
What is Aspirin?
Aspirin belongs to a class of drugs called nonsteroidal anti-inflammatory drugs or NSAIDs which is usally called ‘Dispirin’ in India. The main use of Aspirin is as a pain-killer, though more recently it has shown to prevent cardiovascular (heart) problems and now cancer.
How does it work?
Aspirin blocks the activity of an enzyme in our body called cyclo-oxygenase. Cyclo-oxygenase is needed to produce various chemicals in our body like prostaglandins, prostacyclins and thromboxane.
Pain: Prostaglandins are chemicals produced during injuries because of which we get swellings, inflammation and thereby pain. A high dose of aspirin (300mg and over) prevents the enzyme cyclo-oxygenase from producing these prostaglandins. And Voila! No pain.
Cardiovascular diseases: A lower dose of aspirin blocks cyclo-oxygenase too, but not enough to prevent prostaglandin production. At lower doses, aspirin prevents cyclo-oxygenase’s role in the production of another chemical called thromboxane. Thromboxane is usually produced by blood cells called platelets (with the help of cyclo-oxygenage) to help clot our blood and prevent too much bleeding, when you hurt your knee for example. But clotting of blood within your blood stream can obstruct free flow of blood and result in a stroke or a heart attack. So by preventing the production of thromboxane, blood is less likely to clump together in your blood vessels and cause complications.
Cancer: While the above two uses of Aspirin are relatively well established, it’s role in cancer prevention/cure has been debated since the 70’s by Bennett and Del Tacca. But three recent studies on the topic conducted by Peter Rothwell of the Oxford University however have silenced some skeptics. They conducted a randomized, controlled trials and concluded that a daily low dose of Aspirin for just 3 to 5 years is enough to lower risk of certain cancers, particularly bowel cancer in people who are at risk.
However, it must be noted that all these studies have been epidemiological studies. Though statistics have been proved to be immensely useful to establish correlation between two factors, is it enough? From what I have explored, not many biological reasons for this phenomenon have emerged. If they have then, nobody seems to be talking about them enough.
How is Aspirin doing this?
The biological processes involved in this correlation have still not been established. However there have been some explanations proposed.
As mentioned, Aspirins thins blood, makes it less likely to clot by its effect on blood clotting platelets. Now platelets, save us from bleeding to death no doubt, but they have been show to play a sinister role as well. They prime cancer cells for metastasis ie. They help cancer cells spread from its site of origin. How it does this is detailed in this easy-to-understand article .
So since Aspirin is anti-platelet, and platelets are pro-cancer, this could be one of the mechanisms by which Aspirin cures cancer.
Last month Australian scientists made another explanation.
Co-lead author Tara Karnezis said tumors secret proteins and compounds called growth factors, attracting blood and lymphatic vessels to their vicinity and allowing the cancer to flourish and spread. These growth factors also encourage lymphatic vessels -- or "supply lines" -- to widen, which enables the spread of cancer, she added. "But a group of drugs reverse the widening of the supply line and make it hard for the tumor to spread -- at the end of the day that's what kills people," Karnezis said. "This discovery unlocks a range of potentially powerful new therapies to target this pathway in lymphatic vessels, effectively tightening a tumor's supply lines and restricting the transport of cancer cells to the rest of the body."
So whatever the reason, this doesn’t mean we can simply start gobbling up pills and expect to be Cancer free. There are several concerns that haven’t been addressed.
Aspirin has been known to have side-effects, one of the more serious though rare one is stomach bleeding.
Some critics have noted that some of the doses given in the study were much higher than the 75mg dose typically given in the UK, said a BBC report (Since the article is Lancet, read Elsevier, stuck up folks aren’t letting me read it for free and verify this myself).
The benefit of Aspirin for healthy people is yet to be quantified. The lead author Prof Rothwell himself has said that for most fit and healthy people, the most important things they can do to reduce their lifetime cancer risk is to give up smoking, take exercise and have a healthy diet. Aspirin does seem to reduce the risk further – but only by a small amount if there is no risk factor.
Tuesday, March 20, 2012
Saturday, March 3, 2012
What I found out:-
1) Indian food is deadly spicy.
2) Indians hate Pakistanis
3) It is unheard of to not love SRK
#100WaysToDieInIndia say Sharukh Khan is the shittest actor ever and he's an overrated egghead— akbarghhhh (@akbar_0) March 3, 2012
4) Indian elders regularly beat kids with chappals
5) Cows, goats and elephants trample on us frequently. Cobras also.
#100WaysToDieInIndia get run over by a renegade Elephant.— Taronish Elavia (@Taro_Elavia) March 3, 2012
#100WaysToDieInIndia get run over by a cow— Henry Austin (@henryaustin) March 3, 2012
#100WaysToDieInIndia Provoke a cobra.— Jack Brien (@JackBrien1) March 3, 2012
#100WaysToDieInIndia Trampled by a random sanjay and his elephant.— Liam Boyle (@LBoyle33) March 3, 2012
6) Indian parents have no tolerance for their wayward (read non-engineering/medically inclined) offspring.
#100WaysToDieInIndia "I'd rather be a hairdresser, don't wanna be a doctor" *Dad prepares shotgun*— Denzil Safo-Antwi (@DenzilSafo) March 3, 2012
7) Indians are all vegetarians
'#100WaysToDieInIndia Kill a cow and you'll be toast.' fact.— emmanuel mwisa (@Red_AlertMe) March 3, 2012
8) Indians all have long names
#100WaysToDieInIndia GO TO MACCIES ON JALANDHAR RD AND LAUGH AT THE WORKER CALLED "ALBERT" WHEN CLEARLY HIS NAMES TO LONG FOR THE NAME TAG!!— TWEETHOOLIGAN (@RandyBhambra) March 3, 2012
9) Indians often sell body parts to buy cricket tickets
10) Indian men don't cheat
11) Abusing a Sardar is frowned upon.
#100WaysToDieInIndia abuse a sardar and u will die of guilt— Chemical Locha (@DilFake_aashiq) March 3, 2012
12) We all marry our cousins. And Sanji is a real name.
#100WaysToDieInIndia not marrying your cousin sanji— chris pennicott (@cpennicott) March 3, 2012
13) If not that then at least we must do arranged marriage
As if all of this wasn't enough, we've got these to worry about -
Sunday, February 19, 2012
Joshua Bell, the musician, had just played for a fancy audience - each of whom had paid around $100 for a ticket - a few days ago.
This is what happened.
Bell managed to earn about $32 (excluding the $20 bill he got from a fan who eventually recognised him) from more than a thousand commuters who passed by during that 45 minutes.
How screwed up is that? Imagine how differently we would look at the world if we had no set notions.
There's 2 ways to interpret this.
1. It's possible to wonder if the talent in question is overrated. Maybe Bell is just a mediocre violinist who got a series of lucky breaks. If the crowd didn't listen, does that mean the music wasn't really good?
This is a very valid point, especially in this age where a video of a dog twitching in it's sleep can go viral.
There are so many chance happenings that serendipity has lost its charm today. How do you know if Justin Bieber would be where he is today even if Scooter Braun hadn't 'discovered' him? What is Braun had not updated his flash player or chose this guy instead?
I could go on...
It's all arguable i suppose, but maybe I'm being naive in saying that talents like Joshua Bell, AR Rahman and others are the few for whom luck might not have played as much a role as their gift and their hardwork did.
For them not to have been noticed would have taken life full of lousy luck and bad decision-making.
Which brings us to the second point of view.
2. Let's say these famous guys are really talented (Okay, excepting Snooki, the Kardashians, anybody in Bigggg Boss and Zayed Khan), so there's nothing wrong with a little bit of luck helping them out right?
But imagine if the same amount of luck was given to everyone. How many potential superstars are lurking in the world with no chance of recognition? The supremely overdone example ofcourse is 'How many Sachin Tendulkars might exist among the millions of galli cricket players'.
this was not even a point with which I began this blog entry. I meant to write about how shackled we are by our responsibilities and by perceptions of the society as a whole. How without realizing it, most of us form most of our opinions based on already formed ones.
Sounded really deep in my head, but like wannabe trash on paper. Will publish this still because I'm self destructive that way.