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PhD in USA after B.Tech in Biotechnology

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Dear sir,
I have seen many universities in USA ( like MIT) offer direct PhD after B.Tech. But i have few questions:
1) What is the min. GRE and TOEFL scores required for full scholarship ?
2) Any special requirement like research experiences ?
3) For visa, is it true that a candidate needs to show a certain amount of Bank Balance? If yes How much?

Thanking you.

GATE BT 2016

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sir this year IISC is organising GATE BT 16 so how should i study and can i crack it in 6 months time period.

Final Admission for MTech Biotech at NIT Rourkela

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Hello Sunil,

I am an Indian national and have completed my BS degree in Biochemistry (4 years duration) from the USA. I am currently residing in India and have qualified GATE BT 2015 and have a provisional admission offer for MTech in Biotechnology from NIT Rourkela, through CCMT (didn't make the cutoff for IITs). 
For final admission, apart from the original degree certificates and marksheet, NIT Rourkela is also asking me to submit migration certificate and transfer certificate (as per their document verification checklist)..However, since US universities don't issue such documents, I don't have these with me. Any advice on how I can handle this issue?

Migraine: Diagnosis and Classification of Headaches

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Headache is in almost all cultures and countries among the most common health complaint, and was one of the first conditions to be commented on in ancient medical literature. The great majority of headaches requiring medical attention are manifestations of migraine, which is today the best understood of the headache disorders. The many recent advances in understanding of headache physiology, pharmacological treatment of headache and application of biotechnology to the treatment of headache have been mostly in the area of migraine, which also represents most of the historical cases of headache.

Some of the earliest treatment recommendations for headache involved decompressive skull surgery (trepanation) and evidence of such procedures has been found from as early as 7000 BCE. The Ebers papyrus from about 1500 BCE contains clinical descriptions of headache syndromes consistent with migraine, and the ancient Egyptians developed an extensive pharmacopoeia of herbal medicines, some of them still recommended for migraine. Egyptian therapies also included rubbing the affected side of the head with a fried fish, which is difficult to reconcile with current headache medicine, and binding tightly to the head a clay crocodile containing invocations to the relevant gods. The latter was reported to be effective for chronic headache, and it is possible that the pressure of the linen strips holding to the vessel had a beneficial effect on tension-type headaches [1].

The Hippocratic school of ancient Greek medicine also devoted much attention to headache treatment. The “father of medicine” himself described the prodrome of migraine and the nausea and vomiting that is often associated with migraines and sometimes relieves them. Hippocrates also described the visual scotoma and some other manifestations of the migraine aura and observed the correlation between migraine and exercise, including “immoderate venery”. The occurrence of nausea with migraine and the frequent relief of headache with vomiting led Hippocrates to ascribe the disorder to vapors rising to the head from the stomach, which although incorrect was the ancestor of the neurohumoral theory of migraine pathogenesis that predominates today. Headaches were among the chief symptoms addressed by the priests at the temples of Asklepios, and were often treated by the enkoiemesis or induction of therapeutic sleep, probably by opium, followed by a medicinal diet, both of which may have presaged acute pain management and holistic headache treatments of the present day. In addition to Hippocrates and his disciples, the philosopher Plato often commented on medical topics. Although he was usually wrong when he opined about medicine, Plato did contribute one observation that is germane to headache treatment and to psychosomatic medicine generally: he suggested that in some cases head pain was due to excessive preoccupation with the body and its symptoms [2].

The other precursor of the Western medical tradition in classical antiquity was Roman medicine, epitomized by Galen of Pergamon even though he himself was Greek. Galen took an active interest in headache, and was the first to use the term hemicranias, from which “migraine” was derived. He also identified for the first time the meninges and cerebral blood vessels as the source of head pain, and ascribed pulsatile headache with vomiting, particularly marked in children, to the accumulation of bile in the stomach, giving rise to the still-used term, “bilious attacks”. Arataeus of Cappadocia, another Greek physician in the Roman Empire, at about the same time summarized the features of what are today called classical or common migraine, and distinguished three types of headache: generalized cephalalgia, unilateral and usually migrainous hemicranias and cephalea, headache not in a nerve or blood vessel distribution. Arataeus also advocated cauterization of the scalp and scalp muscle division for refractory headache, modern equivalents of which have lately been used in headache treatment [3].

Headache also received attention in eastern medical traditions. The second-century surgeon Hua To identified acupuncture points useful in treating head pain, and according to legend used acupuncture needles to remove a bulging frontal lesion from a patient suffering from pain between his eyes, after which a canary flew out. Other techniques of ancient Chinese medicine used for headache, such as cupping, the application to the skin of heated glass vessels containing a vacuum to remove toxins, and moxibustion, the first direct and later indirect application of heat and herbal remedies to the skin to rebalance qi or life energy, may date from the 16 [th] century BCE, and their principles are reflected today in western energy medicine and detoxification treatments [4].

The ancient Indian Ayurvedic medical tradition, like the Greeks, postulated that disease was caused by imbalance of doshas or humors. The system derived its name from the Sanskrit for “science of life” or “life knowledge”, and from its beginnings approximately 5,000 years ago emphasized individual variations in disease susceptibility and the role of lifestyle and diet in the production of disease. Headache and pain in general was often ascribed to excess of vata, the energy of movement that is often associated with nervous disease. Headache treatment focused on diet and natural remedies, and some of these techniques are applied today in western holistic medicine as well as Ayurvedic practice [5]. The North and South American “Indian” medical traditions are similar in their approach to headache and other nervous disorders, although sometimes different in the herbal remedies used on account of geography, and appear to have used ritual and spirituality as well as natural medications for several millennia before the arrival of Europeans [6].

As in many areas of medicine, the Islamic world preserved and extended some important ancient insights during the western Dark Ages. The 8 [th] and 9 [th] century medical writers Muhammad al-Razi and Muhammad al-Tabari extensively reviewed the writings of Hippocrates and Galen in their books, and Sabet ibn al-Harani wrote a comprehensive pain textbook which dealt with headache at the start of the 10 [th] century. al-Tabari differentiated migraine from other types of headache, presciently ascribed it to vascular inflammation and described two medical methods of treatment as well as cauterizing the temporal artery for focal temporal pain that may have represented arteritis. Ibn Sina or Avicenna described methods for preparing and testing the efficacy of medicine in his influential Canon of Medicine about a century later, and emphasized the role of exercise in disease treatment and prevention [7].

Byzantine treatments for headache began with purging and bloodletting, preferably from the side opposite to hemicranial headache, often copious and from the the cranial circulation by way of incisions in the nose as well as from the arm. The 1500 medical aphorisms of Maimonides include many concerning headache management, particularly bleeding from palpable pulsating vessels, presumably those involved in the pathogenic events of migraine which were to be clarified centuries later. Beginning with Arataeus, these physicians independently developed the technique of cupping that was being used in Chinese medicine. More benign recommendations of the time included the advice of Oribasius, physician and friend to several late western Roman emperors, to inject soft oil into the ear on the involved side, and the 10 [th] century recommendation by ibn Isa to bind a dead mole tightly to the head, recapitulating the ancient Egyptian method [8].

St. Hildegard of Bingen wrote medical texts in addition to being a philosopher, dramatist, composer and Benedictine abbess. She experienced scintillating visions that are now felt to have been ocular migraines, and described these in writing as well as with drawings that remain classic illustrations of migrainous aura. Her medical works do not reflect her visionary experiences but result from her extensive experience in her abbey’s medicinal garden, and as one of few women schooled in Latin in that day, she was able to write about herbal medicine in a way that most of the women who mainly practiced it at that time could not, and provided the basis for subsequent compendia of medical herbalism. A particular innovation in her recommendations was the application to the scalp of poultices soaked in vinegar and impregnated with opium; it is thought that the vinegar opened the pores of the scalp and facilitated the absorption of the opium [9].

Headache came under the purview of “neurology” when Thomas Willis introduced that term in 1672, and proposed that migraine was the result of cerebral vasodilation, and suggesting that migraine symptoms were correlated with slowly ascending spasms beginning in peripheral nerves and extending centrally. Erasmus Darwin, grandfather of Charles, proposed at the end of the 18 [th] century that patients be spun in a centrifuge in order to redistribute blood from the head to the feet to reduce cerebral vasodilation and head pain. More detailed headache classification was attempted during the 18 [th] century, with the first description of what was later called cluster headache given by van Swieten in 1745, and the differentiation of primary or idiopathic headache from symptomatic headache secondary to an identificable cause and the delineation of 84 headache syndromes by Baur in 1787 [10]. The distinction between migraines with prodromal symptoms, usually visual (migraine ophthalmique), and those without ( migraine vulgaire) was first proposed in 1887 by Louis-Hyacinthe Thomas, by profession a librarian but also a migraineur with keen observational powers [10].

While developing his system of homeopathic medicine in which substances causing a particular symptoms were used in great dilution to cure it, Samuel Hahnemann found that many vasodilatory compounds such as nitroglycerin (Glonoinum) were effective homeopathic remedies for migraine. This supported the predominant vascular theory, but that concept was challenged in 1863 by Edward Living’s treatise on “Megrim and Sick Headache”, which suggested that these represented brain dysfunction due to “nerve storms” that were related to epilepsy. Gowers’ first comprehensive English neurology text in 1888 endorsed this neu1rogenic view, and differentiated between intermittent treatments aimed at aborting attacks and continuous treatment intended to prevent them. He introduced the “Gowers solution” of nitroglycerin in alcohol that was one of the first examples of vasoactive therapy, along with the alkaloid of the ergot fungus that was first used in 1868. Gowers also advocated prophylactic treatment with Cannabis indica, presumably having a neural effect [11].

Headache research became more active and systematic in the 20 [th] century, beginning with the isolation of the therapeutically active ergot ingredient (ergotamine) in 1918 and the demonstration by Wolff and colleagues that the migraine aura corresponded to extracranial vasoconstriction and the headache to vasodilatation. The demonstration in 1941 that blood vessels and meninges were pain-sensitive but the brain itself was not supported the vascular theory, while Lashley’s description of his own migrainous scotomata in 1941 and the identification of cortical spreading depression by Leão in 1944 put in place crucial supports of the present view of the neural origin of migraine. The discovery of serotonin and the effects of a variety of serotoninergic drugs, particularly the demonstration in 1959 of the efficacy of methysergide against migraine, indicated the relationship between a particular neurotransmitter and what were still often called vascular headaches, and it became clear during this period that the correspondence of vasoconstriction with aura and vasodilatation with headache was not sufficient to explain migraines entirely. Spreading cerebral oligemia was demonstrated in migraine with aura by newer methods for measurement of cerebral blood flow in 1981, and oligemia was correlated with cortical spreading depression in animal models the following year. This led to the combination of the vascular and neurogenic theories in 1987 in order to explain migraine on the basis of “neurogenic inflammation”. This is the present consensus, and positron and functional MRI imaging has led to the identification of a probable brainstem migraine generator that sets this in motion. Recent interest has focused on the possibility that migraine may represent an ion channel disorder (channelopathy), and on the role of calcitonin gene-related peptide (CGRP) in the initiation of migraine attacks, while the identification and characterization of serotonin receptors has led to the development of sumatriptan and a dramatic expansion of the armamentarium for effective headache treatment [12].

EPIDEMIOLOGY AND PATHOPHYSIOLOGY OF MIGRAINE

Migraine, which represents about 85 per cent of headaches requiring medical attention , and is ranked 19 [th] among diseases causing disability throughout the world by the World Health Association. In the United States, migraine is thought to affect about 30 million people, many of whom do not seek medical attention for this. The disorder is a particular source of impaired domestic function and workplace productivity, as it predominates during the productive years of 25 to 50, and is 3 times as common in women as among men. A recent study estimated that medical costs for migraine evaluation and treatment approach 2 billion dollars annually, while 13 billion dollars in productivity are lost on account of migraine.

As mentioned earlier, it was suggested in ancient times that the pain of migraine arose from the meningeal coverings and blood vessels of the brain. Harold Wolff elaborated a vascular theory of migraine in the 1940s, based in part on his personal experience with the disorder: he was apparently in the habit of massaging his temples, particularly when he felt the prodromal symptoms of a migraine attack, and noticed that the usually palpable temporal pulse disappeared when he was having a migraine aura but was bounding during the migraine itself, and coincided with the pulsing headache that he experienced. As the technique of cerebral angiography was more frequently used for headache evaluation, constriction of arteries was suggested before the onset of headache, while dilated vessels were seen during the migraine attack. Although most of the brain is insensitive to pain, its blood vessels are richly supplied with pain-sensitive nerve fibers. It was therefore suggested that constriction of the cerebral blood vessels and reduction of cerebral blood flow caused symptoms of migraine aura such as numbness, tingling or visual disturbance, and then led to compensatory dilation resulting in headache, either from edema or inflammation around the affected blood vessels that activated the surrounding nerve fibers [14] . This theory explained the initial premonitory symptoms and subsequent pulsatile headache of the migraine attack, as well as the effectiveness of caffeine, ergotamine and other therapies that constrict blood vessels. Two problems remained, however: most migraine sufferers do not have auras before their attacks, and newer methods of measuring cerebral blood flow have not shown the expected decrease in blood flow during pre-migraine symptoms and increase in blood flow with headache in those who do [15].

These problems and the increasingly-recognized association between migraine and central nervous system conditions like epilepsy and mood disorder have led to a neural theory of its cause. The experimental psychologist Karl Lashley suffered from migraine preceded by one of the most common auras, slow progression and then resolution of decreased vision, and in 1941 carefully mapped his visual loss and suggested that it represented slow inactivation spreading over his visual cortex at a rate of 3 to 5 mm per minute. Two years later, the Brazilian neurophysiologist A. A. P. Leão observed waves of neural hyperactivity followed by suppressed activity moving across the rabbit cerebral cortex at 3 to 4 mm per minute, and termed this “spreading depression”. It was suggested a decade later that the slowly-evolving migraine aura might be due to slowly-progressing spreading depression of the cerebral cortex, preceded by increased neural activity during the migraine headache [16].

The most prevalent view of the cause of migraine today is that genetically susceptible people may have or develop generator sites in the hypothalamus or brainstem (the periacqueductal gray matter of the midbrain) that cause or accentuate waves of spreading depression that may inactivate areas of cerebral cortex and cause auras. The rapid neural firing that occurs at the start of spreading stimulate the release of substances which cause a cascade of inflammation, dilation of cerebral blood vessels and activation of the autonomic nervous system. This makes nerve fibers, particularly branches of the trigeminal nerve which supplies the face and head, more sensitive to pain, and can result in nausea, vomiting and other associated symptoms of migraine. Spreading depression is attended by opening of potassium channels and outward flow of potassium, with a compensatory inward flow of sodium through sodium channels. The associated excitation of neurons results in the inflow of calcium through calcium channels and release of the excitatory transmitter glutamate. The increased neuronal activity also affects the release and reuptake of serotonin. This sequence of events would explain why migraine may be prevented by drugs which affect sodium and potassium channels and glutamate (anticonvulsants), medications which influence serotonin reuptake or bind to serotonin receptors (antidepressants and the migraine-specific triptans) and calcium channel- blocking drugs, as well as those which constrict cerebral blood vessels (ergots) [17].

The susceptibility to migraine is clearly inherited, but the inheritance is complex, with several genes and multiple other factors probably involved. Cortical spreading depression may be due to the abnormal function of ion channels in the cell membranes of neurons, and a number of rare “channelopathies” have been found, causing muscle disorders, seizure disorders, periodic paralysis and some forms of migraine. Familial hemiplegic migraine (FHM) causes migraine headaches with paralysis and is an autosomal dominant disorder (the gene is not carried by the sex chromosomes, and more or less everyone who inherits the gene gets the disorder): attacks of FHM are very similar to some kinds of migraine aura, and 3 causative gene mutations have been identified that result in malfunctioning sodium, potassium and calcium channels [18]. When more than one gene may be involved and the disorder in question is not dominantly inherited, so that some family members will have the gene but not have the disorder, the traditional genetic studies cannot be done, and this is the case for garden variety migraine, particularly migraine without aura. Such disorders can now be studied because the human genome has been essentially deciphered: the Human Genome Project completed the sequencing of human DNA in 2003, and the International HapMap project identified the common patterns of human genetic variation around 2005. The genomes of people with various diseases can be scanned with various markers and compared to the genomes of people without those diseases, in order to identify genetic variants that may be associated with the disease of interest. This is termed a genome-wide association study, and such studies in migraine have suggested 3 genes that regulate the excitatory neurotransmitter glutamate and one that codes for a protein involved in pain perception [19].

It is still uncertain how the molecular alterations of migraine result in inflammation and headache, but it may develop as follows. Cortical spreading depression, responsible for migraine aura, activates pain receptors (nociceptors) such as the protein described above, and this causes the release of chemical factors which dilate blood vessels and initiate inflammation. The trigeminal nerve, subserving sensation in the face and head, is particularly sensitive, and becomes more so as an attack progresses (“central sensitization”). Activation of trigeminal nerve C-fibers, the type which primarily transmit pain, results in the release of substance P (for pain), which causes aggregation of platelets and release of serotonin and thromboxane A2. Clumped platelets, serotonin and thromboxane then activate the production of prostaglandin and kinins (“neurogenic inflammation”) and result in the swelling of the brain’s dural lining, which stretches the pain-sensitive nerve fibers that surround the dural blood vessels and result in the characteristic throbbing pain [20].

Article continues below...

Chromatography columns

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Hello,

Can anyone suggest which out of the four companies Merckmillipore, Agilent, Thermo scientific and Waters is better for chromatographic columns giving a little data supporting their answer?

According to my findings, Agilent columns are the most widely used.

Also, which columns would be more preferred for proteomics application? C18,C8,biphenyl ? and their molecular weight ranges if possible!

Thankyou!

American cfa after bsc!

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Sir I want to ask that if I can pursue for American cfa after bsc in biotechnology. Will I be considered as eligible?

Placement record and salary package of IITs

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What is the placement record for M.Tech in biomedical science and bioengineering or M.tech Biotechnolgy in the IITs?

Biotechnology Competencies

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Hi All,

Does anybody know where I could find
Biotechnology Career Competencies?

Thanks!

AICTE PG Scholarship

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Sir,

Gate scholarship is available for candidates having valid gate score and getting admitted into an institute like iit,nit or any state university through proper counselling. But if somebody having valid gate score takes admission into NIT or any other institute's self-sponsord PG course through the institute's admission test, is he/she eligible for the AICTE Gate stipend? there is a special scheme for non-aicte approved colleges, here is the link, please have a look and give your valuable opinions.

http://www.aicte-india.org/DBT_DEPT.php

Thank you.

Bioprocess engineering

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sir i have started studying numericals from Doran as per recommendation, so can you forward me solution manual for Doran for 2nd Edition.

Graduate Studies in National University Of Singapore

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I have 7.8 cgpa from a reputed university in Tamil Nadu, i will clear TOFEL sir.  In that application form,nothing is mandatory it depends on weightage sir.With this will i be able to get admission in National University Of Singapore for M.Sc (Chemical Engineering) for January 2016 or i must clear GRE to get a confirmed admission,Or any other thing i must do??

Cryptochrome in drosophila

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please tell me some useful information about cryptochrome in drosophila (wild type). how this gene acts? what is it's significance? etc.

Hey guys need some help

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It's regarding choosing of what next to I am a B. E biotechnology graduate 2015 batch. I want suggestions as to what should I pursue next. M. TECH OR MBA?? 
If M. Tech then do I need to do in any specialization and what is the future after doing M. Tech... What is the placement guarantee? 
MBA after B. E..is it advantageous or I should stick to my stream? I really need some help. Would be glad if anyone could help me.

Bioprocess engineering solution manual

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sir i have started studying numericals from Doran as per recommendation, so can you forward me solution manual for Doran for 2nd Edition.

Tips on organizing frozen cells

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Hello! My name is matt and I'm currently working as a Research Associate for a biotech company in which I do cloning and produce stable cell lines.

My question here is more a logistic one...Do any of you have tips on keeping a log of your frozen cells?
We keep them in the usual 10X10 vial boxes thus far and have a crud Excel template where we "try" to log them.
Now we have a binder on top of the excel sheet but trying to consolodate both has proven really time consuming thus far.

Any advice on how you like to log your frozen cells? Tips on keeping a steamlined system? I'd really just like to get an idea of what other people are doing,
as ours seems somewhat inefficient. Thank you in advance for your help!

Best,
Matt

RefFinder and BestKeeper access - URGENT

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Hey everybody,

I am trying to aceess the online program RefFinder, to analyse the best reference genes for my RT-qPCR experiment. But the website seems to be off.

Have someone noticed that??

Anther thing is that, I'm trying to download the Bestkeeper algorithm for my reference genes evaluation. But, they ask for some password.
I've already tried to send an email, but they didn't answer.

What should I do?
Does anyone have acceess in the Bestkeeper?

Thought Of The Day

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“To design the future effectively,
you must first let go of your past.”

jnu ceeb syllaus

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please tell me the syllabus for msc entrance exam conducted by jnu

eligibility for GATE 2016

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Hi Friends,


I am 2012 b.tech Industrial biotechnology graduated. Currently, I am working in e-commerce industry (NON-BIOTECH).  However, my plan is to do higher studies in biotech.

Pls let me know am I eligible for 2016 gate exam or not.



looking forward to your reply.



regards,
Jyoti

Reviews regarding some Private Colleges in Pune,

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Good Afternoon,
I have completed my BSc with Biotechnology from Sautashtra University, Rajkot.
Now planing for MSc from some Private Institutions in Pune,
If you could please provide me with the reviews of these Colleges,
1. Rajiv Gandhi Institute of Information Technology and Biotechnology, Pune and 2. Dr. D Y Patil Biotechnology and Bioinformatics institution, Pune.
I have had even applied for Central University of Gujarat but its waiting list is awaited, Mean while if I am getting fruitful and good reviews regarding the above mentioned two colleges I could go, reserve my seat and take admission.
Thanks, waiting for fruitful Information.
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