As parents, we set our children up for life’s challenges by feeding them, caring for their health, and sending them to school. Many animals also provide for their young, and some do it in inadvertent and surprising ways. Take the red squirrel. The first year of this cute creature’s life is marked by intense competition and imminent death. Its goal is simple: get a territory before winter sets in, or face death by starvation. That goal becomes tougher if there are lots of other competitors around, but a mother squirrel has ways of preparing her pups for these trials. If she hears the sounds of crowded forest, stress hormones surge through her body and begin affecting her pups even before they are born. When they finally pop into the world, they start growing faster. The hormones are a chemical message from mum: Live fast, so you don’t die young.

Red squirrels have a diverse diet, but the seeds of the white spruce are among the most important items on their menu. These trees are “mast seeders” meaning that they all produce tons of seeds every 2 to 6 years and very few seeds in others. In the bonanza years, the squirrels have plenty of spruce seeds to bury in the autumn and snack on through the harsh winter. This means that a bumper autumn for spruce is always followed by a crowded spring for squirrels. That leads to conflict. Red squirrels defend large areas surrounding a central store of spruce cones. They’ll fight for this real estate, because if the youngsters don’t establish a territory before winter sets in, they’ll find themselves bereft of buried grains, and almost certainly die. A team of Canadian scientists has been studying the fates of red squirrels in the Yukon, Canada for the last 22 years. Back in 2006, they showed that the squirrels can actually anticipate gluts of spruce seeds, and produce more young in anticipation. Now, the same team have found that females can also adjust how quickly their young grow up depending on how much competition they will face.

The team, led by Ben Dantzer, now at the University of Cambridge, found that in competitive years following a spruce bonanza, the fastest-growing squirrels fare best and are more likely to survive their first winter. In normal years, these fast-growers have no advantage. This explains why the mothers don’t always give birth to fast-growing young. It comes at a price—squirrels tend to have shorter lifespans if they are born in crowded years, so their early spurt seems to cost them later on in life. It’s a cost that’s only worth paying if there’s some advantage to be gained. To test this link between density and growth, Dantzer’s team carried out a wonderfully simple but beautiful experiment where they simulated the sounds of a crowd. They recorded the loud “rattles” that squirrels make to defend their territories, and played them back to the creatures at two levels—one representing six times more squirrels than the other. If the females heard what sounded like squirrel-infested woods, they gave birth to pups that grew much faster.

How? The answer lies in the mothers’ hormones. The more crowded an area is, the higher the levels of cortisol - a stress hormone - in the squirrels’ bodies. Indeed, if Dantzer’s team created more crowded forests - either genuinely so by feeding the squirrels and boosting their numbers, or dishonestly so by playing the rattle recordings - the females’ cortisol levels went up. Mums with higher cortisol levels gave birth to pups that grew faster. This wasn’t just a correlation. The team also injected some females with extra cortisol, and saw that their offspring grew up 41 percent faster.

Why? This part of the story is less clear. We know from other studies that and early dose of stress hormones can steer the development of young animals, affecting their ability to learn or handle stressful situations. Think of the hormones as an fortune-telling system, plugged into the mother’s senses. It provides the young squirrel with omens of the conditions it will face in the outside world, and prepares its brain and body to deal with those challenges.

Papillomaviruses are a very diverse group of viruses that infect human skin and mucosal cells, which serve as a barrier between the environment and a human being. Most representatives of this group do not cause any symptoms, but highly pathogenic types may cause cancer. Ancient literature contains the first known mention of skin warts. The first classification of warts was introduced by Roman physician Aulus Cornelius Celsus in 25 AD, and the assumption that warts may be transmitted via infection originated even earlier. However, the viral nature of papillomas was not demonstrated until the beginning of the twentieth century (reviewed in 4). The first papillomavirus was isolated in 1933 by the American virologist Richard Shope, who also isolated an influenza virus.

The evolutionary history of papillomaviruses seems to coincide with the origin of higher-order vertebrates, amniotes (including reptiles, birds, and mammals). Mammalian skin structure appears to make them the most suitable hosts for the papillomaviruses, and — today — papillomaviruses are widespread in mammals and rarely found in birds. The relationship between papillomaviruses and similar groups of DNA-viruses, such as polyomaviruses, is not well-demonstrated at the present time. There are more than a hundred types of papillomaviruseshigh-risk that can infect humans. These are collectively referred to as human papilloma viruses or HPV and are divided into (HR) and low-risk (LR) types by their carcinogenic properties. HPV are transmitted through direct skin-to-skin contact, and approximately 30 types are transmitted sexually. LR HPV are much more common than HR HPV among humans and often do not cause any symptoms. In fact, only 18 types of HPV pose a cancer risk, mostly for anogenital cancers.

Current research suggests that LR HPVs produce more virions and infect more human hosts whereas HR types are less virulent but more difficult for the immune system to neutralize. The most dangerous HR HPV types are also the most widespread, HPV16 (reference strain) and HPV18, and the main cause of skin warts (especially in the anogenital zone) are HPV types 6 and 11. These and several other types of HPV attract serious attention.

Human papilloma virus particles lack a lipid envelope and are relatively small, with a diameter of only about 30 nm. In comparison, the human immunodeficiency virus (HIV) and influenza virus virions are enveloped by a lipid bilayer derived from the host cell and are approximately four times larger. The papillomavirus genome consists of double-stranded DNA decorated and packed by histones of the host cell. It encodes two types of proteins, early (E) proteins and late (L) proteins: early HPV proteins maintain regulatory functions (and are responsible for oncotransformation of the host cell in the case of HR types), and late proteins form the capsid of the virion. The life cycle of HPV is bound to the life cycle of its host cells, keratinocytes, and HPV can only be cultivated in special organotypic raft cultures containing a population of cells at different developmental stages — similar to the skin of a living organism. Keratinocytes are the main cells of epidermis, the outermost layer of the skin. Actively dividing young keratinocytes are found near the basal membrane that separates the epidermis from other layers of the skin and move towards the skin surface during maturation. Viral particles infect non-differentiated cells, and new virions are produced inside the keratinocytes during the terminal stage of differentiation.

The HPV early proteins are responsible for maintaining a proper amount of viral DNA inside the host cell nucleus. However, they also coordinate the expression of viral genes. Proteins E1 and E2 form a complex with viral DNA, which recruits the cell replication systems. Proteins E6 and E7 are responsible for the carcinogenic effect in HR HPV types. E6 is able to bind to the tumor suppressor p53 and promote its ubiquitination and degradation. Protein E7 binds several cell proteins and tumor suppressors, including theretinoblastoma protein. The activity of the E6 and E7 proteins leads to uncontrolled cell division.

Late proteins of HPV form the viral capsid and mediate packaging of DNA into the virion. The pentamer-forming L1 protein is the major component of the HPV capsid, and the L2 protein is a minor constituent. The HPV capsid looks roughly spherical, but, in fact, it has a icosahedral symmetry with the triangulation number that equals 7. Rather than a structure based on pentamers mixed with hexamers (like that of the soccer ball), the HPV capsid is composed of 72 L1 pentamers of two different types — 60 hexavalent pentamers and 12 pentavalent pentamers (reviewed in 2, chapter 3). Remarkably, the fold of HPV L1 proteins is similar to that of human nucleoplasmins, the proteins that regulate the assembly of nucleosomes. Whether they share a common ancestor or whether their similarity is the result of convergent evolution is not yet clear. Perhaps the interaction between L1 and nucleosomes on viral DNA is crucial for the encapsidation of the HPV genetic material.

One monomer of L2 is associated with each L1 pentamer of the HPV virion, and current research suggests that L2 is crucial for DNA recruitment to the viral particle. Some hypothesize that L2 — as well as L1 — may interact not with viral DNA but rather with its histones. To date, however, much of the process through which HPV DNA is packed inside the virion remains unknown. One facet of the process that is known may make HPV an important tool in human gene therapy: any segment of DNA less than 8 kb long may be packed inside the capsid [link], which enables the development and use of HPV-based transformation vectors. Interestingly, human cyclophilin participates in HPV capsid unpacking, a mechanism that has also been demonstrated for HIV.

A growing interest in HPV research can be partially — if not wholly — attributed to discovery of the relationship between HPV and cancer and the subsequent Nobel Prize in Physiology or Medicine (2008) awarded for this work. German scientist Harald zur Hausen has shown that nearly all cases of cervical cancer are the result of HPV infection. Vaccines against HPV are currently being actively developed and introduced, and the main targets for such vaccines include the most dangerous and common HPV types: HPV6, HPV11, HPV16, HPV18.

Dr. Christopher Buck from the U.S. National Cancer Institute: Current vaccines against human papillomaviruses (HPVs) are a triumph of applied structural virology. However, the current vaccines, which use recombinant virus-like particles composed of the L1 major capsid protein, do not protect against all disease-causing HPV types. Fortunately, a new generation of HPV vaccines targeting conserved „Achilles’ heel“ epitopes present in the L2 minor capsid protein promise to offer broad protection against all HPVs, including all types that cause cancer, as well as types that cause benign skin warts (for which the papillomavirus family is named). Current knowledge about the structure, dynamics, and function of L2 during the infectious entry process is very limited. This structural information is desperately needed to inform the development of pan-protective HPV vaccines.

Urea is a by-product of protein metabolism by the liver, and is therefore removed from the blood by the kidneys. Urea freely filters through the glomerulous, but is reabsorbed by the renal tubules in a flow-dependent fashion. The higher the flow rate, the greater amount of urea nitrogen is cleared from circulation and eliminated through the kidneys. As a result, the level of circulating urea nitrogen, along with serum creatinine, serves as a primary measure of kidney function. Normal adult Blood Urea Nitrogen (BUN) levels should be between 7 and 21 mg urea nitrogen per 100 mL blood (mg/dL). Azotemia, poor kidney function, will cause elevated BUN levels (≥ 50 mg/dL) and is associated with acute kidney failure or injury, severe acute pancreatitis, congestive heart failure or gastrointestinal bleeding. Azotemia also can occur with dehydration, as a result of alcohol abuse, or high protein diets. Lower than expected BUN levels are usually not clinically predictive, but are primarily associated with liver disease or malnutrition, including malabsorption and low protein diets. Urine and saliva are considered to be acceptable non-invasive samples for measurement of urea nitrogen.

The DetectX® Urea Nitrogen (also called BUN) Detection Kit is designed to quantitatively measure urea nitrogen in a variety of samples. Please read the complete kit insert before performing this assay. A urea nitrogen standard calibrated to NIST reference materials is provided to generate a standard curve for the assay and all samples should be read off the standard curve. Samples are mixed with Color Reagents A and B and incubated at room temperature for 30 minutes. The colored product is read at 450 nm. The concentration of urea nitrogen in the sample is calculated, after making a suitable correction for any dilution, using software available with most plate readers. The results are expressed in terms of mg/dL urea nitrogen. If samples are to be expressed in terms of mg/dL urea, the data can be converted using the multiplier.

Please read this insert completely prior to using the product.

FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC PROCEDURES.

Corticosterone (C₂₁H₃₀O₄, Kendall’s Compound ‘B’) is a glucocorticoid secreted by the cortex of the adrenal gland. Corticosterone is produced in response to stimulation of the adrenal cortex by ACTH and is the precursor of aldosterone. Corticosterone is a major indicator of stress and is the major stress steroid produced in non-human mammals. Studies involving corticosterone and levels of stress include impairment of long term memory retrieval, chronic corticosterone elevation due to dietary restrictions and in response to burn injuries. In addition to stress levels, corticosterone is believed to play a decisive role in sleep-wake patterns.

Assay Principle

The DetectX® Corticosterone Immunoassay kit is designed to quantitatively measure Corticosterone present in serum, plasma, urine, extracted dried fecal samples, and tissue culture media samples. Please read the complete kit insert before performing this assay. This kit measures total corticosterone in serum and plasma and in extracted fecal samples.
A corticosterone stock solution is provided to generate a standard curve for the assay and all samples should be read off the standard curve. We provide protocols on page 8 to prepare assay standards from 5,000 to 78.125 pg/mL or from 10,000 to 78.125 pg/mL. Please choose the standard range that fits your sample concentrations most appropriately.
Standards or diluted samples are pipetted into a clear microtiter plate coated with an antibody to capture sheep antibodies. A corticosterone-peroxidase conjugate is added to the standards and samples in the wells. The binding reaction is initiated by the addition of a polyclonal antibody to corticosterone to each well. After an hour incubation the plate is washed and substrate is added. The substrate reacts with the bound corticosterone-peroxidase conjugate. After a short incubation, the reaction is stopped and the intensity of the generated color is detected in a microtiter plate reader capable of measuring 450nm wavelength. The concentration of the corticosterone in the sample is calculated, after making suitable correction for the dilution of the sample, using software available with most plate readers.

Please read this insert completely prior to using the product

FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC PROCEDURES.

Order : K014-H1 / K014-H5

Frank and Louie the cat, 12, was born with two faces, two mouths, two noses, three eyes , setting the world record for the Oldest living two-faced cat, according to World Record Academy

The Guinness world record for the Longest surviving Janus cat was also set by Frank and Louie, from Millbury, Ohio, USA, which had reached six years of age, thereby outliving all other recorded specimens.

Guinness World Records also recognized the world record for the oldest cat living, set by Pinky, who was born on 31 October 1989 and lives with her owner, Linda Anno (USA), Hoyt, Kansas, USA.

Now, 12 years after Marty Stevens rescued him from being euthanized because of his condition, the exotic blue-eyed rag doll cat is not only thriving, but has also made it into the 2012 edition of Guinness World Records as the longest-surviving member of a group known as Janus cats, named for a Roman god with two faces. 
  
"Every day is kind of a blessing; being 12 and normal life expectancy when they have this condition is one to four days," Stevens said, stroking Frank and Louie's soft fur as he sat on her lap purring. 

"So, he's ahead of the game; every day I just thank God I still have him."

"The condition itself is very rare, and I think that the fact that this cat became an adult, a healthy adult, is remarkable," said Dr. Armelle deLaforcade, an associate professor at Cummings and head of the emergency services section.

Frank and Louie's two faces have a complicated relationship. Both noses work, but one mouth does not have a lower jaw and isn't connected to his one esophagus, so he can't eat with it. Stevens discovered that only after the cat got an MRI later in life.

The animal can see out of only two of his three eyes. The middle one can't even blink and makes Frank and Louie appear to be staring even when his other eyes are closed. 

Frank and Louie does not seem to be bothered by his condition and has developed a friendly personality. The breed is known for its soft and silky fur, docile temperament and penchant for relaxing in a person's arms like a rag doll. 

He is "very, very laid back, not afraid of people, very friendly and he's actually more of a dog than a cat," Stevens said. "He walks on a leash, he goes right in the car; he loves car rides."

The original hedgehog gene was discovered using fruit flies. Rather than the usual smooth cuticle they should have had, the fruit fly embryos defective for hedgehog had spiky bristles - earning the gene its name. The search for corresponding genes (or homologues) in vertebrates revealed 3: Indian Hedgehog (IHH), Desert Hedgehog (DHH) and Sonic Hedgehog (SHH), named for the Sega character. These genes all encode signalling proteins, which bear the same names, and of these 3 sonic hedgehog is the most researched and best understood. 

So what does SHH do? It has key roles in embryonic development, affecting limb and organ creation. The shh protein guides cell growth, cell differentiation and the "patterning" of the embryo. It is also extremely important in creating the facial geometry. Different concentrations of shh in different parts of the embryo guide formation of different cells.

Sometimes the best way to understand what something does is to look at what happens when it's not working. Many defects are associated with mutations to SHH: we've already discussed how it can cause a type of holoprosencephaly (where the forebrain does not split into two hemispheres). Cyclopia accompanies severe holoprosencephaly: like the forebrain, the eyes start out as one and are split into two by shh. Some mutations leave one large eye; others create the two eyes but leave them together in a single middle socket.

The effects on organ development can be seen in mice with both copies of SHH disabled (see image). Their hearts, lungs, kidneys and guts are malformed. The face does not have its usual shape and instead forms a strange trunk, absent of eyes, ears or mouth. They have no paws and are always stillborn.

As hinted at with eye development, shh is key in creating the symmetry of the face. It controls the growth of the what will become the jaws and features. Shh has a lot of control over the width of the face; creatures with too much shh develop very wide faces. Increase the amount of shh even more and the face starts doubling, resulting in a condition known as diprosopus - "two faced". The organism can have two distorted faces, typically united by an eye in the middle.

Read more of the pathogenesis of holoprosencephaly 

In this world of Photoshop and online scams, it pays to have a hearty dose of skepticism at reports of something strange — including an albino fetal shark with one eye smack in the middle of its nose like a Cyclops.

But the Cyclops shark, sliced from the belly of a pregnant mama dusky shark caught by a commercial fisherman in the Gulf of California earlier this summer, is by all reports the real thing. Shark researchers have examined the preserved creature and found that its single eye is made of functional optical tissue, they said last week. It's unlikely, however, that the malformed creature would have survived outside the womb.

"This is extremely rare," shark expert Felipe Galvan Magana of Mexico's Centro Interdisciplinario de Ciencias del Mar told the Pisces Fleet Sportfishing blog in July. "As far as I know, less than 50 examples of an abnormality like this have been recorded." 

Pisces Fleet, a sportfishing company, rocketed the Cyclops shark to viral status online this summer with their photos of the creepy-cute creature. But this isn't the first time that reports of a mythical-seeming creature have spurred media sensations — last week alone, Russian officials announced "proof" of a Yeti, and paleontologists spun a theory about an ancient Kraken-like squid. Few reports of mythical beasts, however, come with proof.

Cyclops shark

Cyclops shark is an exception. While rare, "cyclopia" is a real developmental anomaly in which only one eye develops. Human fetuses are sometimes affected, as in a 1982 case in Israel reported in 1985 in the British Journal of Ophthalmology. In that case, a baby girl was born seven weeks early with no nose and only one eye in the center of her face. The infant, who lived only 30 minutes after birth, also had severe brain abnormalities.

In 2006, a kitten born with one eye and no nose (a rare condition called holoprosencephaly), created a stir online as news organizations and bloggers tried to determine if the bizarre photos of the animal were real. A veterinarian confirmed the kitten's condition; "Cy," as the cat was known, lived only a day. The remains were sold to the creationist Lost World Museum.

The fisherman who discovered the Cyclops shark is reportedly hanging on to the preserved remains, news outlets reported. But scientists have recently examined and X-rayed the fish, authenticating the catch. According to Seth Romans, a spokesman for Pisces Fleet, Galvan Magana and his colleagues will publish a scientific paper about the find within the next several weeks.

Romans told LiveScience that the fisherman who caught the strange shark is "amazed and fascinated" by the attention his catch has drawn.

It's not the first strange shark fetus Galvan Magana has found; he and his colleagues discovered two-headed shark embryos in two different female blue sharks. It's possible that one embryo started to split into twins, but failed to completely separate because of crowding in the womb, the researchers reported in January 2011 in the journal Marine Biodiversity Records.

DNA is known to scientists for more than one hundred years. Swiss biologist Friedrich Miescher and chemist (doctor of education) identify it first in 1868 in the blood-soaked bandages and swabs of bandages for wounded soldiers in Tübingen, and later, after 1870 in Basel - the sperm of salmon of which the first isolate pure DNA. He called the discovery of the substance nuklein and in 1874 managed to break nucleic of protein and acid acid in 1889 was named by his student Richard Altman "nucleic". DNA is recognized as the only carrier of heredity in 1944 as a result of an experiment made ​​by Oswald Avery and his colleagues Colin McCarthy MakLoyd and MacLynn. The structure of the DNA double helix was discovered in 1953 by James Watson and Francis Crick at Cambridge University. For this discovery they received the Nobel Prize in Physiology or Medicine with Maurice Wilkins in whose lab made ​​X-ray crystallographic analysis of DNA, suggested to Watson and Crick's idea of ​​its structure.

The biggest breakthrough in understanding the genetics of cancer before. So Iyls Ross, professor of cancer genetics at the Institute of Cancer Research in London, described the results of an international effort of more than 1,000 scientists, presented in late Wednesday.

Their study - the largest ever study of "faults" of DNA that promote the development of cancer - revealed a series of genetic markers with which can identify people most likely to develop these conditions. In this case for three of the most encountered its forms - prostate, breast and ovarian.

According to London's "Guardian" doctors have said that they can in five years with a simple saliva test based markers make for each risk profile and create a foundation for individual monitoring. For people with an increased risk of developing cancer would go more often reviewing and possibly developing cancer will be detected at an early stage, when there is a much greater chance of prolonging life.

Test based on genetic markers can identify men who are 50% likely to become ill from prostate cancer. This would not only allow the UK have called for a national program. screening of men, it will stop the practice because of inaccurate blood tests a quarter of people with this diagnosis are treated, there was no need.

To identify genetic markers for prostate cancer, the researchers compared the DNA data of 25,000 patients with the disease with the same number of healthy men. So were discovered 23 new "defect" in the DNA, increasing the risk of disease, 16 were identified as "culprits" to reach the most aggressive form. In practice, few men wear markers for prostate cancer, but 1% of them have DNA "defects" that increase the risk of developing it 5 times.

The same procedure has found 49 new DNA "defect" associated with the risk of developing breast cancer.

The third part of the project included the 130 institutes worldwide to compare DNA profiles of women with ovarian cancer with this healthy. This established eight new sections of DNA associated with increased risk of disease.

Professor Iyls believe that a simple test in the GP's office soon enough every patient to have a personal account of the risk of these diseases. Physicians can improve performance by adding factors of lifestyle specific person - the risk of breast cancer, for example, alcohol increases and decreases from birth and breastfeeding.

The big problem started after that - experts disagree on what age should these tests, complement it with ultrasound, magnetic rezonas and biopsies and what kind therapy to apply.

The result of the research was published in Nature Genetics and several other scientific journals.

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