American and Canadian researchers have identified a biomarker which predict which patients are at risk of developing cancer of the prostate or relapsed disease , reported UPI . Andris Zeylstra Medical Center at the University Vanderbilt and John Lewis from the University of Alberta said that some cases of prostate cancer are spread slowly and are not associated with severe symptoms , while others patients experience metastatic disease , often have fatal . Oncologists have long sought biomarkers that identify which patients must pass intensive care

Zeylstra and colleagues examined the protein CD151, which facilitates the migration of cancer cells in the body. Researchers found that when affected by prostate cancer patients CD151 is "free", ie is not bound by his partner, integrin protein, which allows cells to adhere to the surrounding tissue. It turns out that this form of CD151 is important functions in cancer.

"I was surprised we observed that some proteins are CD151 released by the presence of your partner and that it happens when there is a cancer, "said Zeylstra." New in is that it is not about traditional no change the expression of a protein in a protein that modifies molecular state. Namely, it is an indicator of the development of disease. "

The researchers studied tissue samples from 137 patients undergoing to treat a cancer of the prostate in Canada for the past 12 years. The results showed that if patients have "FREE" CD151, the risk of prostate cancer is greater, than for those without detectable "free" CD151.

Researchers at the Massachusetts Institute of Technology (MIT) and the University of Hanyang (Hanyang University) created a "synthetic antibodies". As a basis chemists have used carbon nanotubes, which fluoresce under laser irradiation.

Previously, this phenomenon has been used by other investigators, the carbon nanotubes are coated with the natural antibodies. When meeting with certain molecules such structures either light or dimmed, so you can use them as a sort of sensors. However, such sensors are destroyed in the living cell, which significantly limits their period of operation.

To solve this problem MIT chemists replaced by antibodies specifically synthesized amphiphilic polymers. These macromolecules contain regions that interact with water (hydrophilic) or push it (hydrophobic).

Polymers synthesized so that their hydrophobic portions fixed firmly on the surface nanotubok as armature, and constitute a hydrophilic "loops", which form a kind of crown around the particle. Loops arranged strictly along the tube, and the distance between anchors determines which target molecule can hook into the loop and change the nanotube fluorescence.

The uniqueness of this new approach is that before the polymer is attached to the nanotube is impossible to predict the possibility of molecular recognition, looking at the structure of the target and the polymer. That is, the polymer itself can not selectively detect a particular molecule.

In his article, published in the journal Nature Nanotechnology, researchers publish a description of molecular sensors, specific for riboflavin (vitamin B2), estradiol (female sex hormone) and L-thyroxine (thyroid hormone).

Currently, scientists are actively developing on certain neurotransmitters, carbohydrates and proteins. Another important challenge for the research team is to understand exactly what is happening with the polymer and nanoparticle throughout the whole capture specific target molecule.

The researchers believe that their current and future developments in the field of molecular recognition will open huge opportunities for monitoring of diseases such as cancer, multiple inflammations, diabetes and many others in any living organism.

Severe autoimmunity in childhood can be an indication of a primary immunodeficiency (PID) -- this has now been demonstrated in a 13-year-old patient by a research group from the MedUni Vienna belonging to the CeMM Research Center for Molecular Medicine of the AAS and the St. Anna paediatric hospital. A previously unknown B-cell defect was identified in the teenager with the aid of so-called "next generation sequencing," with which genetic mutations in the genetic material can be detected within a few days. The study has been published in the leading journal Blood.

"Our discovery created a sense of relief in the family as they now know at last what is wrong with the boy," says Kaan Boztug, who works routinely as a doctor at the University Department of Paediatrics and Adolescent Medicine treating seriously ill children, and as a researcher at CeMM, searching for the molecular causes of diseases of the immune system using the most modern genetic technologies. In this specific case a defect in the PRKCD gene was discovered. This causes a malfunction in the regulation of the B lymphocytes which are regarded as "antibody factories." Severe autoimmunity develops as a consequence.

According to Boztug and Elisabeth Förster-Waldl, paediatrician and immunologist at the University Department of Paediatrics and Adolescent Medicine of the MedUni Vienna, not only diagnostic, but also therapeutic, consequences can be derived from the recently successful molecular identification of the deficiency. From early childhood the patient had suffered periodically from severe autoimmunity of the kidneys, lymph nodes and connective tissues. The now 13-year-old had previously been globally immunosuppressed with cortisone for long periods but now the target of the therapy can be precisely isolated. Says Förster-Waldl: "Only when you know the mechanism, an individually-tailored therapy can be appropriately used or developed."

Data from the Anglo-American world assume that the prevalence of a clinically relevant immunodeficiency that can sometimes involve life-threatening consequences for those affected lies at between 1:1200 and 1:2000. Such figures can only be estimated for Austria as the systematic collection of data has only been taking place for the last two years.

At present around 30 to 40 percent of these deficiencies remain without a precise diagnosis according to Förster-Waldl. This could now change with the aid of the latest diagnostic processes including "next generation sequencing." Most immunodeficiencies are classified as so-called "rare diseases." Kaan Boztug: "However, the sum total of all these defects cannot be categorised as rare."

Cells almost don't change their type,just with a few exceptions, once they have become specialized - a heart cell, for example, won't suddenly become a brain cell. However, new findings by researchers at UC Santa Barbara have identified a method for changing one cell type into another in a process called forced transdifferentiation.

With C. elegans as the animal model, lead author Misty Riddle, a Ph.D. student in the Rothman Lab, used transcription factor ELT-7 to change the roundworm's pharynx cells into intestine cells in a single-step process. Every cell has the genetic potential to become any kind of cell. However, the cell's history and the signals it receives changes the transcription factors it contains and thus determines what kind of cell it will become. A transcription factor is a protein that causes genes to turn on.

"This discovery is quite surprising because it was previously thought that only early embryonic cells could be coaxed into changing their identity this readily," Riddle said. "The committed cells that we switched are completely remodeled and reprogrammed in every way that we tested."

Switching one cell type into another to replace lost or damaged tissue is a major focus of regenerative medicine. The stumbling block is that cells are very resistant to changing their identity once they've committed to a specific kind.

"Our discovery means it may become possible to create a tissue or organ of one type directly out of one of another type," says Joel Rothman, professor in UCSB's Department of Molecular, Cellular and Developmental Biology, who heads the lab.

Riddle and her colleagues challenged all C. elegans cells to make the switch to intestine, but only the pharynx cells were able to do this. "We asked skin cells, muscles, neurons to modify but found that only the cells in the pharynx were able to transform," Riddle explained. "So this brings up some big questions. Why aren't other cells changing their identities? What is so special about the cells in the pharynx that allows them to change their identity into intestine?

"Since C. elegans is such an incredible model system we can really tackle these questions," she continued. "By knocking down certain genes and manipulating the animal, we can begin to better understand the conditions under which skin cells and muscles cells might change their identities. That will help us understand what is special about the cells in the pharynx."

Previous studies in the Rothman lab revealed the cascade of transcription factors required for the proper development of the C. elegans intestine. Used in the later stage of intestine development, ELT-7 continues to be expressed for the life of the animal and has important functions not only in gut development but also in gut function.

This study is revolutionary in that researchers have clearly demonstrated that cells are not limited to their original identities. "Think of them as different rooms in a house," Riddle said.

"Like cells, different rooms in your house have different structures and functions. Changing the function of a room is likely to be easier if the structures are similar, say, turning a bedroom into a living room or vice versa. But changing the bathroom into a living room presents a bigger challenge," Riddle explained. "Just as some rooms in a house are more easily converted to others, some cell types may be more easily coaxed into changing their identity to another specific type. This doesn't seem to depend on the relatedness of the cells in terms of when they were born or how closely related they are in their lineage."

Maybe the heart cell can become a brain cell after all.

As demonstrated by another important discovery in the UCSB study, the cells reshaped themselves in a continuous process; there were stages in the remodeling process during which the identity of the cell was mixed. "Going back to the home remodeling example," Riddle said, "the couch and television were added to the bedroom before the bed and dresser were removed."

"The important key of our discovery is that we have observed cells undergoing a process of morphing in which one specialized cell type is converted into another of an entirely different type," Rothman said. "This means that it may be possible to turn any cell into any other cell in a direct conversion. In terms of our understanding of biological constraints over cell identity, we've shown a barrier that we believed absolutely prevents cells from switching their identity does not exist. It may one day be possible to switch an entire organ from one kind to another."