For the first time a gene was identified that allows the repair of damaged nerves in nematodes. The study is from Science Express. A gene that can stimulate the growth of nerve cells was first identified by researchers at the University of Utah (USA), thanks to cutting-edge experimental techniques and a huge genetic screening on a nematode (cylindrical or worm). The neurons, which in the embrio are able to regenerate, in adults have their capacity to "repair" reduced or absent. In other words, damage to the central nervous system (brain or spinal cord) and its consequences - paralysis, loss or reduction of cognitive faculties - are permanent. "In the past molecules have been identified that can inhibit the growth of neurons in different organisms," says the coordinator of research Michael Bastiani, "but their removal in the laboratory had no effect. That is why we went to look for those genes that can stimulate rather than inhibit, the regeneration of nerve. " Taking as a experimental model flat worms (Caenorhabditis elegans), biologists have searched for the genes that trigger the regrowth of motor (neurons that "command" voluntary muscles): in practice, with an experimental technique called RNA interference to "shut down ", one by one, 5000 on 20,000 genes in the DNA of worms (genes similar are also present in humans). The analysis led to the identification of dlk-1, which appears to play a key role in the regeneration of nerve tissue, and three other genes responsible for the formation of axons (parts of the neuron that conduct electrical signal). The researchers found that in nematodes, the gene dlk-1 not only triggers a chain of events known as "Map kinase" behind the growth of neurons, but also that their regeneration can be increased or decreased by stimulating the gene to produce amounts more or less high of the protein dlk-1.

The molecule slows the proliferation of tumor cells while giving the time needed to repair the damage to their DNA. The discovery, made by Italian researchers IEA, is published in Nature. The secret of immortality of cancer stem cells - those that feed it and cause relapses because they're immune to chemotherapy - was unveiled. Their strength is the p21 protein that slows the proliferation, giving them the time needed to repair damage to DNA. In practice, it is as if these cells were able to rejuvenate indefinitely: no age, and thus do not die. By blocking the production of p21, however, you can make them vulnerable and hit the tumor at the root. The research was conducted in the laboratories of the European Institute of Oncology (IFOM-IEO) in collaboration with the universities of Milan and Perugia, and was published this week in Nature. The cells age and die because they accumulate damage and mistakes borne of DNA during cell divisions. To understand why this does not happen in a cancerous stem cell, the researchers observed what happens to a staminale "normal" when you alter one of the genes (oncogenes) that cause cancer (in this case, the acute myeloid leukemia). The study revealed that oncogenes stimulate the activity of another gene, called p21, and thus the production of the corresponding protein, whose effect is to slow the proliferation. In essence, these cells have much more time to repair other damaged DNA, and remain young and active, immune to chemotherapy drugs because they recognize and affect only the cells in rapid proliferation.

By comparing DNA of healthy and cancerous tissue of a single person, there were discovered eight new mutations linked to the disease. The study in Nature The complete genome of a person suffering from cancer was decoded for the first time. The comparison between the DNA of normal and cancerous tissue of a woman suffering from acute myeloid leukemia (AML) has identified ten mutations in the genome of cancer cells, including eight so far unknown, which would be linked to the disease. Researchers of the Washington University School of Medicine (USA), coordinated by Richard K. Wilson, presented their findings in Nature. Scientists have taken a sample of tissue from normal skin and a tumor tissue from bone marrow to a patient suffering from AML - cancer that affects the bone marrow cells that produce red blood cells. Subsequently they have decoded the DNA of the two tissues, comparing all three billion bases of which the genomes were composed, to go back to differences in disease characteristics of the individual. There were ten mutations identified, two already known, eight first ever linked to the disease. Of those, three were found in genes that normally can block the growth of tumors (for example in Ptprt, the tyrosine phosphatase gene, often altered in colon cancer). Four changes instead involved genes regulate the molecular pathways that promote tumor development - particularly in a family of genes, usually expressed in embryonic stem cells, which could stimulate cell renewal. A final disturbing deterioration instead of transporting drugs into the cell. According to scientists, these mutations have occurred one after another, each adding something new to the tumor.

To isolate individual cells of the immune system and study the interaction in order to improve the treatment of cancer. At this will serve the new biosensor prototype developed under the project Cochise (Cell-On-CHIp bioSEnsor), supported by the European Union and coordinated by Roberto Guerrieri, professor of Electronics at the Faculty of Engineering, University of Bologna . The biological approach used to treat cancer patients consisting of interferon, interleukin-2 or other factors stimulating the growth of different cell types and able to reinforce the natural defenses of the body. But these substances are not always well tolerated. An alternative approach is to identify the immune cells able to fight cancer, cultivate them in vitro and then re-introduce them in the body. But here the problem lies in identifying and in isolating the small number of cells that are selectively able to fight cancer. The objective of the project Cochise (which is intended to last three years), is to develop a new class of biosensors capable of isolating cells (not more than 1 in 10 thousand) that are actually effective in fighting cancer cells . As the first objective was developed a prototype, used to demonstrate the possibility of controlling the flow of two individual cells and putting them in a display where you can study the interaction.

A new technique, developed in the laboratories of the Foundation San Raffaele Biomedical Park, facilitates the process of regeneration of muscle tissue. Stem cells, modified at the level of genes, could permit the recovery of tissue degenerated from Duchenne muscular dystrophy (Dmd), even when the disease is in an advanced stage. This is a further step towards developing a therapy, which is being developed for some years by researchers of the Foundation San Raffaele Biomedical Park of Castel Romano, coordinated by Giulio Cossu, University of Milan. The research, published in Nature Medicine, was conducted by Cesare Gargioli and Marcello Coletta, along with Fabrizio de Grandis and Stefano Cannata at the Roman Tor Vergata. From previous studies and experiments on animal models it is known that mesangioblasti, stem cells normally associated with blood vessels, are able to spread easily and merge with and into the muscle tissue regenerating it (cell therapy). In advanced stages, however, this treatment had so far proven ineffective because of difficulties to penetrate between the muscle fibers. The degeneration, in fact, is accompanied by a process of inflammation followed by scarring tissue that impedes the provision of blood (and thus oxygen) to the muscles. Therefore, the muscle fibers are replaced with fatty tissue. To overcome the obstacle, the researchers genetically modified cells derived from the tendons (fibroblasts) so as to make them express the protein metalloproteasi 9 (Mmp9), a molecule that can degrade collagen that accumulates between fibres degeneration.

A study explains how a yeast cell becomes cancerous: the fault is a chromosomal translocation An altering of the genome that causes cancer was finally detected and reproduced in the laboratory. The discovery, crucial for understanding the genesis and development of malignancies, is due to the geneticist Charles V. Bruschi, head of the Laboratory of Molecular Genetics of yeast, International Centre for Genetic Engineering and Biotechnology in Trieste (Icgeb) and coordinator of the Society of Italian scientific yeast (Zymi). Together with his group, Bruschi has uncovered, that the so-called chromosomal translocation is at fault. The yeast cells, whose DNA was sequenced completely in 1996, are a good model because they possess many similarities with mammalian cells and are easily manipulated by genetic engineering. Thanks to technical Bit (Bridge-Induced Translocation), designed by Bruschi and Valentina Tosato in 2005, it was possible to artificially induce the translocation and demonstrate the crucial role of this phenomenon in the formation of cancer. "Although it has long been a correlation between the presence of chromosomal translocations and the appearance of cancer cells," explains Bruschi, "so far it was not clear whether a translocation was the origin of cancer or whether, instead, it was a consequence. This is because we see patients when the cancer has already formed and in the cells already exists a particular translocation. In practice, these observations are made when it is too late to establish a relationship of cause and effect. "

A newly discovered molecule, Isx-9, is able to make stem cells mature into brain cells. The study in Nature Chemical Biology They came across this behavior, while they were stimulating stem cells to give rise to cardiac cells, when researchers from the Southwestern Medical Center at the University of Texas at Dallas, have discovered that some of the molecules tested have matured however into neural cells. Completely random, therefore, this lead to the isolation of Isx-9, the most powerful among the compounds tested, capable, at very low concentrations, to create differentiated neurons. The study, conducted by researchers led by Jay Schneider and Jenny Hsieh was published on the number of Nature Chemical Biology. Scientists began testing 147 thousand molecules for the project in order to isolate those who could stimulate embryonic stem cells to differentiate into cardiac cells. Stunningly, American researchers have noted that five of these compounds caused the stem to rise to neurons. One of these molecules was selected because it was acting to lower concentrations of the other and was more soluble in water. This, has given life to the compound Isx-9 that has been tested on neural stem cells from the brain, particularly those of the hippo campus of laboratory animals. In the test tube, the stem, under the action of Isx-9, could form the clusters and develop the first steps towards the formation of neurons.

An Italian research published on Plos One identified, in rabbits, some areas where neurons grow as from adult tissue A new Italian study has identified in the cerebellum of rabbits some areas in which nerve cells grow from adult tissue, demonstrating that repairing damaged to the brain - in theory - is not impossible. The discovery, fifteen years ago, that even the central nervous system of adult mammals can form new neurons has been a cornerstone of neuroscience and distorting the previous belief that neurogenesis occurs in this animal class, once and for all, during development embryonic, without the possibility of repair after birth. Unlike other vertebrates, in which this process occurs post-natal widely in the brain, in mammals seems limited to a few specific areas.

Cloned cells were transplanted into the brain of mice who suffered from this disease and they replaced sick neurons. The success of therapeutic cloning in mice. Researchers of the Sloan-Kettering Institute in New York, led by neuro-scientist Lorenz Studer, have treated the guinea pigs suffering from Parkinson with the transplantation of embryonic stem cells obtained from the skin of rodents themselves sick. The experiment, described in Nature Medicine, not only has recorded cases of rejection, but also significant improvements in the evolution of clinical pathology. The group Studer - after having caused lesions in the brains of mice that would determine the same effects of Parkinson's disease - has transferred the nuclei of cells inside the tail skin cell mouse egg "emptied" of its nucleus, through the technique known as therapeutic cloning (or Scnt, Somatic Cell Nuclear Transfer). The cloned cells, cultivated, were then developed into blastocysts. The researchers thus generated 187 lines of embryonic stem cells from 24 different mice, most of which later differentiate into neurons capable of producing dopamine.

Satb1 controls the expression of genes that control the growth of tumour mass and the formation of metastases. The discovery in Nature magazine. It is a protein the cause of the aggressiveness of breast cancer. It's called Satb1 and was already known to scientists involved because expression of T cells of the immune system. Only now it has revealed its darkest side, showing that they play a key role in the malignant form of breast cancer. Metastases, which are formed when cells are adding themselves to the tumour to invade tissues nearby and colonize other parts of the body, represent the advanced stage of the disease. Researchers have now discovered that the cells of the breast cancer need their protein Satb1 to become metastatic. The study has just been published in Nature.

The procedural memory remains imprinted in the chemical synapses. It is not the merit of a cell constant. When we drive a car or we tie a shoe knot, we store a series of gestures that are accessed faster and automatically whenever you need that action again. It is the so-called working memory or procedural memory, whose operation resembles that of cache memory of a computer, for example, allows us to more quickly open a website already visited. A study conducted by Gianluigi Mongillo of French Cnrs research, and Omri Barak and Misha Tsodyks the Weizmann Institute (Israel) would seem to refute the widespread belief that this type of memory is fixed thanks to a number of specific neurons. On the contrary, the procedural memory is recorded at the level of chemical changes in cells that remain after the transition pressure in nervous synapses (points of contact and communication between neurons).

Infm-Cnr and Federico II University have developed a technique ultra-miniaturized to study the behavior of red blood cells. In the film "Fantastic Journey" of 1966, to study the physiology of the human body some scientists were miniaturized and were injected with their micro-bus, in the bloodstream. Today is, in a sense, the opposite: to understand the behavior of red blood cells reproduces the circulatory network on a device the size of a chip. The device has been developed by researchers of the center Coherentia at the National Institute for Physics of Matter (Infm-Cnr) and the Department of Chemical Engineering University Federico II of Naples. Their results were presented today at the conference "The research ideas to work" in the Corsican town.