A powerful mixture of antibodies fighting against the AIDS virus attack pulls strong form of the virus in monkeys and then " hold off " weeks , Reuters reported , citing a research team of the U.S. government , led by researchers at Harvard University . Experts have presented findings from two studies in this direction in the journal " Nature "

Researchers found that the rare antibodies produced by 10 to 20 percent of people with HIV, such as to counteract many of the strains of the virus. Such antibodies adhere to those areas of the virus, which are critically important to him, and which are monitored in any strain of HIV. And are attached to the virus , the antibodies do unable to infect other cells.

In the past decade, scientists have tried to develop a vaccine that can cause the body to produce this type of specific antibodies to HIV , but it was quite difficult.

Scientists describe the above antibodies as Ferraris antibody indicates Dr. Dan Baruch , a professor at the Medical College of Harvard University , participated in the research.

For the purpose of both research scientists experienced antibodies on monkeys of the species rhesus infected monkey version of HIV. Rare antibodies were collected from HIV -infected people were then grown in large quantities in the laboratory and were infused in large doses to monkeys. Researchers tested various combinations of antibodies in 35 monkeys. Best working antibody called PGT 121 . Alone or with other antibodies , it gives great results.

Generally antibodies reduced the virus to very low levels in 16 to 18 monkeys within seven days, and this effect was maintained for up to three months. In three animals carry the virus, but in small quantities after treatment he did not reappear.

The effect of the antibodies to be tested on humans. Furthermore, it has not been studied in combination with antiretroviral drugs, which are the standard anti-HIV drugs, used by many thousands of patients in order to control the virus.

According to scientists, however, the combination of antibodies with antiretroviral drugs would make sense because the two treatments have different mechanisms of action. Antiretroviral drugs only attack the mechanism of HIV virus to create copies, while antibodies can directly attack the particles of the virus in blood and in cells that are infected with the virus.

It is not clear whether the antibodies can attack the dormant HIV cells that are hidden in the body and allow the virus to reappear when treatment is discontinued.

New research from the Monell Chemical Senses Center and the U.S. Department of Agriculture (USDA) reveals how diseases can modify animal odors in subtle ways. In a recent study published in the public access journal PLOS ONE, scientists examined how infection with avian influenza (AIV) alters fecal odors in mallards.

Using both behavioral and chemical methods, the findings reveal that AIV can be detected based on odor changes in infected birds.

"The fact that a distinctive fecal odor is emitted from infected ducks suggests that avian influenza infection in mallards may be 'advertised' to other members of the population," notes Bruce Kimball, PhD, a research chemist with the USDA National Wildlife Research Center (NWRC) stationed at the Monell Center. "Whether this chemical communication benefits non-infected birds by warning them to stay away from sick ducks or if it benefits the pathogen by increasing the attractiveness of the infected individual to other birds, is unknown."

In the study, laboratory mice were trained to discriminate between feces from AIV-infected and non-infected ducks, indicating a change in odor. Chemical analysis then identified the chemical compounds associated with the odor changes as acetoin and 1-octen-3-ol.

The same compounds also have been identified as potential biomarkers for diagnosing gastrointestinal diseases in humans. Kimball and colleagues hypothesize that metabolites resulting from viral infection interact in concert with bacteria in the gastro-intestinal system of ducks to produce "odor signatures" indicating presence of the AI virus.

"Avian influenzas are typically asymptomatic in ducks and waterfowl. Infection in these species can only be diagnosed by directly detecting the virus, requiring capture of birds and collection of swab samples. Our results suggest that rapid and simple detection of influenzas in waterfowl populations may be possible through exploiting this odor change phenomenon," said Monell behavioral biologist Gary Beauchamp, PhD, also an author on the paper.

Future work will assess whether odor changes can be used for surveillance of AIV in waterfowl. In particular, researchers are interested in whether the odor change is specific to the AIV pathogen or if it is merely a general response to a variety of pathogens normally found in birds. Other studies will explore communicative functions of the AIV odor to gain greater understanding of how odors can shape social behavior in wildlife populations.

Also contributing to the research, which was funded by the National Wildlife Research Center, were Kunio Yamazaki and Maryanne Opiekun of Monell and Richard Bowen and Jack Muth from Colorado State University. Dr. Yamazaki, who actively contributed to the design and realization of this work, died in April 2103.

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With the discovery of Mimivirus ten years ago and, more recently, Megavirus chilensis, researchers thought they had reached the farthest corners of the viral world in terms of size and genetic complexity. With a diameter in the region of a micrometer and a genome incorporating more than 1,100 genes, these giant viruses, which infect amoebas of the Acanthamoeba genus, had already largely encroached on areas previously thought to be the exclusive domain of bacteria. For the sake of comparison, common viruses such as the influenza or AIDS viruses only contain around ten genes each.

In the article published in Science, the researchers announced they had discovered two new giant viruses:

• - Pandoravirus salinus, on the coast of Chile;
• - Pandoravirus dulcis, in a freshwater pond in Melbourne, Australia.

Detailed analysis has shown that these first two Pandoraviruses have virtually nothing in common with previously characterized giant viruses. What's more, only a very small percentage (6%) of proteins encoded byPandoravirus salinus are similar to those already identified in other viruses or cellular organisms. With a genome of this size,Pandoravirus salinus has just demonstrated that viruses can be more complex than some eukaryotic cells. Another unusual feature of Pandoraviruses is that they have no gene allowing them to build a protein like the capsid protein, which is the basic building block of traditional viruses.

Despite all these novel properties, Pandoraviruses display the essential characteristics of other viruses in that they contain no ribosome, produce no energy and do not divide.

This groundbreaking research included an analysis of thePandoravirus salinus proteome, which proved that the proteins making it up are consistent with those predicted by the virus' genome sequence. Pandoraviruses thus use the universal genetic code shared by all living organisms on the planet.

This shows just how much more there is to learn regarding microscopic biodiversity as soon as new environments are considered. The simultaneous discovery of two specimens of this new virus family in sediments located 15,000 km apart indicates that Pandoraviruses, which were completely unknown until now, are very likely not rare.

It definitively bridges the gap between viruses and cells -- a gap that was proclaimed as dogma at the very outset of modern virology back in the 1950s.

It also suggests that cell life could have emerged with a far greater variety of pre-cellular forms than those conventionally considered, as the new giant virus has almost no equivalent among the three recognized domains of cellular life, namely eukaryota (or eukaryotes), eubacteria, and archaea.

Naked mole rats have what any animal would want. They live long lives—about 30 years—and stay healthy until the very end. Now biologists at the University of Rochester have new insights into the animal's longevity—better-constructed proteins.

Proteins are involved in nearly all functions of an animal cell, and consequently, are essential to all organisms. But before proteins can do their job, they must fold into the appropriate shapes that allow them to connect to and interact with other structures in the cell. In a paper published this week in the Proceedings of the National Academy of Sciences, Vera Gorbunova and Andrei Seluanov describe their discovery of the process in naked mole rats that leads to virtually perfect proteins.

"While this is basic research," said Gorbunova, "we hope our findings encourage further studies on better protein synthesis."

Their work focused on naked mole rat ribosomes—the site of protein creation in the animal's cells—and began by happenstance. Gorbunova and Seluanov were working with ribosome RNA (rRNA) when they made a discovery. After applying a dye to a sample, they studied it under ultraviolet light only to find three dark bands—representing concentrations of different rRNA molecules—not the two bands that are characteristic of all other animals, suggesting that there is a "hidden break" in the naked mole rat rRNA. Since rRNA is an essential part of the protein-creation mechanism, the two biologists decided to see if the broken rRNA affects the quality of naked mole rat proteins.

Ribosome RNA strands act as scaffolds on the ribosome, a protein synthesis machine. Changing the shape of the scaffold can have a profound effect on the organization of the ribosome parts.

Gorbunova and Seluanov discovered that the naked mole rat's rRNA scaffold is indeed unique. The rRNA strands split at two specific locations and discard the intervening segment. Instead of floating off on their own, the two remaining pieces from each strand stay close to each other and act as a scaffold on which ribosomal proteins are assembled to create a functional ribosome—a molecular machine that puts amino acids together to create proteins. And the results are impressive.

When the ribosome connects amino acids together to create a protein a mistake is occasionally introduced when an incorrect amino acid is inserted. Gorbunova and Seluanov found that the proteins made by naked mole rat cells are up to 40 times less likely to contain such mistakes than the proteins made by mouse cells.

"This is important because proteins with no aberrations help the body to function more efficiently," said Seluanov.

The next step for the biologists is to split mouse rRNA in the same way to see if it would lead to improved protein creation.

The two biologists hope their work will eventually result in pharmaceutical treatments that modulate protein synthesis in humans, though any medical solution is a long way off.

The world's first vaccine against smoking has been developed by the company "Selecta (RUS)." Expected in 2018 they arrived at pharmacies, said the site "newsru."

According to Russian scientists, a subsidiary of the large U.S. holding company, it is a means of stimulating the production of antibodies that block nicotine in the blood. To provoke an immune response against the tobacco.

As a result, a person stops experiencing a pleasant sensation of smoking (nicotine can affect the brain).

Thus no point in smoking and it is easy to grips with the psychological addiction.

According to statistics from the World Health Organization (WHO) each year smoking kills about 4 million people.

People do not quit smoking despite injury information on nicotine for smoking bans in public places in many countries and tax increases.

Same group of Russian scientists now developing vaccines against diabetes, hepatitis B and skin cancer.

Meanwhile, a new study of New Zealand scientists shows that smokers are switching to electronic cigarettes to quit the habit have the same chance of success as those using nicotine patches , reported the Associated Press and Reuters .

The first-ever study comparing the efficacy of electronic cigarettes with nicotine patches as standard therapy for smoking.

Scientists from the University of Auckland found that the achievement levels are similar, it is more likely that electronic cigarettes to help their users do to reduce the amount of tobacco you smoke. Moreover, people go to much greater willingness of electronic cigarettes than nicotine patches .

Gentaur provides a wide range of specialist antibodies, primarily to aid research in the cellular stress, heat shock, ion channel and transporter fields of study. However we also provide antibodies as research tools for Apoptosis, Cell Signaling and Post-translational Modification amongst others.

If you need help finding the reagent that meets your requirements, please contact us at This email address is being protected from spambots. You need JavaScript enabled to view it.

HO-1 (Rat) Antibody

Catalog#: SPC-207D
Package size: 100ug
Type: Polyclonal
Datasheet: SPC 207 Heme oxgenase 1 Heat Shock Protein 32 (HO 1)
Description: Anti-HO-1 (Rat)

HSF1 Antibody

Catalog#: SPC-208D
Package size: 100ug
Type: Polyclonal
Datasheet: SPC 208 Heat Shock Factor 1 (HSF1)
Description: Anti-HSF1

LGI1 Antibody

Catalog#: SMC-461D
Package size: 100ug
Type: Monoclonal
Datasheet: SMC 461 LGI1
Description: Anti-LGI1

LRRK2/Dardarin Antibody

Catalog#: SMC-445D
Package size: 100ug
Type: Monoclonal
Datasheet: SMC 445 LRRK2 Dardarin N3
Description: Anti-LRRK2/Dardarin

PEX6 Antibody

Catalog#: SMC-470D
Package size: 100ug
Type: Monoclonal
Datasheet: SMC 470 PEX6
Description: Anti-PEX6

PINK1 Antibody

Catalog#: SMC-450D
Package size: 100ug
Type: Monoclonal
Datasheet: SMC 450 PINK1
Description: Anti-PINK1

Pan-QKI Antibody

Catalog#: SMC-467D
Package size: 100ug
Type: Monoclonal
Datasheet: SMC 467 Pan QKI
Description: Anti-Pan-QKI

SOD1 (UβB) Antibody

Catalog#: SPC-205D
Package size: 100ug
Type: Polyclonal
Datasheet: SPC 205 SOD1 (UBB) Oxidative Stress
Description: Anti-SOD1 (UβB)

SOD1 (EDI) Antibody

Catalog#: SPC-206D
Package size: 100ug
Type: Polyclonal
Datasheet: SPC 206 SOD1 (EDI) Oxidative Stress
Description: Anti-SOD1 (EDI)

TRAP1 Antibody

Catalog#: SPC-209D
Package size: 100ug
Type: Polyclonal
Datasheet: SPC 209 TRAP1 Heat Shock Protein
Description: Anti-TRAP1

A University of Colorado Cancer Center study published today in the journal Cancershows that the current criteria used to match lung cancers with the drug crizotinib may miss some patients who could benefit from the drug. The findings suggest that doctors should look closer at borderline or atypical ALK-negative cases, and could widen the population of lung cancer patients offered treatment with crizotinib or other ALK-inhibitor drugs.

ALK stands for anaplastic lymphoma kinase, a gene that is turned off in most adult tissues in the body, but which can be re-activated to cause cancer when it is fused with another nearby gene. The original and still most widely-used test for ALK-positive lung cancer was co-developed by Leila Garcia, PhD, director of the Cytogenetics Core Resource at the University of Colorado Cancer Center. The test uses the technique known as fluorescence in situ hybridization (FISH) to test for the fusion of the ALK gene with another gene that turns ALK back on, allowing it to drive some lung cancers. When a cancer is ALK positive it can be very effectively treated with crizotinib, a targeted anti-ALK drug.

"The test is fairly definitive -- either a cell is ALK positive or not using the criteria we initially implemented. However, what is less certain is the exact percentage of ALK-positive cells required to label an entire tumor as ALK-positive. Is there an exact threshold of ALK-positive cells that will make a patient respond to crizotinib or other ALK inhibitors?" Garcia says.

"Since the beginning we have looked at the cells in a tumor and if 15 percent or more of these cells show the changes classically associated with an ALK rearrangement, we classify that tumor as ALK-positive and offer treatment with crizotinib," says Ross Camidge, MD, PhD, investigator at the CU Cancer Center and director of the thoracic oncology clinical program at University of Colorado Hospital.

Previous studies indicated that this 15-percent point fell in a clear gap between tumors that were obviously ALK-positive and tumors that were obviously ALK-negative, making it an attractive threshold.

"But what this study shows is that when you look not at tens, but hundreds of cases, tumors clearly exist that come right up to the 15-percent cutoff point," Camidge says.

Another possible gray area is when a gene rearrangement occurs but is very complex -- like shuffling cards rather than just cutting the deck. In this situation the typical separated dot pattern indicative of ALK rearrangement may not be present, but instead doublets or triplets of single or un-separated dots may exist. This atypical cellular footprint can tell an expert that, while officially ALK-negative, the cancer has made some changes in the region of the ALK gene that could still make the cancer sensitive to ALK-inhibitor drugs.

"We believe these data suggest that such borderline and atypical negative cases deserve a closer look, perhaps with new kinds of diagnostic tests," Says Camidge.

The current study tested 1426 samples of non-small cell lung cancer, which included 174 officially positive for an ALK rearrangement and 1252 that were officially negative. Of the ALK-negative tumors, 121 had greater than 10 percent ALK-positivity, but were still below the 15 percent needed to classify the overall tumor as ALK-positive. This means that 8.5 percent of non-small cell lung cancers were "borderline" negative. In the study, 1-2 percent also showed atypical-negative patterns, a group that may also benefit from a closer re-evaluation of their ALK status.

Early in 2013, serendipity provided a chance to test whether at least one of the Colorado team's hypotheses were correct. In a case described in an upcoming article in the Journal of Thoracic Oncology, Dr. Shengxiang Ren from the Shanghai Pulmonary Hospital describes a patient who traveled halfway across the world for a second opinion at the University of Colorado, where much of the research leading to ALK-targeted drugs has taken place.

"We were thrilled this patient had sought out an opinion from one of the leading centers in lung cancer and could not have been happier with the collaboration that developed," Ren says.

The patient was originally classified ALK-negative using the standard FISH assay. However, Dr. Garcia recognized that an atypical negative pattern was present. One way of looking closer at ALK uses the technique of immunohistochemistry (IHC), which looks directly for the protein the aberrant ALK gene creates. Using an IHC assay for ALK conducted within the laboratory of Fred R. Hirsch, MD, PhD, associate director for international programs at the CU Cancer Center, the team quickly confirmed that the patient's tumor was making the ALK protein and should really be considered ALK-positive. Another test called RT-PCR conducted in Shanghai on the same specimen looked at the ALK gene in a third way, confirming the presence of messages coming from the gene that were telling the cell to make the abnormal protein.

"Amazingly, crizotinib was being licensed in China the following week and so we simply wrote the patient a prescription and sent him back to Dr. Ren in Shanghai, where his latest scans show he is responding beautifully to the drug," Camidge says. "All of the early work on ALK positive lung cancer has really helped to clarify what can be achieved by personalized medicine, but we have to keep pushing the envelope to maximize this approach in routine cancer care. For ALK-positive lung cancer, basically our goal now is to make sure that everyone who could benefit from an ALK inhibitor gets an ALK inhibitor."

The CU Cancer Center's Thoracic Oncology Program is world renowned for its pioneering treatment of lung cancer. The program includes a multidisciplinary team of specialists and subspecialists working together to establish the best treatment plan for each patient. Advanced molecular profiling of a patient's tumor, combined with an extensive array of standard and experimental treatments available through clinical trials has led to major advances in patient outcomes in the last few years.

The program's one-year survival rates for advanced lung cancer consistently run twice as high as the national average. The survival rates at five years run four times higher than the national average. Additionally, the Center's new Remote Second Opinion Program now offers access to program experts for patients who prefer not to travel.

According to researchers, they prevent the growth of cancer cells

A new type of therapy can help to effectively treat breast cancer, reported biologists from the University of Aberdeen. It's about the application of the specific type of antibody IgNAR (immunoglobulin new antigen receptor), which are found in cartilage fish - such as sharks. According to researchers unique antibody can prevent the growth of cancer cells.

Over the next three years is to provide a number of studies that confirm the theory and help to create a cure for the most common malignancy in women location. Scientists will focus on the two molecules - HER2 and HER3, which are arranged on the surface of cancer cells. When these molecules are combined, the cancer cells receive signals for growth and division. According to researchers IgNAR can stop the transmission of the signal and to prevent progression of the disease.

Background staining or non-specific staining is an often-encountered problem in immunohistochemistry, in immunofluorescence and in situ stains. Background staining is caused by a number of factors such as cross reactivity of antibodies with the shared epitopes in the tissue, by the presence of natural and/or contaminating antibodies present in the primary antibody and/or the secondary antibody, by ionic interactions, by the presence of carbohydrates and by endogenous biotin present in the tissue. Eradicating background is most important for obtaining background-free specific staining for the ease of qualitative and quantitative evaluation.

PRODUCT DESCRIPTION
Background Buster is a peptide Blocker that eradicates all general background staining. Background Buster removes all background staining caused by primary antibodies, by the staining reagents, by the chromogens, by the fixatives and by endogeneouse biotin present in tissues such as liver and spleen and kidney. Background Buster is used in place of normal sera and other blocking solution for removing background staining in both human and animal tissues.

Background Buster is applicable IHC staining, to immunofluorescence staining and to in situ probe staining in both human and animal tissues. It is also applicable to flow cytometric assays.

Background Buster is a must for animal tissue staining, it is especially essential when staining identical species tissue and antibodies such as mouse antibodies on mouse tissues (Mouse-on-Mouse) and Rabbit-on- Rabbit. A 30-minute incubation with Background Buster is recommended prior to the application of the primary antibody for staining of identical species primary antibodies and tissues. The use of Background Buster is highly recommended for staining of indirect species (non-identical species tissue/ antibody) such as Rat –On-Mouse, Mouse-on- Rat, Mouse-on-Rabbit, etc. A 20-minute incubation with Innovex Background Buster is recommended prior to the application of the primary antibody for staining of Indirect (non-identical species primary antibodies and tissues).

In immunoperoxidase-IHC staining, another type of background and non-specific staining is caused by red blood cell staining; this is due to endogenous peroxidase enzyme present in red blood cells. This type of background requires a pre-treatment step with 3% freshly made hydrogen peroxide (H2O2) in water, this blocking step should precede the blocking step with Innovex Background Buster.

NB306 Background Buster 125 ml qty 419 EUR
NB306-50 Background Buster 50 ml qty 325 EUR

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Immunolocalization of electrogenic sodium-bicarbonate cotransporters pNBCI and kNBCI in the rat eye

IMMNLINOLOCALIZATION  OF SODIUM.BICARBONATE  COTRANSPORTERS

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