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Researchers from China reported, in Acta Biochimica et Biophysica Sinica, a way to improve antibody production. Traditionally, antibody production uses recombinant fusion protein as an antigen to raise antibodies against the epitope, part of the molecule recognized by the immune system, of a target protein. At noted by the authors however is the issue that “the concomitant anticarrier antibody in resulting antiserum reduces the production of the desired antibody and brings about unwanted non-specific immune reactions.” To alleviate these issues the authors used a green fluorescent protein transgenic mouse. The carrier protein mouse produced a higher concentration of antibodies against the desired target protein compared to control mice.

This is an interesting but already developed way to use transgenic animals.  Medarex has been using transgenic mice since 2001 to make 100% human protein antibodies for use in therapeutics. The more pressing question is the application of this technology. For years Medarex has been promising that they would have a product out with one of their partners; a long list including Bristol-Myers Squibb, Pfizer, Amgen, Roche, Genmab, and Eli Lilly. However this promise is still on the back burner. The closest they have come to being on the market is the work they have done with Centocor. This product, CNTO 1275, is in the process of getting Biologica License Approval. Hopefully Medarex will finally perform as stated but, if I was an investor I would be concerned as the stock has taken a dive in the last six months from above $17/share to the current price of $8.77/share.

MicroRNA’s are short single stranded ribose nucleic acids which regulate gene expression. They have been found in heart and muscle tissue, and some exclusively in the brain. The term was first introduced in 2001 in Science. Researchers at Rockefeller University have discovered that microRNA’s also help create our skin to protect us from bacteria and possible prevent skin cancer.

The lead authors, Yi and Fuchs, used mouse models to find where the microRNA was expressed. During the first 13th days of development, mouse skin is primarily composed of undifferentiated stem cells. On the 15th day, these stem cells exit the inner layer of the skin and begin to differentiate into cells that form the outermost, protective layer. During this time the expression of microRNA-203 skyrockets, suggesting that during development microRNA-203 has some responsibility in creating the skin barrier. When they compared this expression to humans, chickens, and zebrafish they found the pattern was identical. Yi was quoted saying “If it has been expressed in this very specific tissue for a long time and across several species, it means that it probably plays an important role there.” This group further found that the microRNA-203 suppresses a protein, p63, which stimulates skin cell growth. Without the presence of the RNA the skin grows uncontrolled, a possible reason for some skin cancers.

This is a great find to further introduce new targets for cancer drugs. In this case the authors suggest recovering microRNA-203 expression if it fails to prevent these type of cancers. In mice models this would be great evidence that certain squamous cell carcinomas are due to the lack of microRNA-203, however this could be extremely difficult to do in humans. Another possible cheaper alternative would be to design an inhibitor to the protein, p63.

Investigators at Saint Jude Children’s Research Hospital have announced new research which has advanced the understanding of how cells undergo Apoptosis. Apoptosis is intentional programmed cell death and is believed to be one of the main reasons for the existence of cancer which hijacks apoptosis and prevents it from occurring. A report on this work can be found in the advanced online publication in Nature.

James Ihle, Ph.D., and senior author describes the work, “This is probably the first description of what is happening mechanistically that contributes to the ability of cells to delay apoptosis,(…)it provides incredible insights into how three proteins work and how they can control apoptosis.” The researchers demonstrated in mouse lymphocytes that a protein, Hax1, is required to suppress apoptosis. Briefly, Hax1 interacts with the protease Parl which allows HtrA2 to be presented to Parl. Ultimately the presence of HtrA2 prevents Bax to become activated, and Bax is known as one way to initiate apoptosis.

This detailed look at the mechanisms behind apoptosis are extremely beneficial to further preventing cancer. Similar to pharmaceutical companies targeting Angiogenesis, Apoptosis drugs is believed to be another way to slow down or even prevent many forms of cancer. By figuring out ways to initiate apoptosis in cancer you effectively rid cancer, remember cancer is define as uncontrolled cell growth due to the lack of cells undergoing apoptosis. With this type of research the drug industry will be screening and targeting proteins found in this paper and hopefully have similar success stories such as Avastin from Genetech. 

Researchers at Purdue University, have published in Nature, a new technology for detection of toxins and food-borne pathogens. The research group claims the technology is able to detect several pathogens in thousands of food and water samples in a couple of hours. Interestingly, it can also estimate the number of microbes present in a sample and determine whether that amount poses an active health hazard.

The technology uses live mammalian cells, B-cell hybridoma, PED-2E9, in a type I collagen matrix, that release a chemical, alkaline phosphatase, when harmed. This chemical can be detected uses optical equipment, such as laser scanning cytometry or cryo-nano scanning electron microscopy. The group developed software which can then analyze the signal and determine the quantity of harmful microbes present. Since the bio-sensor uses live cells it only detects actively harmful pathogens and ignores those that are inactive and harmless. Most test on the market currently detect dead or alive microbes and are prone to high false alarm rates or use a lengthy incubation periods, up to 20 hours or more, to grow only living microbes for detection.

This is an interesting application for live cells but is not novel. BAE systems has had this algae detector on the market for some time now. Even with this being said, the food market is lacking a fast, relatively speaking, detection method for Listeria monocytogenes. We at Biotech Mashup will follow this group to see if they are able to spin this out of the laboratory.

A group of scientists from Cardiff University, University of London, and Max Planck Institute for Ornithology have reported in PLoS ONE, for the first time, that when birds eat small invertebrates contaminated with environmental pollutants, significant changes occur in both the bird’s behavior and their brain. Surprisingly, male European starlings that have been exposed to higher levels of natural and synthetic estrogen, found in sewage effluent, sing longer and more complex songs than their controlled male counterparts. What is so unique about this research is that the group of scientists were able to show that the key brain area controlling male song complexity (HVC) was significantly enlarged due to the pollution. Not surprisingly, female songbirds prefer to mate with birds who sing songs which are stronger and go on for a longer period of time, and thus choose males with higher pollution levels.

Although this seems beneficial in reality more harm than good is happening to these hyped up polluted birds. As predicted by the scientists, the birds that have exposure to pollutants have suppressed cell-mediated and humoral immune functions. As a result, females choose to mate with polluted male birds despite their reduced immune functions. The scientists conclude that “[O]ur data suggest that female starlings would bias their choice towards exposed males, with possible consequences at the population level.” 

Although we feel troubled by the fact that these birds are negatively affected by the sewage waste, it is surprising that the pollution improves the songbirds song – a key evolutionary function in these birds. Yet, we remain hopeful that the reporting of the pollution problem will subsequently save these songbirds and other species from extinction.

Julie Steenhuysen (Reuters) reported on a recent study published in PLoS Genetics which found that genes that helped early humans adapt to cold climates may be driving metabolism-related diseases such as obesity or diabetes. U.S. researchers at the University of Chicago found a strong correlation between climate and genetic adaptations that influence the risk of metabolic syndrome, a group of related disorders such as obesity, high cholesterol, heart disease and diabetes. “Climate over a long period of time has shaped the distribution of genetic variants that may be associated with the risk of these common metabolic disorders,” said Anna Di Rienzo, a professor of human genetics at the University of Chicago. Anthropologists have long argued that differences in skin pigmentation, for instance, are related to early human migration. “There are all of these traits, body mass or skin pigmentation, that we know are strongly correlated with environmental variables,” Di Rienzo said. Di Rienzo and colleagues wanted to see if genes that were once useful for tolerating cold climates were playing a role in metabolic diseases. “To survive in these climates, they had to adapt,” said Di Rienzo.

To test the hypothesis that climate shaped variation in metabolism genes in humans, the team used a bioinformatics approach to select 82 candidate genes for common metabolic disorders. They then genotyped 873 tag SNPs in the genes in 1,034 people from 54 populations. They saw several clusters of different genetic variations related to metabolic syndrome in colder climates. Interestingly, one haplotype was associated with higher body mass index and altered concentrations of the hunger-satiety hormones ghrelin and leptin, suggesting that it conferred a selective advantage on energy metabolism. Biotech Mashup thinks that we might be able to use some of the SNPs from this study to better understand our hunger pains. Furthermore, the SNP tests offered by companies such as 23andme and Navigenics might be more insightful in light of these studies.

What do you get when you pit two bacteria in a death ring match? Researchers at MIT did this for their amusement, which they claim was research, and found out the winner uses a unique weapon to dominate its opponent.

Professor Anthony Sinskey’s laboratory at MIT was doing a weekly bacteria battle royale fight when they noticed that the soil-dwelling bacteria, Rhodococcus, who always loses these fights, won. Kazuhiko Kurosawa, postdoctoral associate, was intrigued by the winner’s fighting spirit and decided to try and stress the bacteria by placing it in different environments to see if it would produce any new antibiotics, it did not. Finally, Kurosawa decided to pit the bacteria in more death-match fights against a new competitor, Streptomyces. Normally Streptomyces produces an antibiotic which kills other bacteria but this time around Rhodococcus did the killing by making its own antibiotic.

The researchers realized these games had actually produced a new compound which they isolated and called rhodostreptomycin. This new antibiotic proved be very effective against other strains of bacteria such as Helicobacter pylori, the now famous bacteria which is known to cause stomach ulcers. More amazing is that this new antibiotic, an aminoglycoside, is actually a novel new molecule, it has a ring structure which has never been seen before. This new structure could be used as a building block for newer antibiotics, something that the medical community is in dire need of with the recent stories on Methicillin-resistant Staphylococcus aureus (MRSA) and multidrug-resistant Tuberculosis. This battle royale technique could be used to make more antibiotics that have previously been undiscovered, the only step left is for MIT to stream the fights over the Internet so everyone can enjoy the action.

The Scripps Research Institute is reporting on a new way to fight HIV. According to one of lead authors, Chi-Huey Wong, Scripps Research Chemistry Professor, the approach was developed with two ideas in mind:

“This new approach capitalizes on two recent findings in the field of HIV research. One is the discovery that HIV takes a Trojan horse approach to reach cells it needs to infect deep inside the human body. Scientists have described how, when the virus enters the body through sexual contact, it hitches a ride with the dendritic cells of the immune system that stand guard for invaders at the mucosal lining of tissues. The virus outsmarts these cells, however, and latches onto a particular receptor protein, known as DC-SIGN, on the dendritic cells. By sticking to these immune system fighters, HIV manages to evades immune detection while the dendritic cells travel to the ultimate goal of the virus: immune T-Cells in the lymphoid system, which HIV then invades, setting up a deadly infection that spreads.

The second discovery is that an antibody exists that can signal immune destruction of the virus. The antibody, 2G12, protects people who have it against HIV progression, but very few of those who are infected put up such an immune reaction, said the study’s first author, Sheng-Kai Wang, a graduate student in Wong’s laboratory. Scientists at Scripps Research have defined the details of the action of the antibody and found that recognizes a dense cluster if sugars on one region of the virus’s spiky protein coating—which is, strikingly, the same area that HIV uses to bind to the DC-SIGN protein on dendritic cells.”

To achieve the goals of this new approach the group has created glycodendrons. Glycodendrons first set up an immune response because the sugar molecules on the molecule mimic 2G12 prompting the production of destructive antibodies, secondly it binds to the DC-SIGN on dendritic cells preventing HIV from piggybacking deeper into the body.

This new method to tackle HIV is smart and elegant and addresses the other lead authors, Dennis Burton, past commentary. Dennis Burton’s criticized VaxGen’s HIV vaccine trial because he believed you should not just try anything and that no science existed behind the companies vaccine candidate. Besides VaxGen, many other groups have tried to tackle this issue but typically have used little intelligence behind the vaccine development. This new idea, using intelligent design, is very exciting and hopefully will have continued success. Read more about this research in this weeks online Early Edition of the Proceedings of the National Academy of Sciences (PNAS).

Nanotechnology, considered morally unacceptable by the public, has benefited a variety of fields and is once again making strides in medicine. The University of Michigan has reported a novel technique using nanoemulsions to vaccinate against infectious diseases. The group uses nanometer diameter oil-based emulsions that are sprayed into the nose to produce a strong immune response. Previously, this technique was successful in vaccinating against influenza and can now add smallpox and HIV to the list.

Nanoemulsion vaccines developed at the Center for Biologic Nanotechnology at the University of Michigan are based on a mixture of soybean oil, alcohol, water and detergents emulsified into ultra-small particles smaller than 400 nanometers wide, or 1/200th the width of a human hair. This new technology uses surface tension from the nanoemulsions to disrupt membranes and destroy microbes without much or any damage to human cells. Laboratory results with mice indicate that treatment of their nares with nanoemulsion prior to exposure to pathogens offers protection against pathogen challenge. The emulsion also acts as a mucosal adjuvant by presenting the pathogen to the immune system, which can induce protective immunity in the absence of an active infection. In contrast, the presentation of other forms of inactivated pathogens does not yield an effective immune response, suggesting that the nanoemulsion-killed organisms are uniquely immunogenic.

Dilute emulsions showed stability when stored at 40°C for over 1 year and at room temperature for over 3 years. They can also withstand several cycles of heating and cooling. The technology has been licensed out to NanoBio Corporation. If successful in commercialization, this could become a disruptive technology, eliminating the current technique of needle vaccinations.

Korean researchers report the development of a robot powered by heart muscle cells from a rat. The researchers coated a biocompatible polymer with heart cells that pulse in synchony in the presence of glucose, obviating the need for an external power supply. These beating cells permit the robot to move its six legs. The robot has three short front legs and three longer back legs, which are all attached to a central rectangular body. As the heart cells contract, the longer rear legs bend inwards. This creates a difference in friction between the front and rear legs, which pushes the robot forward. The scientists measured the robot’s average speed at about 100 micrometers per second (or about 2.2E-10 MPH). The lead designer, Sukho Park at Chonnam National University, Korea, says these crab-like robots could be used inside the body to clear blocked tubes or arteries.

This made me think of another really neat use for the heart muscle cells, which would be to make a glucose-powered electricity generator. The basic concept would be to coat a micro-balloon with the cells and use their contracting force to drive a nano-machined generator. The concept is shown below. The advantage would be that you could power small electronics or anything else that runs off electricity using only glucose. Although each single generator may not make much power, linking thousands of nano-generators together may generate usuable quantities of power.

Heart muscle cells coat a micro balloon and contract in synchrony. The expelled fluid drives a generator using nano-machined gears.