A nice forward
Have you ever experienced a moment in your life when you just ran out of
words and you go...
s i l e n t ???
Let me assist you in recalling...
.. the moment when you left your home for the first time and you look
back at your parents who are worried that their son/daughter are
leaving them yet happy that their child took the first step towards
independence.
... the moment when the girl/boy you like most.. smiled back at you!
You don't say anything.. you just smile back..
... the moment when you get better marks than you expected... those
"numb" moments of ecstasy n surprise "is that true?"...
... the moment when you are parting with your old friend(s) and the
train has just started... and you are standing on the door of the
wagon.. waving "bye-bye" with your heart beating fast...
... the moment after the HR manager has just called you and told
you,"You are through! Congrats!"
... the moment when you sit alone in your room after having told
everyone that you cleared that exam you prepared for 6 months!!
You can go on remembering your "special" moments!
I had always wondered why I never said anything to myself at those
moments.. as if it was "understood"... happiness, joy, pain.. all
feelings just flowed ceaselessly in the 'years' that passed in those
flash moments!
They say.. the best way to communicate is through "silence".
Love. Joy. Grief. Surprise. Anger. Hope. Expectations. Support.
Non-cooperation...
Can you imagine the importance of a silent moment in a song??
When Bryan Adams stops for a while along with music, before he goes
on in his husky voice...
... Please forgive me. I can't stop loving you!
Ever had those moments when you thought you were tired enough that
you reach for your bed after dinner.. but find yourself wide awake
looking at the roof of your room silently...
But you sure are 'thinking'... those moments of self-talk are the
most important in our lives. Those moments when we listen to our own
hearts! Those promises... those decisions... those are the moments
when we make our destinies!
Next time you go silent... listen carefully to what your heart is
saying.. listen to its joy...listen to its pain.. listen to its
fears.. listen to its desires..
Don't make it shut up and go off to sleep...
LISTEN TO THAT VOICE and ACCEPT EVERYTHING IT SAYS!
That voice alone can lead you to the abode of peace that your sleep
lacks... peace that awaits you!
Be in touch with your true self... be silent once a day,
every day!
...........................
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Web feed
Web feed From Wikipedia, the free encyclopedia A web feed is a document (often XML-based) which contains content items, often summaries of stories or weblog posts with web links to longer versions. Weblogs and news websites are common sources for web feeds, but feeds are also used to deliver structured information ranging from weather data to "top ten" lists of hit tunes. The two main web feed formats are RSS (which is older and far more widely used) and Atom (a newer format that has just completed the IETF standardization process.) The terms "publishing a feed" and syndication are used to describe making available a feed for an information source, such as a blog. Like syndicated print newspaper features or broadcast programs, web feed contents may be shared and republished by other web sites. (For that reason, one popular definition of RSS is Really Simple Syndication.) More often, feeds are subscribed to directly by users with aggregators or feed readers, which combine the contents of multiple web feeds for display on a single screen or series of screens. Depending on the aggregator, subscription is done by manually entering the URL of a feed, by clicking a feed: link in a web browser or by various other methods. Web feeds are designed to be machine readable, so there is no requirement that they be destined only for human readers. For example, business partners could use web feeds to exchange sales data or other information without any human intervention. Web feeds are most commonly found in various RSS formats or the standardised Atom format. This e-Mail may contain proprietary and confidential information and is sent for the intended recipient(s) only.
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Atom (standard) - Web Feed Format
Atom (standard) From Wikipedia, the free encyclopedia Atom is the name of a specific web feed format. Web feeds, from a user's perspective, allow Internet users to subscribe to websites that change or add content regularly. To use this technology, site owners create or obtain specialized software (such as a content management system) which, in the machine-readable XML format, presents new articles in a list, giving a line or two of each article and a link to the full article or post. Unlike subscriptions to many printed newspapers and magazines, most web subscriptions are free. Web feeds in general provide web content or summaries of web content together with links to the full versions of the content, and other meta-data in a developer-friendly standardized format. Atom in particular delivers this information as an XML file called an Atom feed, webfeed, Atom stream, or Atom channel. In addition to facilitating syndication, web feeds allow a website's frequent readers to track updates on the site using an aggregator. Atom, from a technical perspective, is an open standard that includes both: an XML-based web syndication format used by weblogs, news websites and web mail and, an HTTP-based protocol for remote editing of Atom-based weblogs The development of Atom was motivated by perceived deficiencies in the RSS 2.0 format and associated XML-RPC APIs [1]. Atom is now a formal IETF proposed standard detailed in the recently released RFC 4287. This e-Mail may contain proprietary and confidential information and is sent for the intended recipient(s) only.
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Web syndication
Web syndication From Wikipedia, the free encyclopedia Web syndication is a form of syndication in which a section of a website is made available for other sites to use. This could be simply by licensing the content so other people can use it, but more commonly web syndication refers to making Web feeds available from a site so other people can display an updating list of content from it (for example one's latest forum postings, etc.). This originated with news and blog sites but is increasingly used to syndicate any information. Although the format could be anything transported over HTTP, such as HTML or JavaScript, it is more commonly XML. The prevalence of web syndication is also of note to online marketers, since web surfers are becoming increasingly weary of providing personal information for marketing materials (such as signing up for a newsletter) and expect the ability to subscribe to a feed alternatively. The two main families of web syndication formats are RSS and Atom. This e-Mail may contain proprietary and confidential information and is sent for the intended recipient(s) only.
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RSS (file format)
RSS (file format) From Wikipedia, the free encyclopedia RSS is a family of web feed formats, specified in XML and used for Web syndication. RSS is used by (among other things) news websites, weblogs and podcasting. The abbreviation is variously used to refer to the following standards: Rich Site Summary (RSS 0.91) RDF Site Summary (RSS 0.9 and 1.0) Really Simple Syndication (RSS 2.0) Web feeds provide web content or summaries of web content together with links to the full versions of the content, and other metadata. RSS in particular, delivers this information as an XML file called an RSS feed, webfeed, RSS stream, or RSS channel. In addition to facilitating syndication, web feeds allow a website's frequent readers to track updates on the site using an aggregator. This e-Mail may contain proprietary and confidential information and is sent for the intended recipient(s) only.
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Schizophrenia...
If you remember movie - 'A beautiful Mind' then you can remember that in
this movie the subject - John Nash has got some mental illness
Schizophrenia is the name of that mental disorder.
I got some details on this from Wikipedia.com.
For more detailed description kindly visit the site itself :
http://en.wikipedia.org/
Schizophrenia is a mental disorder characterized by persistent defects in
the perception or the expression of reality. A person experiencing
untreated schizophrenia typically demonstrates disorganized thinking, and
may also experience delusions or auditory hallucinations. Although the
disorder primarily affects cognition, it can also contribute to chronic
problems with behavior or emotions. Due to the many possible combinations
of symptoms, it is difficult to say whether it is in fact a single
psychiatric disorder; and Eugen Bleuler deliberately called the disease
"the schizophrenias" (plural) when he coined the present name.
Diagnosis is based on the self-reported experiences of the patient, in
combination with secondary signs observed by a psychiatrist or other
competent clinician such as a doctor of psychology. There is no objective
biological test for schizophrenia, though studies suggest that genetics and
biochemistry are important contributing factors. Current research into the
development of the disorder often focuses on the role of neurobiology,
although a reliable and identifiable organic cause has not been found. In
the absence of objective laboratory tests to confirm the diagnosis, some
question the legitimacy of schizophrenia's status as a disease.
The term "schizophrenia" translates roughly as "shattered mind," and comes
from the Greek σχίζω (schizo, "to split" or "to divide") and φρήν (phrēn, "
mind"). Despite its etymology, schizophrenia is not synonymous with
dissociative identity disorder, also known as multiple personality disorder
or "split personality"; in popular culture the two are often confused.
Although schizophrenia often leads to social or occupational dysfunction,
there is little association of the illness with a predisposition toward
aggressive behavior.
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Influenza - Avian Flu - Bird Flu
Bird Flu (WHO website:
http://www.who.int/csr/don/2004_01_15/en/)
Avian influenza (“bird flu”) and the significance of its transmission to humans
The disease in birds: impact and control measures
Avian influenza is an infectious disease of birds caused by type A strains of the influenza virus. The disease, which was first identified in Italy more than 100 years ago, occurs worldwide.
All birds are thought to be susceptible to infection with avian influenza, though some species are more resistant to infection than others. Infection causes a wide spectrum of symptoms in birds, ranging from mild illness to a highly contagious and rapidly fatal disease resulting in severe epidemics. The latter is known as “highly pathogenic avian influenza”. This form is characterized by sudden onset, severe illness, and rapid death, with a mortality that can approach 100%.
Fifteen subtypes of influenza virus are known to infect birds, thus providing an extensive reservoir of influenza viruses potentially circulating in bird populations. To date, all outbreaks of the highly pathogenic form have been caused by influenza A viruses of subtypes H5 and H7.
Migratory waterfowl – most notably wild ducks – are the natural reservoir of avian influenza viruses, and these birds are also the most resistant to infection. Domestic poultry, including chickens and turkeys, are particularly susceptible to epidemics of rapidly fatal influenza.
Direct or indirect contact of domestic flocks with wild migratory waterfowl has been implicated as a frequent cause of epidemics. Live bird markets have also played an important role in the spread of epidemics.
Recent research has shown that viruses of low pathogenicity can, after circulation for sometimes short periods in a poultry population, mutate into highly pathogenic viruses. During a 1983–1984 epidemic in the United States of America, the H5N2 virus initially caused low mortality, but within six months became highly pathogenic, with a mortality approaching 90%. Control of the outbreak required destruction of more than 17 million birds at a cost of nearly US$ 65 million. During a 1999–2001 epidemic in Italy, the H7N1 virus, initially of low pathogenicity, mutated within 9 months to a highly pathogenic form. More than 13 million birds died or were destroyed.
The quarantining of infected farms and destruction of infected or potentially exposed flocks are standard control measures aimed at preventing spread to other farms and eventual establishment of the virus in a country’s poultry population. Apart from being highly contagious, avian influenza viruses are readily transmitted from farm to farm by mechanical means, such as by contaminated equipment, vehicles, feed, cages, or clothing. Highly pathogenic viruses can survive for long periods in the environment, especially when temperatures are low. Stringent sanitary measures on farms can, however, confer some degree of protection.
In the absence of prompt control measures backed by good surveillance, epidemics can last for years. For example, an epidemic of H5N2 avian influenza, which began in Mexico in 1992, started with low pathogenicity, evolved to the highly fatal form, and was not controlled until 1995.
A constantly mutating virus: two consequences
All type A influenza viruses, including those that regularly cause seasonal epidemics of influenza in humans, are genetically labile and well adapted to elude host defenses. Influenza viruses lack mechanisms for the “proofreading” and repair of errors that occur during replication. As a result of these uncorrected errors, the genetic composition of the viruses changes as they replicate in humans and animals, and the existing strain is replaced with a new antigenic variant. These constant, permanent and usually small changes in the antigenic composition of influenza A viruses are known as antigenic “drift”.
The tendency of influenza viruses to undergo frequent and permanent antigenic changes necessitates constant monitoring of the global influenza situation and annual adjustments in the composition of influenza vaccines. Both activities have been a cornerstone of the WHO Global Influenza Programme since its inception in 1947.
Influenza viruses have a second characteristic of great public health concern: influenza A viruses, including subtypes from different species, can swap or “reassort” genetic materials and merge. This reassortment process, known as antigenic “shift”, results in a novel subtype different from both parent viruses. As populations will have no immunity to the new subtype, and as no existing vaccines can confer protection, antigenic shift has historically resulted in highly lethal pandemics. For this to happen, the novel subtype needs to have genes from human influenza viruses that make it readily transmissible from person to person for a sustainable period.
Conditions favourable for the emergence of antigenic shift have long been thought to involve humans living in close proximity to domestic poultry and pigs. Because pigs are susceptible to infection with both avian and mammalian viruses, including human strains, they can serve as a “mixing vessel” for the scrambling of genetic material from human and avian viruses, resulting in the emergence of a novel subtype. Recent events, however, have identified a second possible mechanism. Evidence is mounting that, for at least some of the 15 avian influenza virus subtypes circulating in bird populations, humans themselves can serve as the “mixing vessel”.
Human infection with avian influenza viruses: a timeline
Avian influenza viruses do not normally infect species other than birds and pigs. The first documented infection of humans with an avian influenza virus occurred in Hong Kong in 1997, when the H5N1 strain caused severe respiratory disease in 18 humans, of whom 6 died. The infection of humans coincided with an epidemic of highly pathogenic avian influenza, caused by the same strain, in Hong Kong’s poultry population.
Extensive investigation of that outbreak determined that close contact with live infected poultry was the source of human infection. Studies at the genetic level further determined that the virus had jumped directly from birds to humans. Limited transmission to health care workers occurred, but did not cause severe disease.
Rapid destruction – within three days – of Hong Kong’s entire poultry population, estimated at around 1.5 million birds, reduced opportunities for further direct transmission to humans, and may have averted a pandemic.
That event alarmed public health authorities, as it marked the first time that an avian influenza virus was transmitted directly to humans and caused severe illness with high mortality. Alarm mounted again in February 2003, when an outbreak of H5N1 avian influenza in Hong Kong caused 2 cases and 1 death in members of a family who had recently travelled to southern China. Another child in the family died during that visit, but the cause of death is not known.
Two other avian influenza viruses have recently caused illness in humans. An outbreak of highly pathogenic H7N7 avian influenza, which began in the Netherlands in February 2003, caused the death of one veterinarian two months later, and mild illness in 83 other humans. Mild cases of avian influenza H9N2 in children occurred in Hong Kong in 1999 (two cases) and in mid-December 2003 (one case). H9N2 is not highly pathogenic in birds.
The most recent cause for alarm occurred in January 2004, when laboratory tests confirmed the presence of H5N1 avian influenza virus in human cases of severe respiratory disease in the northern part of Viet Nam.
Why H5N1 is of particular concern
Of the 15 avian influenza virus subtypes, H5N1 is of particular concern for several reasons. H5N1 mutates rapidly and has a documented propensity to acquire genes from viruses infecting other animal species. Its ability to cause severe disease in humans has now been documented on two occasions. In addition, laboratory studies have demonstrated that isolates from this virus have a high pathogenicity and can cause severe disease in humans. Birds that survive infection excrete virus for at least 10 days, orally and in faeces, thus facilitating further spread at live poultry markets and by migratory birds.
The epidemic of highly pathogenic avian influenza caused by H5N1, which began in mid-December 2003 in the Republic of Korea and is now being seen in other Asian countries, is therefore of particular public health concern. H5N1 variants demonstrated a capacity to directly infect humans in 1997, and have done so again in Viet Nam in January 2004. The spread of infection in birds increases the opportunities for direct infection of humans. If more humans become infected over time, the likelihood also increases that humans, if concurrently infected with human and avian influenza strains, could serve as the “mixing vessel” for the emergence of a novel subtype with sufficient human genes to be easily transmitted from person to person. Such an event would mark the start of an influenza pandemic.
Influenza pandemics: can they be averted?
Based on historical patterns, influenza pandemics can be expected to occur, on average, three to four times each century when new virus subtypes emerge and are readily transmitted from person to person. However, the occurrence of influenza pandemics is unpredictable. In the 20th century, the great influenza pandemic of 1918–1919, which caused an estimated 40 to 50 million deaths worldwide, was followed by pandemics in 1957–1958 and 1968–1969.
Experts agree that another influenza pandemic is inevitable and possibly imminent.
Most influenza experts also agree that the prompt culling of Hong Kong’s entire poultry population in 1997 probably averted a pandemic.
Several measures can help minimize the global public health risks that could arise from large outbreaks of highly pathogenic H5N1 avian influenza in birds. An immediate priority is to halt further spread of epidemics in poultry populations. This strategy works to reduce opportunities for human exposure to the virus. Vaccination of persons at high risk of exposure to infected poultry, using existing vaccines effective against currently circulating human influenza strains, can reduce the likelihood of co-infection of humans with avian and influenza strains, and thus reduce the risk that genes will be exchanged. Workers involved in the culling of poultry flocks must be protected, by proper clothing and equipment, against infection. These workers should also receive antiviral drugs as a prophylactic measure.
When cases of avian influenza in humans occur, information on the extent of influenza infection in animals as well as humans and on circulating influenza viruses is urgently needed to aid the assessment of risks to public health and to guide the best protective measures. Thorough investigation of each case is also essential. While WHO and the members of its global influenza network, together with other international agencies, can assist with many of these activities, the successful containment of public health risks also depends on the epidemiological and laboratory capacity of affected countries and the adequacy of surveillance systems already in place.
While all these activities can reduce the likelihood that a pandemic strain will emerge, the question of whether another influenza pandemic can be averted cannot be answered with certainty.
Clinical course and treatment of human cases of H5N1 avian influenza
Published information about the clinical course of human infection with H5N1 avian influenza is limited to studies of cases in the 1997 Hong Kong outbreak. In that outbreak, patients developed symptoms of fever, sore throat, cough and, in several of the fatal cases, severe respiratory distress secondary to viral pneumonia. Previously healthy adults and children, and some with chronic medical conditions, were affected.
Tests for diagnosing all influenza strains of animals and humans are rapid and reliable. Many laboratories in the WHO global influenza network have the necessary high-security facilities and reagents for performing these tests as well as considerable experience. Rapid bedside tests for the diagnosis of human influenza are also available, but do not have the precision of the more extensive laboratory testing that is currently needed to fully understand the most recent cases and determine whether human infection is spreading, either directly from birds or from person to person.
Antiviral drugs, some of which can be used for both treatment and prevention, are clinically effective against influenza A virus strains in otherwise healthy adults and children, but have some limitations. Some of these drugs are also expensive and supplies are limited.
Experience in the production of influenza vaccines is also considerable, particularly as vaccine composition changes each year to match changes in circulating virus due to antigenic drift. However, at least four months would be needed to produce a new vaccine, in significant quantities, capable of conferring protection against a new virus subtype.
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Details from wikipedia can be followed here:
http://en.wikipedia.org/wiki/H5N1Avian Flu
H5N1 is a subtype of the species called avian influenza virus (bird flu). Avian flu is a disease and avian flu virus is a species. The avian flu virus subtypes are labeled according to an H number and an N number.
The avian influenza subtypes that have been confirmed in humans, ordered by the number of known human deaths, are: H1N1 caused "Spanish Flu", H2N2 caused "Asian Flu", H3N2 caused "Hong Kong Flu", H5N1 is the current pandemic threat, H7N7 has unusual zoonotic potential, H1N2 is currently endemic in humans and pigs, H9N2, H7N2, H7N3, H10N7.
The annual flu (also called "seasonal flu" or "human flu") kills an estimated 36,000 people in the United States each year. The dominant strain of annual flu virus in January 2006 was H3N2 which is now resistant to the standard antiviral drugs amantadine and rimantadine.
Avian influenza virus H3N2 is endemic in pigs ("swine flu") in China and has been detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Human influenza viruses can reassort with H5N1 in pigs and mutate into a form which can pass easily among humans. This is one of many possible paths to a pandemic.
Technical
H5N1 is a type of avian influenza virus (bird flu virus) that has mutated[10] through antigenic drift into dozens of highly pathogenic varieties, but all currently belonging to genotype Z of avian influenza virus H5N1. Genotype Z emerged through reassortment in 2002 from earlier highly pathogenic genotypes of H5N1[11] that first appeared in China in 1996 in birds and in Hong Kong in 1997 in humans[12]. The "H5N1 viruses from human infections and the closely related avian viruses isolated in 2004 and 2005 belong to a single genotype, often referred to as genotype Z." [1]
This infection of humans coincided with an epizootic (an epidemic in nonhumans) of H5N1 influenza in Hong Kong’s poultry population. This panzootic (a disease affecting animals of many species especially over a wide area) outbreak was stopped by the killing of the entire domestic poultry population within the territory. The name H5N1 refers to the subtypes of surface antigens present on the virus: hemagglutinin type 5 and neuraminidase type 1.
Genotype Z of avian influenza virus H5N1 is now the dominant genotype of H5N1. Genotype Z is endemic in birds in southeast Asia and represents a long term pandemic threat.
The species called the avian flu virus has a subtype called H5N1 which has a strain called highly pathogenic H5N1 which includes genotype or strain Z which has been divided into two genetic clades which are known from specific isolates. Among H5N1 viruses, only clade one infects humans.
Terminology
"Virus" refers to either the complete virus assemblage or when distinguishing between its parts it refers to the molecules (RNA in the case of H5N1) comprising the genome that is surrounded (encapsidated) by a protective coat of protein called a capsid which binds directly to the viral genome. This complex of protein and nucleic acid is called the nucleocapsid. The complete virus assemblage is referred to as a virion. In normal useage "H5N1 virus" refers to the H5N1 nucleocapsid which is the same as the H5N1 virion since the H5N1 lacks an envelope (a membranous lipid structure that surrounds the nucleocapsid).
Avian influenza is not a genus of Orthomyxoviridae. The term "avian influenza" denotes a disease not a virus. The orthomyxovirus family consists of 5 genera: Influenzavirus A, Influenzavirus B, Influenzavirus C, Isavirus, and Thogotovirus. Influenzavirus A is not the same as "avian influenza": the former is a genus of viruses, the latter is an illness.
In phylogenetics based taxonomy the "RNA viruses" includes the "negative-sense ssRNA viruses" which includes the Order "Mononegavirales" which includes the Family "Orthomyxoviridae" which contains five genera, classified by variations in nucleoprotein (NP and M) antigens. One of these is the Genus "Influenzavirus A" which consists of a single species (or "type species") called "Influenza A virus" (AI) and one of its subtypes is H5N1.
H5N1 (like the other avian flu viruses) has strains called "highly pathogenic" (HP) and "low-pathogenic" (LP). "Avian influenza viruses that cause HPAI are highly virulent, and mortality rates in infected flocks often approach 100%. LPAI viruses are generally of lower virulence, but these viruses can serve as progenitors to HPAI viruses. The current strain of H5N1 responsible for die-offs of domestic birds in Asia is an HPAI strain; other strains of H5N1 occurring elsewhere in the world are less virulent and, therefore, are classified as LPAI strains. All HPAI strains identified to date have involved H5 and H7 subtypes." The distiction is about pathogenicity in poultry, not humans. Normally a highly pathogenic avian virus is not highly pathogenic to either humans or non-poultry birds. This current strain of H5N1 is unusual in being deadly to so many species.
The species called the avian flu virus has a subtype called H5N1 which has a strain called highly pathogenic H5N1 which includes genotype or strain Z which has been divided into two genetic clades which are known from specific isolates. Only clade one infects humans but all clade one are resistant to adamantanes. Each specific known genetic variation is known from a virus isolate of a specific case of infection.[13]
Influenza virus isolates are notated as in this example: A/New York/348(H1N2):
A stands for the species of influenza (A, B, or C).
New York is the place this specific virus was isolated.
348 is the number of the specimen it was isolated from.
H1 stands for the first of several known types of the protein hemagglutinin.
N2 stands for the second of several known types of the protein neuraminidase.
[edit]
H5N1 virus structure
Virus - A virus is one type of microscopic parasite that infects cells in biological organisms.
Orthomyxoviridae - The Orthomyxoviridae are a family of RNA viruses which infect vertebrates. It includes those viruses which cause influenza. Viruses of this family contain 7 to 8 segments of linear negative-sense single stranded RNA.
Influenza virus - "Influenza virus" refers to a subset of Orthomyxoviridae that create influenza. This is not a phylogenetics based taxonomic category.
Avian influenza virus - Avian influenza viruses have 10 genes on eight separate RNA molecules (called: PB2, PB1, PA, HA, NP, NA, M, and NS). HA, NA, and M specify the structure of proteins that are most medically relevant as targets for antiviral drugs and antibodies. This segmentation of the influenza genome facilitates genetic recombination by segment reassortment in hosts who are infected with two different influenza viruses at the same time[1]. Avian influenza viruses compose the Influenzavirus A genus of the Orthomyxoviridae family and are negative sense, single-stranded, segmented RNA viruses.
"The influenza virus RNA polymerase is a multifunctional complex composed of the three viral proteins PB1, PB2 and PA, which, together with the viral nucleoprotein NP, form the minimum complement required for viral mRNA synthesis and replication."[14]
Surface antigen encoding gene segments (RNA molecule): (HA, NA)
HA codes for hemagglutinin which is an antigenic glycoprotein found on the surface of the influenza viruses and is responsible for binding the virus to the cell that is being infected. Hemagglutinin forms spikes at the surface of flu viruses that function to attach viruses to cells. This attachment is required for efficient transfer of flu virus genes into cells, a process that can be blocked by antibodies that bind to the hemagglutinin proteins. One genetic factor in distinguishing between human flu viruses and avian flu viruses is that "avian influenza HA bind alpha 2-3 sialic acid receptors while human influenza HA bind alpha 2-6 sialic acid receptors. Swine influenza viruses have the ability to bind both types of sialic acid receptors."[15] A mutation found in Turkey in 2006 "involves a substitution in one sample of an amino acid at position 223 of the haemoagglutinin receptor protein. This protein allows the flu virus to bind to the receptors on the surface of its host's cells. This mutation has been observed twice before — in a father and son in Hong Kong in 2003, and in one fatal case in Vietnam last year. It increases the virus's ability to bind to human receptors, and decreases its affinity for poultry receptors, making strains with this mutation better adapted to infecting humans." Another mutation in the same sample at position 153 has as yet unknown effects. [16]
NA codes for neuraminidase which is an antigenic glycoprotein enzyme found on the surface of the influenza viruses. It helps the release of progeny viruses from infected cells.
Internal viral protein encoding gene segments (RNA molecule): (M, NP, NS, PA, PB1, PB2)[17]
M codes for the matrix proteins (M1 and M2) that along with the two surface proteins (hemagglutinin and neuraminidase) make up the capsid (protective coat) of the virus. It encodes by using different reading frames from the same RNA segment.
M1 is a protein that binds to the viral RNA.
M2 is a protein that uncoats the virus exposing its contents (the eight RNA segments) to the cytoplasm of the host cell. The M2 transmembrane protein is an ion channel required for efficient infection [18]. The amino acid substitution (Ser31Asn) in M2 some H5N1 genotypes is associated with amantadine resistance[19].
NP codes for nucleoprotein.
NS: NS codes for two nonstructural proteins (NS1 and NEP). "[T]he pathogenicity of influenza virus was related to the nonstructural (NS) gene of the H5N1/97 virus"[20][21]
NS1: Non-structural: nucleus; effects on cellular RNA transport, splicing, translation. Anti-interferon protein. NS1 described in detail. The "NS1 of the highly pathogenic avian H5N1 viruses circulating in poultry and waterfowl in Southeast Asia might be responsible for an enhanced proinflammatory cytokine response (especially TNFa) induced by these viruses in human macrophages"[22]. H5N1 NS1 is characterized by a single amino acid change at position 92. By changing the amino acid from glutamic acid to aspartic acid, the researchers were able to abrogate the effect of the H5N1 NS1. [This] single amino acid change in the NS1 gene greatly increased the pathogenicity of the H5N1 influenza virus."[23]
NEP: The "nuclear export protein (NEP, formerly referred to as the NS2 protein) mediates the export of vRNPs" [24]
PA codes for the PA protein which is a critical component of the viral polymerase.
PB1 codes for the PB1 protein and the PB1-F2 protein.
The PB1 protein is a critical component of the viral polymerase.
The PB1-F2 protein is encoded by an alternative open reading frame of the PB1 RNA segment and "interacts with 2 components of the mitochondrial permeability transition pore complex, ANT3 and VDCA1, [sensitizing] cells to apoptosis. [...] PB1-F2 likely contributes to viral pathogenicity and might have an important role in determining the severity of pandemic influenza."[25] This was discovered by Chen et. al. and reported in Nature[26].
PB2 codes for the PB2 protein which is a critical component of the viral polymerase. 75% of H5N1 human virus isolates from Vietnam had a mutation consisting of Lysine at residue 627 in the PB2 protein; which is believed to cause high levels of virulence.[27][28] Until H5N1, all known avian influenza viruses had a Glu at position 627, while all human influenza viruses had a lysine.
The hemagglutinin, neuraminidase, and M2 proteins are essential viral proteins with functions that can be inhibited by antiviral drugs such as oseltamivir and rimantadine or bound by virus-inactivating antibodies produced by the immune system.
Influenza viruses have a relatively high mutation rate that is characteristic of RNA viruses. The H5N1 virus has mutated into a variety of types with differing pathogenic profiles; some pathogenic to one species but not others, some pathogenic to multiple species[29]. The ability of various influenza strains to show species-selectivity is largely due to variation in the hemagglutinin genes. Genetic mutations in the hemagglutinin gene that cause single amino acid substitutions can significantly alter the ability of viral hemagglutinin proteins to bind to receptors on the surface of host cells. Such mutations in avian H5N1 viruses can change virus strains from being inefficient at infecting human cells to being as efficient in causing human infections as more common human influenza virus types[30]. This doesn't mean one amino acid substitution can cause a pandemic but it does mean one amino acid substitution can cause an avian flu virus that is not pathogenic in humans to become pathogenic in humans.
In July 2004, researchers led by H. Deng of the Harbin Veterinary Research Institute, Harbin, China and Professor Robert Webster of the St Jude Children's Research Hospital, Memphis, Tennessee, reported results of experiments in which mice had been exposed to 21 isolates of confirmed H5N1 strains obtained from ducks in China between 1999 and 2002. They found "a clear temporal pattern of progressively increasing pathogenicity"[31]. Results reported by Dr. Webster in July 2005 reveal further progression toward pathogenicity in mice and longer virus shedding by ducks.
Recent research of Taubenberger et al [32] has shown that the 1918 virus, like H5N1, was also an avian influenza virus. Furthermore, Tumpey and colleagues [33] who reconstructed the H1N1 virus of 1918 came to the conclusion that it is was most notably the polymerase genes and the HA and NA genes that caused the extreme virulence of this virus. The sequences of the polymerase proteins (PA, PB1, and PB2) of the 1918 virus and subsequent human viruses differ by only 10 amino acids from the avian influenza viruses. Human forms of seven of the ten amino acids have already been identified in currently circulating H5N1. It is not unlikely that the other mutations eventually will surface and make the H5N1 virus capable of human-to-human transmission. Another important factor is the change of the HA protein to a binding preference for alpha 2,6 sialic acid (the major form in the human respiratory tract). In avian virus the HA protein preferentially binds to alpha 2,3 sialic acid, which is the major form in the avian enteric tract. It has been shown that only a single amino acid change can result in the change of this binding preference. Altogether, only a handful of mutations need to take place in order for H5N1 avian flu to become a pandemic virus like the one of 1918.
--------------------------------------
Glossary from Wikipedia
Antigenic drift refers to mutations in the influenza virus that cause changes in the virus's surface proteins over time. Those proteins (hemagglutinin and neuraminidase) are the causes of the body's immune reaction (i.e., they are antigens). Mutations occur almost yearly in the influenza virus, and while the change might not be a major one (which would then be called an antigenic shift), they are sufficient to lessen your body's ability to protect you with antibodies. For this reason, vaccination is required on a yearly basis, with the vaccine adjusted to the new antigen. In influenza, mutations happen frequently because the virus has no way of checking its RNA for errors. Antigenic drift has been responsible for heavier than normal flu seasons in the past, like the outbreak of influenza A Fujian(H3N2) in the 2003 - 2004 flu season. All influenza viruses experience some form of antigenic drift, but it's most pronounced in the influenza A virus. Antigenic drift is not the same as antigenic shift, which is the process by which two different strains of influenza combine to form a new subtype having a mixture of the surface antigens of the two original strains.
Antigenic shift is distinct from antigenic drift, which is a slower mode of genetic change in viruses.
Antigenic shift is the process by which two different strains of influenza combine to form a new subtype having a mixture of the surface antigens of the two original strains. The term antigenic shift is specific to the influenza literature; in other viral systems, the same process is called reassortment or viral shift.
Antigenic shift is contrasted with antigenic drift, which is the natural mutation over time of known strains of influenza (or other things, in a more general sense) to evade the immune system. Antigenic drift occurs in all types of influenza including influenza A, B and C. Antigenic shift, however, occurs only in influenza A because it infects more than just humans. Affected species include other mammals and birds, giving influenza A the opportunity for a major reorganization of surface antigens. Influenza B and C only infect humans, minimizing the chance to mutate drastically
Influenza, commonly known as the flu or the grippe, is a contagious disease of the upper airways and the lungs, caused by an RNA virus of the orthomyxoviridae family. It rapidly spreads around the world in seasonal epidemics, imposing considerable economic burden, in the form of health care costs and lost productivity. Three influenza pandemics in the 20th century, each following a major genetic change in the virus, killed millions of people all over the world.
It is not connected to gastroenteritis, commonly known as "stomach flu" or the "24 hour flu".
The term influenza has its origins in 15th century Italy, where the cause of the disease was ascribed to unfavorable astrological influences. Evolution in medical thought led to its modification to "influenza di freddo", meaning "influence of the cold", which by the 18th century became the prevalent terminology in the English-speaking world as well
The
Orthomyxoviridae are a family of RNA viruses which infect vertebrates. It includes those viruses which cause influenza ?
Orthomyxoviridae
Virus classification
Group:
Group V ((-)ssRNA)
Family:
Orthomyxoviridae
Genera
Influenzavirus A
Influenzavirus B
Influenzavirus C
Isavirus
Thogotovirus
Influenzavirus A is a genus of a family of viruses called Orthomyxoviridae in virus classification. Influenzavirus A has only one species in it; that species is called "influenza A virus". Influenza A virus causes "avian influenza" (also known as bird flu, avian flu, influenzavirus A flu, type A flu, or genus A flu). It is hosted by birds, but may infect several species of mammals. All known subtypes are endemic in birds. It was first identified in Italy in the early 1900s and is now known to exist worldwide.
Influenzavirus B is a genus in the virus family Orthomyxoviridae. The only species in this genus is called "Influenza B virus". Influenza B viruses are known to infect humans and seals, giving them influenza. The annually updated trivalent flu vaccine consists of hemagglutinin (HA) surface glycoprotein components from influenza H3N2, H1N1, and B influenza viruses.
Influenzavirus C is a genus in the virus family Orthomyxoviridae. The only species in this genus is called "Influenza C virus". Influenza B viruses are known to infect humans and pigs, giving them influenza. Flu due to the type C species is rare compared to types A or B, but can be severe and can cause local epidemics.
An
RNA virus is a virus that either uses ribonucleic acid (RNA) as its genetic material, or whose genetic material passes through an RNA intermediate during DNA replication. For example, Hepatitis B virus is classified as an RNA virus, even though its genome is double-stranded DNA, because the genome is transcribed into RNA during replication. The basis for this classification is error-prone replication of RNA through DNA: All RNA viruses have very high mutation rates because they lack DNA polymerases which can find and edit out mistakes, conducting the equivalent of DNA repair of damaged genetic material. DNA viruses have considerably lower mutation rates. Retroviruses integrate their genome into the host genome, and suffers this problem considerably less.
Although RNA usually mutates rapidly, recent work found that the SARS virus and related RNA viruses contain a gene that mutates very slowly. [1] The gene in question has a complex three-dimensional structure which is hypothesized to provide a chemical function necessary for viral propagation, perhaps as a ribozyme. If so, most mutations would render it unfit for that purpose and would not propagate.
Some RNA viruses:
Arenaviridae
Bunyaviridae
Coronaviridae: SARS
Flaviviridae: Dengue fever - Hepatitis - West Nile virus - Yellow fever
Furovirus
Orthomyxoviridae: Influenza
Paramyxoviridae: Mumps
Picornaviridae: Polio
Pomovirus
Reoviridae
Retroviridae: Human Immunodeficiency Virus
Rhabdoviridae: Rabies - Vesicular stomatitis virus
Tobamovirus: tobacco mosaic virus
Togaviridae
Tymoviridae
Filoviridae: Ebola
-------------------
Hemagglutinin (HA) is an antigenic glycoprotein found on the surface of the influenza viruses and is responsible for binding the virus to the cell that is being infected. The name hemagglutinin comes from the protein's ability to cause erythrocytes to clump together (Nelson 2005).
Subtypes: - There are at least 16 different HA antigens. These subtypes are labeled H1 through H16. The last, H16, was discovered only recently on influenza A viruses isolated from black-headed gulls from Sweden and Norway (Fouchier 2005). The first three hemagglutinins, H1, H2, and H3, are found in human influenza viruses.
A highly pathogenic avian flu virus of H5N1 type has been found to infect humans at a low rate. It has been reported that single amino acid changes in this avian virus strain's type H5 hemagglutinin have been found in human patients that "can significantly alter receptor specificity of avian H5N1 viruses, providing them with an ability to bind to receptors optimal for human influenza viruses" (Gambaryan 2005, Suzuki 2005). This finding seems to explain how an H5N1 virus that normally does not infect humans can mutate and become able to efficiently infect human cells. The hemagglutinin of the H5N1 virus has been associated with the high pathogenicity of this flu virus strain, apparently due to its ease of conversion to an active form by proteolysis (Senne 1996, Hatta 2001).
HA has two primary functions:
1. the recognition of target vertebrate cells, accomplished through the binding of these cells' sialic acid-containing receptors, and
2. the fusion of host and viral endosomal membranes (White 1997), accomplished through the recruitment of HA molecules to the fusion site where some undergo conformational alterations to destabilize the lipid bilayer, thence cooperatively forming a fusion intermediate which associates the two bilayers
------------------
Neuraminidase is an antigenic glycoprotein enzyme (EC 3.2.1.18) found on the surface of the Influenza virus.
Subtype:- Nine neuraminidase subtypes are known; many occur only in various species of duck and chicken. Subtypes N1 and N2 have been positively linked to epidemics in man.
Structure:- The neuraminidase enzyme exists as a mushroom-shape projection on the surface of the influenza virus. It has a head consisting of four co-planar and roughly spherical subunits, and a hydrophobic region that is embedded within the interior of the virus' membrane. It is comprised of a single polypeptide chain that is oriented in the opposite direction to the hemagglutinin antigen. The composition of the polypeptide is a single chain of six conserved polar amino acids, followed by hydrophilic, variable amino acids.
-------------------------
A
glycoprotein is a macromolecule composed of a protein and a carbohydrate (an oligosaccharide). The carbohydrate is attached to the protein in a cotranslational or posttranslational modification. The addition of sugar chains can happen either at asparagine, and is termed N-glycosylation, or at hydroxylysine, hydroxyproline, serine, or threonine, and is termed O-glycosylation. Possible carbohydrates include glucose, glucosamine, galactose, galactosamine, mannose, fucose, and sialic acid.
The sugar group can assist in protein folding or improve its stability. Glycoproteins are often used in proteins that are at least in part located in extracellular space (that is, outside the cell). Glycoproteins are important for immune cell recognition, especially in mammals. Examples of glycoproteins in the immune system are:
molecules such as antibodies (immunoglobulins), which interact directly with antigens
molecules of the major histocompatibility complex (or MHC), which are expressed on the surface of cells and interact with T-cells as part of the adaptive immune response.
Other examples of glycoproteins include:
components of the zona pellucida, which surrounds the oocyte, and is important for sperm-egg interaction.
Soluble glycoproteins often show a high viscosity, for example, in egg white and blood plasma.
Erythrocytes/Red blood cells are the most common type of blood cell and are the vertebrate body's principal means of delivering oxygen from the lungs or gills to body tissues via the blood.Red blood cells are also known as RBCs or erythrocytes (from Greek erythros for "red" and kytos for "hollow", with cyte nowadays translated as "cell"). A schistocyte is a red blood cell undergoing fragmentation, or a fragmented part of a red blood cell.
An antigen is a substance that stimulates an immune response, especially the production of antibodies. Antigens are usually proteins or polysaccharides, but can be any type of molecule, including small molecules (haptens) coupled to a carrier-protein.
International Atomic Energy Agency (IAEA) Safeguards.
India signed IAEA Safeguards on July 18 '05.
Few details about IAEA Safeguards.
* IAEA was established in 1957
Most countries around the world use nuclear technologies for a wide variety
of peaceful purposes — for generating electricity, diagnosing disease and
treating cancer, for numerous industrial applications and for food and
medical sterilization. At least 30 countries have nuclear power reactors.
There are scores of other major facilities containing nuclear material in
over 70 countries that are “safeguarded” under IAEA agreements with
governments.
Safeguards are a set of activities by which the IAEA seeks to verify that a
State is living up to its international undertakings not to use nuclear
programmes for nuclear weapons purposes. The safeguards system is based on
assessment of the correctness and completeness of the State’s declarations
to the IAEA concerning nuclear material and nuclear-related activities. To
date, 145 States have entered into such agreements with the IAEA,
submitting
nuclear materials, facilities and activities to the scrutiny of IAEA’s
safeguards inspectors.
IAEA verification helps to provide assurance that such items are not
diverted or misused in order to assemble nuclear weapons and that no items
required to be declared under safeguards are undeclared. This, in turn,
helps to allay security concerns among States with respect to the
development of nuclear weapons.Verifying the Peaceful Uses of Nuclear
Energy
For more details you can visit:
http://www.iaea.org/OurWork/SV/Safeguards/index.html
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Six Step Weekly Planning Process
Six Step Weekly Planning Process
Nice web site for planning
Quote for Oscar Schindler
"Whoever saves one life, saves the world entire"Schindler's List - I have seen this movie couple of times. A great movie.. an abode to a Great Man - Oscar Schindler.
'No one will ever know exactly what made this complex man do what no German had the courage to do. Oscar Schindler rose to the highest level of humanity, walked through the bloody mud of the Holocaust without soiling his respect for human life - and gave his Jews a second chance at life.' - Extract from website www.aushwithz.dk
To unfold.. visit:
http://www.aushwitz.dk/lamus.htm
Lung Cancer
In one of the mail I recieved today - Non Small Cell Lung Cancer was mentioned. So just thought of gathering some info on same and got it from http://www.cancer.org/
The complete link is:
http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_is_lung_cancer_26.aspHere is the extract.
What Is Lung Cancer? Your lungs are two sponge-like organs found in your chest cavity. Your right lung is divided into 3 sections, called lobes. Your left lung has 2 lobes. It is smaller because your heart takes up more room on that side of the body. When you breathe, air goes into your lung through the trachea (windpipe). The trachea divides into tubes called the bronchi, which divide into smaller branches called the bronchioles. At the end of the bronchioles are tiny air sacs known as alveoli. Many tiny blood vessels run through the alveoli, absorbing oxygen from the inhaled air into your bloodstream and releasing carbon dioxide. Taking in oxygen and getting rid of carbon dioxide are your lungs’ main function. A slippery lining, called the pleura, surrounds the lungs. This lining protects your lungs and helps them slide back and forth as they expand and contract during breathing.
Most lung cancers start in the lining of the bronchi. That is why another term for lung cancer is bronchogenic cancer. Lung cancer can also form in glands below the lining of the bronchi, frequently in the periphery of the lungs. Lung cancers are thought to develop over a period of many years. First, there may be areas of precancerous changes in the lung. These changes do not form a mass or tumor. They cannot be seen on an x-ray and they do not cause symptoms. But, these precancerous changes can be found by analyzing cells in the lining of the airways of smoke-damaged lungs. Recently, molecular abnormalities believed to be precancerous have been identified in cells from individuals at high risk to develop lung cancers (for example, survivors from one prior lung cancer). These precancerous changes often progress to true cancer. As a cancer develops, the cancer cells may produce chemicals that cause new blood vessels to form nearby. These new blood vessels nourish the cancer cells, which can continue to grow and form a tumor large enough to see on x-rays. Cells from the cancer can break away from the original tumor and spread to other parts of the body. As noted earlier, this process is called metastasis. Lung cancer is a life-threatening disease because it often spreads in this way even before it can be detected on a chest x-ray.
Types of Lung Cancer There are two major types of lung cancer:
small cell lung cancer (SCLC)
non-small cell lung cancer (NSCLC).
If a lung cancer has characteristics of both types it is called a mixed small cell/large cell carcinoma. This is uncommon. These two types of lung cancer are discussed separately because they are treated very differently.
Small Cell Lung Cancer About 13% of all lung cancers are the small cell type (SCLC), named for the small round cells that make up these cancers. SCLC tends to spread widely through the body. This is important because it means that treatment must include drugs to kill the widespread disease. The cancer cells can multiply quickly, form large tumors, and spread to lymph nodes and other organs such as the bones, brain, adrenal glands, and liver. This type of cancer often starts in the bronchi near the center of the chest. Small cell lung cancer is almost always caused by smoking. It is very rare for someone who has never smoked to have small cell lung cancer. Other names for SCLC are oat cell carcinoma and small cell undifferentiated carcinoma.
Non-small Cell Lung Cancer The remaining 87% of lung cancers are non-small cell (NSCLC). There are three sub-types of NSCLC. The cells in these sub-types differ in size, shape, and chemical make-up.
squamous cell carcinoma: About 25% - 30% of all lung cancers are squamous cell carcinomas. They are associated with a history of smoking and tend to be found centrally, near a bronchus.
adenocarcinoma: This type accounts for about 40% of lung cancers. It is usually found in the outer region of lung. People with one type of adenocarcinoma, known as bronchioloalveolar carcinoma (sometimes called bronchoalveolar carcinoma or bronchioalveolar carcinoma) tend to have a better outlook (prognosis) than those with other types of lung cancer.
large-cell undifferentiated carcinoma: This type of cancer accounts for about 10% - 15% of lung cancers. It may appear in any part of the lung, and it tends to grow and spread quickly resulting in a poor prognosis.
*For more details please visit the website:
http://www.cancer.org/docroot/CRI/content/CRI_2_4_1X_What_is_lung_cancer_26.asp*Information provided here is purely for my own understanding of this topic and for easy reference if required in future.
India, Inc.'s new mantra: Serve thy motherland
India, Inc.'s new mantra: Serve thy motherland
CHAITALI CHAKRAVARTY AND BHANU PANDE
NEW DELHI: Even Indians are buying the India Story. Corporate executives
are refusing plum foreign postings and settling for the home turf to prove
their mettle. Search firms believe the phenomenon has come to the forefront
in the last six months and will gather steam in ’06-07.
“As many as 7 out of 10 top executives prefer domestic assignments to
overseas postings. The trend has reversed in the last five years,” says
Ronesh Puri, MD of search firm Executive Access.
Adds Deepak Gupta of Korn Ferry, “My conservative estimate is that 60% of
the CEOs in multinational companies wouldn’t take up a foreign offer.”
Search firms attribute it to several reasons. But the primary ones are
developed markets have shrunk to such an extent that it’s no fun working
there anymore.
Second, salary differentials have narrowed down considerably, so dollar
salaries are not top in the priority list and most importantly, the quality
of the life index in India has improved so much that executives don’t
hanker after international postings like they used to be in the past.
“Which country offers farmhouses measuring several acres to CEOs?” asks a
head hunter.
Also, family life and kids’ education have assumed importance in the last
few years. Executives are willing to sacrifice cushy foreign postings if
they find that their children’s education would suffer.”
ET is withholding names of executives who have refused overseas postings
because they are currently finalising fresh assignments in India.
Market sources said that Rohit Srivastava, head of planning in ad agency
Contract, has repeatedly declined an overseas posting, a few senior
Gillette executives have recently declined plum offers in Europe and
exploring opportunities with companies in India, and some point to the fact
that during the last few months even Hindustan Lever saw some top
executives declining cushy overseas assignment for a position in India
itself.
The investment banking community is also saying no to foreign offers.
According to Mr Gupta, vacancies in the Middle East have become even more
difficult to fill. “The tax-free regime of the Middle East used to be a big
draw a few years ago. Not anymore. There’s so many opportunities in India
that even expats are coming in droves,” he says.
According to Preety Kumar, managing partner of search firm Amrop
International, the developed markets including Europe have become staid
with petering growth, and the US has its own issues.
“The scale and complexity of what can be achieved in India is something no
other comparative market can match and top executives are increasingly
warming up to this idea,” she adds.
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How much does it cost to celebrate?
A nice forward:
How much does it cost to celebrate?
Maggi noodles.
A hostel room.
4.25 a.m.
A winter evening.
Four friends.
One barsaat.
Four glasses of chai.
Hundred bucks of gas.
A rusty old bike.
And an open road.
3 old friends.
3 separate cities.
3 coffee mugs.
1 internet messenger.
Rain on a hot tin roof.
Pakoras deep-frying.
Neighbours dropping in.
A party.
You and mom.
A summer night.
A bottle of coconut oil.
A head massage.
Gossiping about absent family members.
You can spend
hundreds on birthdays,
thousands on festivals,
lakhs on weddings,
but to celebrate
all you have to spend is your Time.
It doesn't take much after all ........................
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Bill Gates and Narayan Murthy Interviewed by Prannoy Roy
PRANNOY ROY : To me and many of us at TiE, it is a special moment. We have
with us together two icons of our times - Mr. Bill Gates and Mr. Narayana
Murthy. Both iconic entrepreneurs, but in fact both much more than that. As
you look into their lives there are so many similarities. Like both started
life as hardcore software guys. Mr. Bill Gates wrote the basic compiler and
Mr. Murthy, in the early 70s, also wrote the first basic compiler. Both
today have given up being CEOs and taken a step back to help with the
bigger kind of picture with bigger vision. Both of them have superb right
hand people i.e: Steve Ballmer and Nandan Nilekani. Both have huge
businesses but even larger social goals with larger hearts. Both have
wives, Melinda and Sudha, who infact are even more
committed to changing society, to philanthropy and charity. As icons they
have to resist tremendous pressures, sometimes to enter politics. Both
remarkable men, that come once in a lifetime, once in a generation. Both
used to travel economy class, some say they were stingy, for some it is
about principles. If it is stingy, certainly it is not visible in their
charity. Ironically both are voracious readers, books are their passion.
One major similarity - both really believe in spreading wealth among their
employees through ESOPs but now both have stopped that and the list of
their similarities is endless.
PRANNOY ROY : What are the defining moments in your life?
BILL GATES : Certainly the opportunity to use a computer at young age, I
was only 13 at that time and I was 16 when I first understood the magic of
chips with double power every two years. The school teacher asked me to
teach computer to the class. That was when I got fascinated and completely
immersed. My decision to leave school and start a company, that’s a nice
milestone since it worked. In my case I thought the time was very important
to get in and be the very first. So this chip computer comes out and I
decided to go to Paul Allen and provide the software for the very first
personal computer, which again was incredibly limited. The willingness to
take the risk before anybody else was doing it, I think that was a big help
to us. My parents thought that I was going on leave and will come back as
the company will not succeed, even Harvard was nice enough to say that I
could come back and even today they are willing to take me back.
NARAYANA MURTHY : There have been atleast three defining moments in my
life. First when I was incarcenated in Bulgaria, a communist country and
without food and water for 96 hours. Later I decided that I don’t want to
be a part of this system and I will go back to India to pursue
entrepreneurship and create wealth legally and ethically. Second was in
1990, we had started the company in 1981. It didn’t progress because there
was so much of friction in business in India. There was an offer from
somebody to acquire us for $1mn, from this offer six of my group members
got excited but towards the end I decided that I am not going to sell it
off. Third was frankly getting listed on NASDAQ. In fact it was a small
step for NASDAQ but a giant leap for Infosys and Indian software industry.
I would say that these were the three defining moments in my life.
PRANNOY ROY : How do you keep yourself motivated to work on and on and on?
BILL GATES : I love my work, I get to work with smart people and it’s a
field that’s constantly changing. Every couple of year’s people say that a
new company will throw you out of the business and we get to show people
“not this time”. My vision was not about sales or profits but it was about
this computer, what it could do and we don’t have that computer yet. We
cannot talk to the machine and it cannot talk to us and we are still
looking for that computer. I have a dream of having a computer in every
home, in every desk. We are not even half way in achieving that goal, here
in India we are scratching the surface. So there is still lot of work to be
done as there is no finish line anywhere near.
NARAYANA MURTHY : Most passionate people in the world are held by larger
goals. At Infosys, we have a vision to become a globally respected
organization, not only in India but also in US, Japan, Germany, Australia
UK and that’s still a long marathon. Maybe 10,000 or 12,000 Infosysians
have already made some money but there are 30,000 other Infosysians who
still have to make that kind of money and it is our responsibility to give
our best, our commitment to make sure that they and future Infosysians can
make money.
PRANNOY ROY : Both of you started ESOPs and both of you have given it up.
Why?
BILL GATES : Microsoft shared more wealth than any other company has in the
history of capitalism. If you get to a point where industry is so hot, it
almost hyped then you start to get deviations that not only go up but they
also fluctuate, so to pass the risk of those market conditions on to the
employees may not be right. But we are actually into shares now where you
get your salary and shares of stock and so we cut the variance down and so
the predictability is much greater and still plenty of personal wealth. We
are still sharing the wealth but in a different way and it wasn’t to do
anything with the new accounting principles.
NARAYANA MURTHY : I always believed that leadership does not succeed in a
vacuum, you need people who are smarter than you, who have same or higher
level of passion and energy. If you want to bring those people on board
then you need some equitable paradigm and that is why Infosys adopted the
ESOPs model. We suspended it because we have to expense it out according to
US regulations and then we realized that it is not the best model for us
anymore. And then as it was pointed out, we made an analysis and found that
by creating a paper or variable performance model, we will be able to
provide a decent compensation for all.
PRANNOY ROY : India has got a new energy with Democracy as its foundation.
People have started questioning. Is democracy important in taking business
decisions?
BILL GATES : Democracy means right way of looking at resources. It is the
real commitment to the future. It is a must and we, US, stand for it.
NARAYANA MURTHY : We value knowledge as the most intangible asset. However,
the important question now is, Is it really paying? There has to be a
greater premium on time. We waste lot much of it in discussions. One of my
friends from Harvard aptly quoted, “Two of my greatest challenges are – How
to get my Japanese students to speak up and Indian students to shut up”. We
have to come to conclusion out of discussions and get to execution.
PRANNOY ROY : Does a anti-American wave affect you? Lack of US sensitivity
in handling international affairs to the world issues affects your
relationships with
your partners.
BILL GATES : The world depends on the US to do certain things right whether
it is funding science or whether setting a good example for free trade. I
won’t say we lost business or have some impact it is because of the US
politics. Everybody resents the most successful country and everybody loves
the most successful country. It is all the love-hate relationship. In the
US there are mixed feelings about what they think the US is doing good and
not doing well. It is for the world to understand the benefits of free
trade system. The US should be imitated by others. The way we run our
university system should be learnt by everyone. We stand for – Be good in
every way, innovation in products, markets, etc. People talk of India
versus China, why not India plus China. India should learn from China and
China should learn from India. I am proponent of the combined best
practices of India, China and the US.
PRANNOY ROY : Does the use of force by US in international affairs worry
you?
BILL GATES : It is best to use when the stake is very dramatic. Even in US,
people say we need more evidence (in Iraq issue) but then for us it is
good, for it is for the democracy.
PRANNOY ROY : Is it love-hate relationship? Even we say “Yankee go home,
but take me with you”
NARAYANA MURTHY : I am unabashed admirer of US for their openness. I don’t
know of any other society as open as the US. It is for us to work harder to
convince the US people, decision makers, law makers, that there is good
value for them (inoutsourcing). If there is an outcry, dissatisfaction, I
see it as our failure. ‘The day you say market is wrong, you are finished’,
this should be learnt by US.
PRANNOY ROY : Now we will take some of the questions from the audience.
A1. My question is for Mr. Narayana Murthy. What challenges are faced by
large and small companies in attracting, keeping and retaining best talent?
NARAYANA MURTHY : It is all about creating the dream and vision and
articulating that everybody is able to take the rainbow and put in pocket.
It is all about making sure that people will get their value, people will
automatically come to you.
A2. My question is for Mr. Bill Gates. After the internet, what technology
will take the world now?
BILL GATES : We need to get a device which will get us value at the low
cost. Like speech recognition, mapping devices etc. I see natural interface
technology as the important area that shall dominate the sphere.
A3. My question is for Mr. Bill Gates. What human qualities are important
for success?
BILL GATES : You need passion, intelligence and some kind of integrity to
understand what your limits are. Very strong combination of all the three
shall help to achieve success.
A4. My question is for Mr. Narayana Murthy. Very large companies are
created in US. What do we need to do to have the same in India?
NARAYANA MURTHY : We need a more competitive market. Corporations have to
realize the importance of innovation, good venture capital system,
environment that enhances the quality of education system that focuses on
problem solving and good set of mentoring who will take care of
entrepreneurs’ linkages with the requisite networks.
BILL GATES : We always talk big companies like Yahoo, Microsoft, Google,
etc. We don’t think of numerous companies that fail. It is all market
economy that survives.
A5. My question is for Mr. Bill Gates. What is the fundamental difference
between managing a startup and a large corporation?
BILL GATES : The leadership styles are quite different. When the companies
grow, you acquire skill sets, create a system, take a step back, monitor
the people and manage the managers.
PRANNOY ROY : The last question - Will you ever enter into politics?
BILL GATES : No
NARAYANA MURTHY : No
PRANNOY ROY: Thank you very much.
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Fw: Bug in Windows
One more bug in Microsoft Windows!
This is quite interesting
1) Create a folder on the desktop and name it as "Notepad"
2) Open a webpage (any) in IE and see its view source.
Its Just AMAZING !!!
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Seven Deadly Sins
Pride
Sloth -
a disinclination to work or exert yourself
any of several slow-moving arboreal mammals of South America and
Central America; they hang from branches back downward and feed on
leaves and fruits
apathy and inactivity in the practice of virtue (personified as one
of the deadly sins)
Gluttony
habitual eating to excess
eating to excess (personified as one of the deadly sins)
wrath
intense anger
belligerence aroused by a real or supposed wrong (personified as one
of the deadly sins)
envy
a feeling of grudging admiration and desire to have something
that is possessed by another
feel envious towards; admire enviously
spite and resentment at seeing the success of another
(personified as one of the deadly sins)
be envious of; set one's heart on
lust
Greed
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My Stupid Suicide Plan... by Chetan Bhagat
My Stupid Suicide Plan
- CHETAN BHAGAT
Last week, an IITian committed suicide. People who commit suicide do it
when they feel there's no future. But wait, isn't IIT the one place where a
bright and shining future is a foregone conclusion? It just doesn't add up,
does it? Why would a young, hardworking, bright student who has the world
ahead of him do something like this? But the answer is this-in our constant
reverence for the great institution (and I do believe IITs are great), we
forget the dark side. And the dark side is that the IITs are afflicted by
the quintessential Indian phenomenon of academic pressure, probably the
highest in the world.
I can rant about the educational system and how it requires serious fixing,
or I can address the immediate-try my best to prevent such suicides. For
this column I have chosen the latter, and I do so with a personal story.
News of a suicide always brings back one particular childhood
memory. I was 14 years old when I first seriously contemplated suicide. I
had done badly in chemistry in the Class X half yearly exam. I was an IIT
aspirant, and 68% was nowhere near what an IIT candidate should be getting.
I don't know what had made me screw up the exam, but I did know this, I was
going to kill myself. The only debate was about method.
Ironically, chemistry offered a way. I had read about copper
sulphate, and that it was both cheap and poisonous. Copper sulphate was
available at the kirana store. I had it all worked out.
My rationale for killing myself was simple-nobody loved me, my
chemistry score was awful, I had no future and what difference would it
make to the world if I was not there. I bought the copper sulphate for two
rupees-probably the cheapest exit strategy in the world.
I didn't do it for two reasons. One, I had a casual chat with the aunty
next door about copper sulphate, and my knowledgeable aunty knew about a
woman who had died that way. She said it was the most painful death
possible, all your veins burst and you suffer for hours. This tale made my
insides shudder. Second, on the day I was to do it, I noticed a street dog
outside my house being teased by the neighborhood kids as he hunted for
scraps of food. Nobody loved him. It would make no difference to the world
if the dog wasn't there. And I was pretty sure that its chemistry score
would be awful. Yet, the dog wasn't trotting off to the kirana store. He
was only interested in figuring out a strategy for his next meal. And when
he was full, he merely curled up in a corner with one eye open, clearly
content and not giving a damn about the world. If he wasn't planning to die
anytime soon what the hell was I ranting about? I threw the copper sulphate
in the bin. It was the best two bucks I ever wasted.
So why did I tell you this story? Because sometimes the pressure gets too
much; like it did for the IITian who couldn't take it no more. On the day
he took that dreadful decision, his family and friends were shattered, and
India lost a wonderful, bright child. And as the silly but true copper
sulphate story tells you-it could happen to any of us or those around us.
So please be on the lookout, if you see a distressed young soul, lend a
supportive, non-judgmental ear. When I look back, I thank that aunt and
that dog for unwittingly saving my life. If God wanted us to take our own
life, he would have provided a power off button. He didn't, so have faith
and let his plan for you unfold. Because no matter how tough life gets and
how much it hurts, if street dogs don't give up, there is no reason why we,
the smart species, should. Makes sense right?
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BSE Sensex touched 10000 mark on (06-02-2005) for the first time
The Sensex journey: 1,000 to 10,000!
rediff Business Desk | February 06, 2006
Bombay Stock Exchange, the oldest stock exchange in Asia, was established
in 1875 as the Native Share and Stock Brokers Association at Dalal Streetin
Mumbai. A lot has changed since then when 318 persons became members upon
paying Re 1.
In 1956, the BSE obtained permanent recognition from the Government of
India -- the first stock exchange to do so -- under the Securities
Contracts (Regulation) Act, 1956.
The Sensex, first compiled in 1986, is a 'Market Capitalisation-Weighted'
Index of 30 component stocks representing a sample of large and financially
sound companies. The BSE-Sensex is the benchmark index of the Indian
capital markets.
The BSE Sensex comprises these 30 stocks: ACC, Bajaj Auto, Bharti Tele,
BHEL, Cipla, Dr Reddy's, Gujarat Ambuja, Grasim, HDFC, HDFC Bank, Hero
Honda, Hindalco, HLL, ICICI Bank, Infosys, ITC, L&T, Maruti, NTPC, ONGC,
Ranbaxy, Reliance, Reliance Energy, Satyam, SBI, Tata Motors, Tata Power,
TCS, Tata Motors and Wipro.
The Sensex on Monday scaled a new high as it breached the historic 10,000
mark* during mid-session.
Here's a timeline on the rise and rise of the Sensex through Indian stock
market history.
The 1000-mark
On July 25 1990, the Sensex touched the magical four-digit figure for the
first time and closed at 1,001 in the wake of a good monsoon and excellent
corporate results.
The 2000-mark
On January 15, 1992, the Sensex crossed the 2,000-mark and closed at 2,020
followed by the liberal economic policy initiatives undertaken by the then
finance minister and current Prime Minister Dr Manmohan Singh.
The 3000-mark
On February 29, 1992, the Sensex surged past the 3000 mark in the wake of
the market-friendly Budget announced by the then Finance Minister, Dr
Manmohan Singh.
The 4000-mark
On March 30, 1992, the Sensex crossed the 4,000-mark and closed at 4,091 on
the expectations of a liberal export-import policy. It was then that the
Harshad Mehta scam hit the markets and Sensex witnessed unabated selling.
The 5000-mark
On October 8, 1999, the Sensex crossed the 5,000-mark as the BJP-led
coalition won the majority in the 13th Lok Sabha election.
The 6000-mark
On February 11, 2000, the infotech boom helped the Sensex to cross the
6,000-mark and hit and all time high of 6,006.
The 7000-mark
On June 20, 2005, the news of the settlement between the Ambani brothers
boosted investor sentiments and the scrips of RIL, Reliance Energy,
Reliance Capital and IPCL made huge gains. This helped the Sensex crossed
7,000 points for the first time.
The 8000-mark
On 8th September 2005, the Bombay Stock Exchange's benchmark 30-share index
-- the Sensex -- crossed the 8000 level following brisk buying by foreign
and domestic funds in early trading.
The 9000-mark
The Sensex on November 28, 2005 crossed the magical figure of 9000 to touch
9000.32 points during mid-session at the Bombay Stock Exchange on the back
of frantic buying spree by foreign institutional investors and well
supported by local operators as well as retail investors.
The 10,000-mark *
The Sensex on Monday crossed the magical figure of 10,000 and touched a
life-time peak of 10,003 points during mid-session at the Bombay Stock
Exchange on the back of frantic buying spree by foreign institutional
investors and well supported by local operators as well as retail
investors.
* During mid-session trading.
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Some Facts
* The lowest temperature ever recorded in the world was 129 degrees below 0 at Vostok, Antarctica, on July 21, 1983.
* The low frequency call of the humpback whale is the loudest noise made by a living creature.
* The lowest point that a person can reach on Earth, outside of riding a submarine or going down a mine shaft, is where the Jordan River enters the Dead Sea. It's 1,290 feet below sea level.
* The left lung is smaller than the right lung to make room for the heart.
* The letter "W" is the only letter in the alphabet that doesn't have just one syllable; it has three.
* The letter J does not appear ANYWHERE in the periodic table of elements.
* The last thing to happen is the ultimate. The next-to-last is the penultimate, and the second-to-last is the antepenultimate.
* The lead in a normal pencil would draw a line of 35 miles.
* The Leaning Tower of Pisa was built on the site of a river estuary. The land under the town has several layers of silt and soft clay. The 15,000-ton tower tilts to the south because the subsoil is too unstable.
