Sunday, August 30, 2009

How to get rid of insomnia?



In order to lead a healthy life good sleep is one of the vital things you should take care off because sleep can do miracles for your body because of its role as a rejuvenator of not only your mind but also your body. Not getting enough sleep or suffering from insomnia can be quite difficult for your organism so here are some tips that should help you get rid of insomnia.

In order to prevent insomnia the good thing to start with is usually a regular daily time for sleep, even ancient nations knew that regular sleeping time habit helps against insomnia. One thing you should avoid though is daily nap because this can totally disrupt your regular daily time for sleep.

Sometimes when you can not fall a sleep exercises can do the trick. It is important to know that maximum benefits cannot be achieved with exercises just prior to going to bed, in order to achieve maximum effect you should do exercise 4-6 hours before going to bed.

Many people think how alcohol can help you to sleep good but this is not true, alcohol as well as caffeine can in fact make your insomnia worse, after all we all know that drinking lots of coffee can remove your desire for sleep.

Cosy, warm bed is something that should be also quite helpful, especially in combination with hot tub in the evening so you could also try this. Proper diet can also have big effect on good sleep so make sure to avoid strong, spicy food, and stick with easily digestible food. Also a glass of warm milk can sometimes be enough to make your eyes sleepy.

If you're not afraid of dark make sure to sleep in dark room, light is definitely not good for eyelids that are not sleepy. I also forgot to mention that you should try anything that relaxes and soothes you because relaxed organism has much better chance of falling into sleep than not relaxed one.

It is always good to try these natural options before switching for medicines like sleeping pills.

3D Medical Animation: Tonsillectomy Surgery

3D Medical Animation Upper GI Endoscopy

3D Medical Animation: Endometrial Biopsy of the Uterus

McRoberts Maneuver for Shoulder Dystocia Birth Injury

3D Medical Animation - Lumpectomy, Mastectomy Breast Cancer Surgery

Atherosclerosis

Inguinal Hernia Repair Surgery

Skin Cancer


Skin cancer occurs if there's uncontrollable growth of abnormal cells on the skin. Learn more about the different types of skin cancer.

Functions of the Skin

The skin is the largest organ of the body. It serves many important functions, including protecting the body from infection, and regulating body temperature and fluids. The skin is primarily composed of three layers.

Layers of the Skin

  • The epidermis is the outer layer of skin and contains basal and squamous cells. Melanocytes are also found in the epidermis; these are cells that contain pigment, which allows the skin to tan and which also protect the deeper layers of skin from the effects of UV sunlight exposure.

  • The dermis, which lies below the epidermis, contains blood vessels, connective tissue, hair follicles, and sweat glands.

  • The subcutaneous layer, which is the deepest layer of skin, contains fat cells and collagen.

How Skin Cancer Develops


Skin cancer occurs when there is an uncontrollable growth of abnormal cells in a layer of the skin. There are three common forms of skin cancer that are distinguished by the types of cells affected.

Types of Skin Cancer

  • Basal cell carcinoma is the most common form of skin cancer. This type of skin cancer does not typically spread, but does require treatment. Basal cell carcinomas most often develop in areas of the skin exposed to the sun.

  • Squamous cell carcinomas develop in the middle layer of the epidermis. This type of cancer can spread and can be life threatening if not treated appropriately.

  • Abnormal growths of melanocytes, called malignant melanomas, are the most aggressive form of skin cancer. Melanomas can spread quickly to other parts of the body and to organs. This type of skin cancer can be fatal if not detected and treated early. People with fair skin are at increased risk for developing this form of cancer.

A few hours after a person or animal dies, the joints of the body stiffen and become locked in place. This stiffening is called rigor mortis. Depending on temperature and other conditions, rigor mortis lasts approximately 72 hours. The phenomenon is caused by the skeletal muscles partially contracting. The muscles are unable to relax, so the joints become fixed in place.

More specifically, what happens is that the membranes of muscle cells become more permeable to calcium ions. Living muscle cells expend energy to transport calcium ions to the outside of the cells. The calcium ions that flow into the muscle cells promote the cross-bridge attachment between actin and myosin, two types of fibers that work together in muscle contraction. The muscle fibers ratchet shorter and shorter until they are fully contracted or as long as the neurotransmitter acetylcholine and the energy molecule adenosine triphosphate (ATP) are present. However, muscles need ATP in order to release from a contracted state (it is used to pump the calcium out of the cells so the fibers can unlatch from each other). ATP reserves are quickly exhausted from the muscle contraction and other cellular processes. This means that the actin and myosin fibers will remain linked until the muscles themselves start to decompose.

Rigor mortis can be used to help estimate time of death. The onset of rigor mortis may range from 10 minutes to several hours, depending on factors including temperature (rapid cooling of a body can inhibit rigor mortis, but it occurs upon thawing). Maximum stiffness is reached around 12-24 hours post mortem. Facial muscles are affected first, with the rigor then spreading to other parts of the body. The joints are stiff for 1-3 days, but after this time general tissue decay and leaking of lysosomal intracellular digestive enzymes will cause the muscles to relax. It is interesting to note that meat is generally considered to be more tender if it is eaten after rigor mortis has passed.

DNA Extraction

DNA Extraction is typically the first step in a longer laboratory process. DNA first needs to be purified away from proteins and other cellular contaminants.

So Where do we begin?

We first need to collect cell from the test subject. The skin inside of our mouths losses thousands of cells everyday. These cells are ideal for DNA Extraction. Once the “Cheek Cells” are collected you will need to place the swab used for collection in a Eppendorf Tube

Now using a Micropipette, add Lysis a solution with the greek meaning “to separate” into the Eppendorf tube containing the swap used to collect the cheek cells. Once the Lysis has been added you will need to place the tube in a “Warm Water Bath Machine”.
The Lysis solution we just added contains two important ingredients, the first being “Detergent” and the second being “Proteinase K”. The Detergent disrupts the cel membrane and nucleus envelope. Causing the cells to burst open and release their DNA. The DNA is still wrapped very tightly around proteins called histones, and the Proteinase K cuts apart the histones to free the DNA.

The cells have now been in warm water long enough (the cells themselves are not in warm water but merely the Eppendorf tube is) for the DNA freed from the cells, and we have removed the swab from the tube.

Now we must add concentrated salt to the Eppendorf tube containing the DNA. The salt causes the proteins and the cellular debris to clump together. To complete this process we must now place the Eppendorf tube into a centrifuge. In order the balance the centrifuge we have to add a second Eppendorf tube into it that contains only water on the opposite side of the tube containing the DNA sample.DNA extraction4.gif (23962 bytes)

Inside the centrifuge, the tube spin a high speed. The heavy clumps and cellular debris sink to the bottom of the tube, while the DNA strands stays distributed in the liquid above .

Now using a Micropipette we must very carefully remove the liquid above (which contains DNA) the debris and cellular contaminants and place it into a new clean Eppendorf tube, the debris and cellular contaminants will be left behind since they are no longer needed.

Now we will need to add Isopropyl into the Eppendorf tube containing the DNA strands, Inverting the tube several times mixes the Isopropyl alcohol into the DNA solution. Because DNA is not soluble, in Isopropyl alcohol it comes out of the solution. We will then be able to see the DNA with your naked eye.

Again we will have to place the tube into a centrifuge. This time after the sample spins in the centrifuge, the DNA sinks to the bottom of the Eppendorf tube.

Now what’s next? Nothing. The solution left in the tube is the final part of the DNA extraction. Depending on the circumstances you may want to let the solution dry out so it could be frozen for later use, for years even. This can now be used in another forensic laboratory investigation to match that DNA with other DNA found at a crime scene for example.

Asphyxia


Asphyxia occurs when the body is deprived of oxygen that arises from being unable to breathe normally. Asphyxia causes Generalized Hypoxia which primarily effects organs and tissues. Examples of Asphyxia include choking, smothering, and drowning (Asphyxia can also be induced by inhalation of toxic chemicals, certain toxins can interfere with the uptake of O2 by the blood cells’ use of oxygen in the body). Asphyxia is referred to as traumatic or crush Asphyxia in relation to accidents.

Mechanisms of Asphyxial death include Mechanical Constriction, Airway Obstruction, and Cardiac Arrhythmia. Several classic signs that help medical examiners acknowledge if a particular persons demise was caused by Asphyxiation, include congestion of the face due to venous congestion (venous return to the heart is prevented), facial oedema due to increased venous pressure causes tissue fluid transudation, cyanosis (excess de-oxygenated hemoglobin the venous blood), and petechial hemorrhagen the skin and eyes (particularly the eyelids, conjunctiva, sclera, face, lips and behind the ears) due to raised venous pressure. Categories in which Asphyxial deaths are classified include neck compression, chest compression, postural/positional Asphyxia, airway obstruction and exhaustion or displacement of environmental oxygen.

The air we take into our lungs contains oxygen. After it’s in the lungs’ air sacs, the O2 crosses into the blood, combines with the hemoglobin of the red blood cells, and departs with those red blood cells throughout the body. Normal air contains approximately twenty one percent oxygen. When this percentage drops to ten – fifteen, judgement and coordination are greatly impaired. You lose consciousness when the oxygen concentrations fall below ten percent, thereafter death will occur at around eight percent.

In a Stranglehold

Strangulation is the compression of the neck that leads to unconsciousness or death. In turn causing an increasingly hypoxic state in the brain. Fatal strangling typically occurs in cases where violence, accidents, and as the mechanism of suicide in hangings. Stranglings are not always fatal; limited or interrupted strangling is an important technique in many self-defence and combat sports, strangling is also ‘practiced’ in erotic asphyxiation, and in the “Fainting or Choking game”.

Strangulation is divided into three main categories. Hanging, suspension from a cord wound around the neck. Ligature strangulation, strangulation without suspension using some form of cord-like object or rope. Manual strangulation, strangulation using the fingers or other extremity.

Inside the Lungs: Drowning

Drowning is death by suffocation (Asphyxia) induced by liquid entering the lungs, in turn preventing the absorption of oxygen leading to cerebral hypoxia and myocardial infarction. Near drowning is the survival of a drowning event involving unconsciousness or water inhalation and can be the path to serious secondary complications including death (secondary complications/drowning is when biological and chemical changes occur after a near drowning incident, that can lead to death up to seventy two hours after the orginal incident).

Drowning is a common fear and a decidedly unpleasant demise. As you drown, your lungs fill with water, and they lose their ability to transfer oxygen into the bloodstream. While you struggle to breathe, you force water into your sinuses. Coughing triggers an inhalation reflex, which pulls even more water into the lungs. The loss of an air supply combines with energy you consume in the struggle for survival, and the oxygen level in the blood rapidly falls. You loose consciousness in one to two minutes. The heart stop shortly after.

Saturday, August 29, 2009

Origin of swine flu virus


Researchers use evolutionary history to trace the early days of the pandemic.Closely related forms of the H1N1 strain of influenza virus circulated undetected in swine for years, a study published online June 11 in Nature reports. The virus, which has spread to multiple continents, has now been classified by the World Health Organization as a pandemic. "Based on this report, we had a virus circulating in pigs for 10 years and nobody knew anything about it because we were not doing proper surveillance," says Daniel Perez, an influenza expert at the University of Maryland in College Park.

Researchers traced the sordid past of the H1N1 virus by comparing mutations among different strains of the virus. Genetic sequences of 15 swine influenzas from Hong Kong and two human H1N1 viruses were compared with 796 sequences representing a large spectrum of related strains from humans, birds and pigs.

Analyzing numbers of mutations allowed an international team of researchers to estimate how long ago the strains first existed. Virus strains more than 90 percent identical to the current H1N1 strain were circulating in pigs between 9.2 and 17.2 years ago, the researchers found. The current strain "evidently spread without anyone noticing it for 10 years," says Michael Worobey, an evolutionary biologist at the University of Arizona in Tucson and one of the study's authors. "We need to spend more energy looking at what's in pigs."

"Any estimate like this has a certain amount of uncertainty to it," Worobey says. Although the numbers are not exact, he says, the data clearly show that a similar version of the virus was around long before anyone was aware of it. The report also shows that each bit of the current virus's DNA had been circulating on its own and primarily in pigs for years before combining to form the virus responsible for the current pandemic. Some genes have been in pigs for decades. "Across the genome, this is something that came from pigs," Worobey says.

Some of these DNA segments came from a North American swine influenza virus, which itself is made of bits of avian, human and swine influenzas (called a triple-reassortant strain). Other segments came from Eurasian swine with avian virus components. The combination of the triple-reassortant strain from North America and the avianlike strain from Eurasia probably happened as live pigs were transported between North America and Eurasia, the authors say.

"We can do all the surveillance we want in humans, but if we really want to prevent pandemic influenza..., a fundamental change in efforts on the animal health side has to be made," Perez says. On the same day the new report appeared, the World Health Organization classified the H1N1 outbreak as a pandemic, defined as showing sustained person-to-person transmission in many parts of the world.

WHO Director-General Margaret Chan said that the organization is raising the alert level after determining that flu cases are now showing up in people who didn't bring it from another region and weren't in contact with such travelers. "Further spread is considered inevitable," Chan said in a news conference.

"This does not mean that there is any difference in the level of severity of the flu," he said. Rather, the pandemic label "is important because it does send the strong message that the virus is here, it's in all likelihood here to stay, and it's important that we continue our aggressive efforts to prepare and respond." So far no decision has been made to mobilize pharmaceutical companies to start mass-producing vaccines aimed specifically at the novel H1N1 virus. But preliminary steps to make that a seamless move have already been taken.

Source: www.sciencenews.org

H1N1 fever- Swine flu Doubts


As the Swine flu is at its kill, everyone is having many doubts. You can clear many of them here

How do you catch H1N1 (swine) flu?

Spread of H1N1 (swine) flu can occur in two ways:

Through contact with infected pigs or environments contaminated with swine flu viruses.
Through contact with a person with H1N1 (swine) flu. Human-to-human spread of H1N1 (swine) flu has been documented also and is thought to occur in the same way as seasonal flu. Influenza is thought to spread mainly person-to-person through coughing or sneezing of infected people.



How does this new H1N1 virus spread?

Spread of this H1N1 virus is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing by people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.


Are there medicines to treat H1N1 (swine) flu?

Yes. CDC recommends the use of oseltamivir (brand name Tamiflu ®) or zanamivir (brand name Relenza ®) for the treatment and/or prevention of infection with these H1N1 (swine) influenza viruses. Antiviral drugs are prescription medicines (pills, liquid or an inhaler) that fight against the flu by keeping flu viruses from reproducing in your body. If you get sick, antiviral drugs can make your illness milder and make you feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms).


How long can an infected person spread H1N1 (swine) flu to others?

People with H1N1 (swine) influenza virus infection should be considered potentially contagious as long as they are symptomatic and possible for up to 7 days following illness onset. Children, especially younger children, might potentially be contagious for longer periods


What can I do to protect myself from getting sick?

There is no vaccine available right now to protect against H1N1 (swine) flu. There are everyday actions that can help prevent the spread of germs that cause respiratory illnesses like influenza. Take these everyday steps to protect your health:

Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.
Wash your hands often with soap and water, especially after you cough or sneeze. Alcohol-based hand cleaners are also effective.
Avoid touching your eyes, nose or mouth. Germs spread this way.
Try to avoid close contact with sick people.
If you get sick with influenza, CDC recommends that you stay home from work or school and limit contact with others to keep from infecting them.


How can someone with the flu infect someone else?

Infected people may be able to infect others beginning 1 day before symptoms develop and up to 7 or more days after becoming sick. That means that you may be able to pass on the flu to someone else before you know you are sick, as well as while you are sick.


Can people catch H1N1 (swine) flu from eating pork?

No. H1N1 (swine) influenza viruses are not transmitted by food. You can not get H1N1 (swine) influenza from eating pork or pork products. Eating properly handled and cooked pork and pork products is safe. Cooking pork to an internal temperature of 160°F kills the H1N1 (swine) flu virus as it does other bacteria and viruses


Do pigs carry this virus and can I catch this virus from a pig?

At this time, there is no evidence that swine in the United States are infected with this new virus. However, there are flu viruses that commonly cause outbreaks of illness in pigs. Most of the time, these viruses do not infect people, but influenza viruses can spread back and forth between pigs and people.


How long can influenza virus remain viable on objects (such as books and doorknobs)?

Studies have shown that influenza virus can survive on environmental surfaces and can infect a person for up to 2-8 hours after being deposited on the surface.


What surfaces are most likely to be sources of contamination?

Germs can be spread when a person touches something that is contaminated with germs and then touches his or her eyes, nose, or mouth. Droplets from a cough or sneeze of an infected person move through the air. Germs can be spread when a person touches respiratory droplets from another person on a surface like a desk, for example, and then touches their own eyes, mouth or nose before washing their hands.


Is there a risk from drinking water?

Tap water that has been treated by conventional disinfection processes does not likely pose a risk for transmission of influenza viruses. Current drinking water treatment regulations provide a high degree of protection from viruses. No research has been completed on the susceptibility of the novel H1N1 flu virus to conventional drinking water treatment processes. However, recent studies have demonstrated that free chlorine levels typically used in drinking water treatment are adequate to inactivate highly pathogenic H5N1 avian influenza. It is likely that other influenza viruses such as novel H1N1 would also be similarly inactivated by chlorination. To date, there have been no documented human cases of influenza caused by exposure to influenza-contaminated drinking water.


Can the new H1N1 flu virus be spread through water in swimming pools, spas, water parks, interactive fountains, and other treated recreational water venues?

Influenza viruses infect the human upper respiratory tract. There has never been a documented case of influenza virus infection associated with water exposure. Recreational water that has been treated at CDC recommended disinfectant levels does not likely pose a risk for transmission of influenza viruses. No research has been completed on the susceptibility of the H1N1 influenza virus to chlorine and other disinfectants used in swimming pools, spas, water parks, interactive fountains, and other treated recreational venues. However, recent studies have demonstrated that free chlorine levels recommended by CDC (1–3 parts per million [ppm or mg/L] for pools and 2–5 ppm for spas) are adequate to disinfect avian influenza A (H5N1) virus. It is likely that other influenza viruses such as novel H1N1 virus would also be similarly disinfected by chlorine.


Can H1N1 influenza virus be spread at recreational water venues outside of the water?

Yes, recreational water venues are no different than any other group setting. The spread of this novel H1N1 flu is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing of people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.

Tuesday, August 11, 2009

Discussion

You can ask doubts regarding medical field here. Your doubts will be cleared within 1 week.
Genuine doubts will also be given place in this blog
Thanks

Monday, August 10, 2009

Man With Twin Living Inside Him


Sanju Bhagat's stomach was once so swollen he looked nine months pregnant and could barely breathe.Living in the city of Nagpur, India, Bhagat said he'd felt self-conscious his whole life about his big belly. But one night in June 1999, his problem erupted into something much larger than cosmetic worry.

An ambulance rushed the 36-year-old farmer to the hospital. Doctors thought he might have a giant tumor, so they decided to operate and remove the source of the bulge in his belly. "Basically, the tumor was so big that it was pressing on his diaphragm and that's why he was very breathless," said Dr. Ajay Mehta of Tata Memorial Hospital in Mumbai. "Because of the sheer size of the tumor, it makes it difficult [to operate]. We anticipated a lot of problems."

Mehta said that he can usually spot a tumor just after he begins an operation. But while operating on Bhagat, Mehta saw something he had never encountered. As he cut deeper into Bhagat's stomach, gallons of fluid spilled out -- and then something extraordinary happened. "To my surprise and horror, I could shake hands with somebody inside," he said. "It was a bit shocking for me."

Removing the Mutated Body

One doctor recalled that day in the operating room.

"He just put his hand inside and he said there are a lot of bones inside," she said. "First, one limb came out, then another limb came out. Then some part of genitalia, then some part of hair, some limbs, jaws, limbs, hair." Inside Bhagat's stomach was a strange, half-formed creature that had feet and hands that were very developed. Its fingernails were quite long.

"We were horrified. We were confused and amazed," Mehta said.

A Mutated Body Within a Body

At first glance, it may look as if Bhagat had given birth. Actually, Mehta had removed the mutated body of Bhagat's twin brother from his stomach. Bhagat, they discovered, had one of the world's most bizarre medical conditions -- fetus in fetu. It is an extremely rare abnormality that occurs when a fetus gets trapped inside its twin. The trapped fetus can survive as a parasite even past birth by forming an umbilical cordlike structure that leaches its twin's blood supply until it grows so large that it starts to harm the host, at which point doctors usually intervene.

According to Mehta, there are fewer than 90 cases of fetus in fetu recorded in medical literature.

What is deja vu?


The term deja vu is French and means, literally, "already seen." Those who have experienced the feeling describe it as an overwhelming sense of familiarity with something that shouldn't be familiar at all. Say, for example, you are traveling to England for the first time. You are touring a cathedral, and suddenly it seems as if you have been in that very spot before. Or maybe you are having dinner with a group of friends, discussing some current political topic, and you have the feeling that you've already experienced this very thing -- same friends, same dinner, same topic. Ddeja vu occurs most often in young people.

The phenomenon is rather complex, and there are many different theories as to why deja vu happens. Swiss scholar Arthur Funkhouser suggests that there are several "deja experiences" and asserts that in order to better study the phenomenon, the nuances between the experiences need to be noted. In the examples mentioned above, Funkhouser would describe the first incidence as deja visite ("already visited") and the second as deja vecu ("already experienced or lived through"). As much as 70 percent of the population reports having experienced some form of deja vu. A higher number of incidents occurs in people 15 to 25 years old than in any other age group. Deja vu has been firmly associated with temporal lobe epilepsy. Reportedly, deja vu can occur just prior to a temporal-lobe seizure. People suffering a seizure of this kind can experience deja vu during the actual seizure activity or in the moments between convulsions.

Since deja vu occurs in individuals with and without a medical condition, there is much speculation as to how and why this phenomenon happens. Several psychoanalysts attribute deja vu to simple fantasy or wish fulfillment, while some psychiatrists ascribe it to a mismatching in the brain that causes the brain to mistake the present for the past. Many parapsychologists believe it is related to a past-life experience. Obviously, there is more investigation to be done

Man with tiny brain


A man with an unusually tiny brain manages to live an entirely normal life despite his condition, which was caused by a fluid build-up in his skull. Scans of the 44-year-old man's brain showed that a huge fluid-filled chamber called a ventricle took up most of the room in his skull, leaving little more than a thin sheet of actual brain tissue (see image, right).

"It is hard for me [to say] exactly the percentage of reduction of the brain, since we did not use software to measure its volume. But visually, it is more than a 50% to 75% reduction," says Lionel Feuillet, a neurologist at the Mediterranean University in Marseille, France. Feuillet and his colleagues describe the case of this patient in The Lancet. He is a married father of two children, and works as a civil servant.

Not retarded

The man went to a hospital after he had mild weakness in his left leg. When Feuillet's staff took his medical history, they learned that, as an infant, he had had a shunt inserted into his head to drain away hydrocephalus - water on the brain. The shunt was removed when he was 14. But the researchers decided to check the condition of his brain using computed tomography (CT) scanning technology and another type of scan called magnetic resonance imaging (MRI). They were astonished to see "massive enlargement" of the lateral ventricles - usually tiny chambers that hold the cerebrospinal fluid that cushions the brain. Intelligence tests showed the man had an IQ of 75, below the average score of 100 but not considered mentally retarded or disabled. "The whole brain was reduced - frontal, parietal, temporal and occipital lobes - on both left and right sides. These regions control motion, sensibility, language, vision, audition, and emotional and cognitive functions," Feuillet told New Scientist.

Brain adaptation

The findings reveal "the brain is very plastic and can adapt to some brain damage occurring in the pre- and postnatal period when treated appropriately," he says. "What I find amazing to this day is how the brain can deal with something which you think should not be compatible with life," comments Max Muenke, a paediatric brain defect specialist at the National Human Genome Research Institute in Bethesda, Maryland, US. "If something happens very slowly over quite some time, maybe over decades, the different parts of the brain take up functions that would normally be done by the part that is pushed to the side," adds Muenke, who was not involved in the case.

Friday, August 7, 2009

The Deadliest Snakes in the World











1) Fierce Snake or Inland Taipan (Oxyuranus microlepidotus ), Australia.
The most toxic venom of any snake. Maximum yield recorded (for one bite) is 110mg. That would porbably be enough to kill over 100 people or 250,000 mice. It is 750 times more poisonous than common cobra. The Fierce Snake is native to the arid regions of central Australia.Fierce Snakes are known to live in holes, and feed on small rodents such as mice and rats. Despite its name, Fierce Snakes are not known to be particularly aggressive, but docile. They will strike if provoked, however, injecting their incomparably toxic venom.No fatalities have been attributed to this species, and all known bites have been to people who keep them in captivity or actively seek them out in the wild.

















(2) Australian Brown Snake (Pseudonaja textilis ), Australia.
One 1/14,000 of an ounce of this vemon is enough to kill a person. It is the world's second most poisonous land snake mostly found in Australia. and may also be found on the peninsulas of Papua New Guinea and Indonesia. They are very fast moving and highly aggressive. When agitated, they will hold their necks high, appearing in a somewhat upright S-shape. The snake will occasionally chase an aggressor and strike at it repeatedly.















(3) Malayan or Blue Krait (Bungarus candidus ), Southeast Asia and Indonesia.
50% of the bites from this snake are fatal even with the use of antivenin treatment. Kraits are ophiophagous, preying primarily upon other snakes (including venomous varieties) and are cannibalistic, feeding on other kraits. They will also eat small lizards.
All kraits are nocturnal. The snake is more docile during the daylight hours, becoming more aggressive during the night. However, they are rather timid and will often hide their heads within their coiled bodies for protection. When in this posture, they will sometimes whip their tail around as a type of distraction.

















4) Taipan (Oxyuranus scutellatus ), Australia.
The venom delivered in a single Taipan bite is enough to kill up to 12,000 guinea pigs. The common taipan is the third-most venomous snake on Earth and arguably the second-largest venomous snake in Australia















5) Tiger Snake (Notechis scutatus ), Australia.
All Notechis species have a very potent neurotoxic venom, which may cause neurotoxic, hemolytic, coagulopathic, and myolytic reactions; paralysis or death can ensue in as short as 30 minutes, but if it occurs it is usually on the timespan of 6-24 hours after the bite. Prior to the development of specific antivenom, Tiger Snake bite fatalities probably approached 60-70% in cases of severe bites. Specific antivenoms are available for the treatment of tiger snake bites. Fortunately the snake will generally flee if intruded upon, but will become aggressive if cornered.













6) Beaked Sea Snake (Enhydrina schistosa )
This is a species of sea snake.It is found in the Arabian Sea and Persian Gulf (off Oman), south of the Seychelles and Madagascar, the seas off South Asia (Pakistan, India and Bangladesh), Southeast Asia (Myanmar (formerly Burma), Thailand, Vietnam), and Australia (Northern Territory and Queensland) and New Guinea.
Found in mangrove swamps.






















7) Saw Scaled Viper (Echis carinatus ), Middle East Asia.
Echis carinatus is a venomous viper species found in parts of the Middle East and Central Asia, and especially the Indian subcontinent. It is the smallest of the Big Four dangerous snakes of India. Five subspecies are currently recognized, including the typical form described here.
This species is mostly crepuscular and nocturnal, although there have been reports of activity during daylight hours. During they daytime they hide in all kinds of places, such as deep mammal burrows, rock fissures an fallen rotted logs. In sandy environments, they may bury themselves leaving only the head exposed. Often, they are most active after rains or on humid nights.
When alarmed, they put on a distinctive threat display.

They move about mainly sidewinding: a method at which they are considerably proficient and alarmingly quick. They are also capable of other forms of locomotion, but sidewinding seems to be best suited to moving about in their usual sandy habitats. It may also keep them from overheating too quickly, as they leave only two points of contact with the hot surface.
This species is often found climbing in bushes and shrubs, sometimes as much as 2 m above the ground. When it rains, up to 80% of the adult population will climb into bushes and trees. Once, it was observed how some 20 individuals had massed on top of a single cactus or small shrub.






















8 ) Coral Snake (Micrurus fulvius ), North America.


The coral snakes are a large group of elapid snakes that can be divided into two distinct groups, New World coral snakes and Old World coral snakes. There are three genera among New World coral snakes that consist of over 65 recognized species.
Coral snakes vary widely in their behavior, but most are very secretive, fossorial snakes which spend the vast majority of their time buried in the ground or in leaf litter of a rainforest floor, only coming to the surface during rains or during breeding season. Some species, like Micrurus surinamensis are almost entirely aquatic and spend most of their lives in slow moving bodies of water that have dense vegetation.
Like all elapid snakes, coral snakes use a pair of small fangs, which are fixed in the front of their top jaw, to deliver their venom. Due to the time it takes for the venom take effect, coral snakes have a tendency to hold on to a victim when biting, unlike vipers which have retractable fangs and tend to prefer to strike and let go immediately. Coral snakes are not aggressive or prone to biting however, and account for less than a single percent of the number of snake bites each year in the United States. Most coral snake bites occur because of accidental handling of the snake while engaged in an activity like gardening.
Due to the small size of coral snakes, along with their having much smaller fangs than pit vipers, bites are frequently ineffective and have some difficulty penetrating shoes or even thick clothing. This along with the fact that coral snakes are quite shy and reclusive makes bites quite rare. However, coral snakes are highly venomous, being the only relative of the cobra found in the New World. Despite their relatively small size, their venom is a powerful neurotoxin, quite capable of killing an adult human. Any bite from a coral snake should be considered life threatening and immediate treatment should be sought. Often there is very little reaction around the bite area, as opposed to the pain and swelling usually associated with a viper bite, and systemic effects can delay manifestation for 8-24 hours. This potential delay in symptoms makes treating coral snake bites particularly tricky, and often results in preventative treatment whether one is displaying symptoms or not. Once the neurotoxin takes effect, it causes the neurotransmitters between the brain and muscles to malfunction. Initially symptoms are slurred speech, double vision, difficulty swallowing, but can quickly progress to muscular paralysis, and even respiratory or cardiac failure if not treated.



















9) Boomslang (Dispholidus typus ), Africa.
A boomslang, Dispholidus typus is a large, venomous colubrid snake native to sub-Saharan Africa. It is the only species in its genus. Its name means “tree snake” in Afrikaans and Dutch.Boomslangs are largely arboreal, are very fast moving, and are oviparous. Their diet includes chameleons and other arboreal lizards, frogs, and occasionally small mammals, birds and eggs from nesting birds, which they swallow whole.
Most members of the colubrid family are harmless, or have relatively weak venom, but the boomslang is an exception. It has a highly potent venom which it delivers through large, deeply grooved fangs that are (like in most other venomous colubrids) located in the rear of the jaw. This type of venomous apparatus is called opisthoglypha. The boomslang is the most dangerous of the snakes with this method of venom delivery, due to its relatively large fangs and its relatively anterior position of the fangs compared to other opisthoglyphic taxa. The bite of the boomslang can be fatal, and has been reported to be not unlike bites from vipers. In 1957, well known herpetologist, Karl Schmidt died after being bitten by a boomslang. D.S. Chapman states that between 1919 and 1962 there were eight serious human envenomations by boomslangs, two of which were fatal. The South African Vaccine Producers (formerly South African Institute of Medical Research) manufactures a monovalent antivenom for boomslang venom. The venom of the boomslang is primarily a hemotoxin. This means that the venom attacks and destroys the hemoglobin in the red blood cells, destroying the blood in its victim. The venom of a boomslang disables blood clotting process and the victim often dies out of numerous internal and external bleedings. Other symptoms include: headache, nausea, sleepiness and mental disorders. Being a relatively slow-acting venom, the symptoms may occur many hours after the bite. On one hand, this provides time for arranging the serum, while on the other hand it may lead victims to underestimate the bite (especially when, as with other snakes, not every bite injects venom).
An adult snake has 4-8 mg of venom. 5 mg is said to be enough to kill a man.
The boomslang is a timid snake, and bites generally occur only while attempting to handle, catch or kill the snake.













10) Death Adder (Acanthopis antarcticus ), Australia and New Guinea.
Death adders are very viper-like in appearance, having triangular shaped heads and small subocular scales. They also have vertical pupils and many small scales on the top of the head. Like vipers, they have short, fat bodies (normally 50 – 90 cm (20 – 36 inches) long). Their fangs are also longer and more mobile than for most other elapids, although still far from the size seen in some of the true vipers. Despite their name and appearance, they are not vipers at all, but elapids (like all Australian venomous snakes). This is a case of convergent evolution.
It normally takes 2 – 3 years to reach adult size. Females are generally slightly larger than the males. They can also be easily distinguished from other Australian snakes because of a short spine protruding from their tails. Most have large bands around their bodies, though the color itself is variable. Colors are usually grey or red, but also include brown, greenish-grey, or yellow.
Death adders inject on average 40 – 100 mg of extremely toxic venom (0.4 – 0.5 mg/kg murine LD50, subcutaneous) with a bite. This makes an untreated death adder bite one of the most dangerous in the world (rated in top 10 in the CSL list).
Death adder venom is highly neurotoxic. It blocks the post-synaptic neuromuscular transmission from the acetylcholine receptor. Unlike other snakes of its type, it does not contain either procoagulants or myolysins, making treatment easier.
A bite from a death adder causes paralysis. While this paralysis is very minor at first, it can cause death from a complete respiratory shutdown in as little as six hours. Symptoms peak in 24 – 48 hours.
Symptoms of envenomation can be reversed through the use of death adder antivenom, or using anticholinesterases, which break the synaptic blockade by making acetylcholine more available to the brain.
Before antivenom was introduced, 50% of death adder bites were fatal. Now, with the antivenom, and due to the slow progression of envenomation symptoms, fatalities from death adder bites are very rare in Australia. In New Guinea, deaths from these snakes are still common.

Monday, August 3, 2009

Rabies - Hydrophobia

Rabies is caused by a bite from an infected animal but occasionally by other forms of contact. In some countries it is a significant killer of livestock. The rabies virus makes its way to the brain by following the peripheral nerves.

RABIES OR hydrophobia is a viral neuroinvasive disease that causes acute encephalitis (inflammation of the brain) in warm-blooded animals. It is zoonotic (ie transmitted by animals), most commonly by a bite from an infected animal but occasionally by other forms of contact. It is fatal if left untreated. In some countries it is a significant killer of livestock.

The rabies virus makes its way to the brain by following the peripheral nerves. The incubation period of the disease depends on how far the virus must travel to reach the central nervous system, usually taking a few months. Once the infection reaches the central nervous system and symptoms begin to show, the untreated infection is usually fatal within days. In the beginning stages of rabies, the symptoms are malaise, headache and fever, while in later stages it includes acute pain, violent movements, uncontrolled excitements, depressions and the inability to swallow water (hence the name hydrophobia).


In the final stages, the patient begins to have periods of mania and lethargy, and coma. Death generally occurs due to respiratory insufficiency. The term is derived from the Latin rabies, "madness." This, in turn, may have come from the Sanskrit rabhas, "to do violence.

The Greeks derived the word "lyssa," which is derived from "lud" or "violent," this terminology is used in the name of the genus of rabies lyssavirus. The rabies virus is the type species of the Lyssavirus genus, which encompasses other similar viruses.

Lyssa-viruses have helical symmetry, with a length of about 180nm and a cross-sectional diameter of about 75nm. These viruses are enveloped and have a single stranded RNA genome with negative-sense. The genetic information is packaged as a ribonucleoprotein complex, in which RNA is tightly bound by the viral nucleoprotein.

The RNA genome of the virus encodes five genes whose order is highly conserved. These genes are nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G) and the viral RNA polymerase (L). From the point of entry, the virus travels quickly along the neural pathways into the central nervous system (CNS) and then further into other organs. The salivary glands receive high concentrations of the virus thus allowing further transmission.

The Museum of Human Brains



Diana Rivas says it only takes her a few seconds to look at a brain to know what afflicted its owner.

"This one belonged to an alcoholic...This one belonged to somebody who had Alzheimer's disease," Rivas said as she passes row after row of brains suspended in preserving liquid and stacked on shelves in a tiny room in central Lima.

Rivas is a neuropathologist who runs a little-known brain museum in the Peruvian capital. She claims it is the only public display of human brains in the world.

The museum has an inventory of 2,998 specimens and is still growing. Rivas studies neurological diseases and psychiatric disorders but, unlike prestigious brain banks around the world, she also lets

the public in to wander around.

It is not a tour for the queasy. On display in one room are several human fetuses with neurological disorders. Another exhibit shows a brain afflicted by the human form of mad cow disease which is known as variant Creutzfeldt-Jakob disease.

About 4,000 people, most of them children from local schools, paid the 30 cents entrance fee to trundle past Rivas' brains last year.

Foreign doctors from Germany, Japan and France also visited the museum which sits at the end of a decrepit street where many taxis fear to go.

The museum started collecting samples of diseased brains in 1942. Rivas said she works with researchers on the effects of cysticercosis, an infection caused by pork tapeworm, on the human brain.

But her primary goal is to educate the public.

"The main purpose is for people to see what brain sicknesses look like, and realize that many of them can be healed or prevented," she said showing how a healthy brain differs from one that has been damaged by drug abuse.

"Its true. Alcohol and drugs kill brain cells."

The museum is tucked in behind a 300-year-old building that is now the National Neurological Science Institute hospital. It operates on a shoe-string budget.The "museum" brain ", as is known, was inaugurated on August 26, 1997 by the then head of the Department of Neuropathology, Luis Palomino, who was collecting the cuttings from the brain autopsy on their first service in 1942.