BD Biosciences, a part of global medical technology company BD (Becton, Dickinson and Company), has launched a high-performance research flow cytometry cell analyzer BD LSRFortessa X-20 that can be configured with up to five lasers to detect up to 20 parameters simultaneously.

According to the company, the BD LSRFortessa X-20 cell analyzer delivers high-performance multi color analysis with the most compact footprint in its class at 30”x29” and a height of 30”. Recognizing that space is a valuable commodity in today’s research environment, BD Biosciences designed the new cell analyzer to be compact without compromising the power needed

While popular laser choices include blue, red, violet, yellow-green and UV, a wide range of up to 34 available laser choices are available as excitation sources. Each excitation source is supported by new polygon detector arrays, and each polygon can support up to eight detectors for maximum flexibility in optical configuration, the company said in a statement.

The new cell analyzer enables customers to configure BD flow cytometers and cell sorters to fit precise research and assay needs. This program is tailored to meet the needs of researchers at the leading edge of biomedical discovery.

“The new BD LSRFortessa X-20 cell analyzer will enable researchers to conduct complex experiments with the additional parameters and increased sensitivity they need,” said Alberto Mas, president, BD Biosciences. “Uncovering dim staining and rare cell populations is extremely valuable to complex multi color assays, which are tools for advanced disease or drug development research.”

 

Biocon – India’s leading biotechnology company has launched a new drug to treat a skin disease called psoriasis. This condition takes place when the immune system mistakes a normal skin cells as a pathogen.

“Psoriasis is a common disease which affects 3% of the world population and which 2% of population affects India approximately 1.2 billion people. The global psoriasis market size is estimated to cross $8 billion by 2016,” the company said in a statement here on Sunday.

“The drug is an outcome of our path-breaking research and will bring a paradigm shift in the management of skin disorder. The molecule has potential to treat multiple auto-immune diseases and make a difference to a larger patient population worldwide,” Biocon chairperson Kiran Mazumdar-Shaw said in the statement.

An infusion drug to treat psoriasis, Alzuma will be manufactured after regulatory clearances

“With a unique mechanism, the drug offers safety profile compared to other therapies, and has a long remission period with low opportunistic infection rate,” Shaw said.

The new drug also demonstrated pre-clinical and post-clinical evidence in treating other autoimmune diseases like rheumatoid arthritis, psoriatic arthritis and multiple sclerosis.

“We are committed to address the unmet need of patients suffering from psoriasis through the new drug, which has better safety and efficacy profile to patients with longer remission periods and lower infection rates,” said Biocon president (marketing) Rakesh Bamzai in the statement.

Chemists at Johannes Gutenberg University Mainz (JGU) have developed a new method for parallel protein analysis. This study shows a capable of identifying thousands of different proteins.

This method could be used to find the presence of viruses and their type in tiny samples. As well as it is very fast and cost-effective. “We see possible applications of this technique in medicine, where it could be used, for example, for the rapid diagnosis of a wide range of diseases. It would be almost as easy to use as a pregnancy test strip,” said Professor Carsten Sonnichsen of the Institute of Physical Chemistry.

The test involves blood, saliva, or other body fluid on a test strip, which is then placed in a device developed at the JGU Institute of Physical Chemistry. This device is able to identify the specific proteins in the fluid and allows us to differentiate between harmless microorganisms and dangerous pathogens.

In order to detect the many different substances present in a small sample, the sensors need to be as tiny as possible, preferably the size of nano-particles. Sonnichsen’s team of scientists has designed a sensor no larger than the head of a pin but capable of performing a hundred different individual tests on a surface that is only of one-tenth of a square millimeter in area.

The ‘test strips’ consist of glass capillary tubes that have gold nano-particles as sensor elements on their internal surfaces. “We first prepare our nano-particles using short DNA strands, each of which binds to a specific type of protein,” explained Janak Prasad, who developed this method.

When a protein docks with one of these special DNA strands, called aptamers, the corresponding nano-particle changes its color. The color changes can be detected with the aid of a spectrometer. For this purpose, the capillary tubes are placed under a microscope and provided with the necessary software by the Mainz-based team of chemists.

 

Researchers have discovered an enzyme responsible for repairing single DNA strands damaged through cell division, and hope this will lead to treatments for cancer, Parkinson’s and Alzheimer’s disease.

As we grow, the number of cells in our body must grow as well.  In order to multiply, a cell’s DNA must divide into two strands, creating two identical templates for the genomes of the “daughter” cells.

Cell division occurs every time, the cell’s genome is exposed, and this very important genetic material is left vulnerable to attacks from reactive oxygen species (ROS) – toxic molecules created through respiration.  If damaged by an ROS, the genetic information carried in a cell may change, and these genetic mutations can lead to disorders associated with DNA damage, such as cancer and neurodegenerative diseases.

Human body has a natural way of repairing DNA through the replication process, and researchers from the University of Texas Medical Branch in Galveston (UTMB), have found that how the process works could lead to cancer treatments and even the reversal of age-related diseases.

“We have so much damage cells so we can use a system of repair before that damage is replicated,” lead author Dr. Sankar Mitra, “If repair doesn’t occur, replication is going to happen with the damaged genome.”

How it works:

The National Academy of Sciences, Mitra and his team describe the work of an enzyme called NEIL1, a molecule that had been previously associated with the replication process.  In order to understand NEIL1’s mechanisms, the researchers suggest comparing DNA strand separation to the opening of a zipper.

As the zipper opens (or the strand divides), the DNA’s nucleo bases are exposed, so that a group of proteins known as the pre-replication complex can bind to the single strands and copy them back into double strands.  The NEIL1 enzyme is part of this protein package.

However, it is during this copying process that the DNA’s bases are most susceptible to ROS damage.

“The most common genome damage is oxygen damage; it is the most chemical damage you’re exposed to,” Mitra said. “You cannot survive without oxygen, but because you’re breathing huge liters of oxygen every day

According to Mitra, ROS damage occurs rather frequently throughout cell division and replication.  Fortunately, as soon as this damage occurs, NEIL1 recognizes the genetic change, and subsequently binds to the damaged site.  Once attached to the changed bases, it halts the replication process in its tracks.

“When they bind to that damage, the NEIL1 enzymes don’t allow replication to proceed,” Mitra explained. “When genome replication stops, the mechanism then is regression of the replication fork. So going backwards, like a zipper, the two strands come back together again.”

Once the strands have joined together, the NEIL1 – still bound to the damaged area – then fixes the genetic mutation before falling off the cell’s DNA.

Mitra and his team discovered NEIL1’s mechanisms through a series of in vitro experiments in their lab. They argue that knowing NEIL1’s function in the replication process could have huge implications for the future of cancer therapies.  For example, blocking or inhibiting the expression of NEIL1 in cancer cells could make them more susceptible to current cancer medications.

“All cancer drugs kill cells by targeting the DNA, because if the genome is damaged and if it’s not repairable, it causes the cancer cell to die.  But most of the time cancer comes back because some resistance occurs, and one mechanism of resistance is repair activity,” Mitra said. “But if you increase susceptibility of cancer cells to genome damage, then they’ll be much more sensitive to the drugs, and they can be killed more easily.”

Mitra also noted an even more incredible byproduct of his research: reversing the damage done by age-related diseases such as Parkinson’s and Alzheimer’s.  He said that boosting NEIL1 expression could potentially repair ROS-related genome damage in the elderly population.

“We don’t know how to increase the level of this enzyme, however there are ways to increase its expression,” Mitra said.  “Epigenetically, you can change the level of NEIL1 by changing a particular chromosomal function so that the level of this enzyme goes up.”

But most importantly, a better understanding of the cell replication repair process is crucial to the future of genetic research, according to Mitra.

“Genome damage repair is essential for survival of the human species, and we need to understand the mechanisms,” Mitra said. “If we have a comprehensive picture of how this damage repair occurs in various situations, then we can provide the window to developing new approaches to improving the process.”

 

Scientists have found that a new molecule in severe tumors prevents cancer cells from responding and surviving when starved of oxygen and it is the new treatment, according to new research published in the Journal of the American Chemical Society on July 26.

Cancer Research UK scientists at the University of Southampton found that this molecule targets the master switch  HIF-1 that cancer cells use to adapt to low oxygen levels, a common feature in the disease.

The researchers uncovered a way to stop cancer cells using this switch through an approach called ‘synthetic biology’. By testing 3.2 million potential compounds, made by specially engineered bacteria, they were able to find a molecule that stopped HIF-1 from working.

All cells need a blood supply to provide them with the oxygen and nutrients they require to survive. Cancer tumors grow rapidly and as the tumor gets bigger it outstrips the supply of oxygen and nutrients that the surrounding blood vessels can deliver.

But, to cope with this low-oxygen environment, HIF-1 acts as a master switch that turns on hundreds of genes, allowing cancer cells to survive. HIF-1 triggers the formation of new blood vessels around tumors, causing more oxygen and nutrients to be delivered to the starving tumor, which in turn allows it to keep growing.

Dr Ali Tavassoli, a Cancer Research UK scientist whose team discovered and developed the compound at the University of Southampton, said: “We’ve found a way to target the steps that cancer cells take to survive and we hope that our research will one day lead to effective drugs that can stop cancers adapting to a low oxygen environment, stopping their growth. The next step is to further develop this molecule to create an effective treatment.”

Dr Julie Sharp, senior science information manager at Cancer Research UK, said: “Finding ways to disrupt the tools that cancer cells use to adapt and grow when starved of oxygen has been a hot topic in cancer research, but finding drugs that do this effectively has proved elusive.

“For the first time our scientists have found a way to block a master switch controlling cells response to low levels of oxygen — an important step towards creating drugs that could halt cancer in its tracks.”