This creepy looking robot is Simroid which translates as Pain Girl. This high-tech robot simulates a dental patient complete with pain noises and cavities. Of course, she is controlled by a human, which gives it the chooses the proper responses from a multitude of possibilities. Creepy stuff

Italian researcher Alessandra Luchini wins the first edition of "The Prize Award” with a paper of a system to identify those molecules that signal the presence of a tumor (tumor markers) that are beyond the traditional methods of investigation. To do this requires making a hydrogel containing certain microscopic nano-spheres that once inserted in the samples of blood taken for analysis diagnostic trap some markers and protect them from deterioration. "These nano-spheres, made of the same plastic as hydrated soft contact lenses are equipped with special molecules that, once in the blood, snap-specific tumor markers and incorporate them. In this way, they protect them from enzymes that would otherwise deteriorate them. Usually blood tests fail to identify precisely because these markers are destroyed prematurely, " says researcher Alessandra Luchini. "The beauty of this system," says the researcher, "is that it does not need very sophisticated tools, which is simple and economical: with one hundred U.S. dollars we can make nano-spheres for more than two hundred patients." The new method is not going to replace the standard, but acts at a stage prior to analysis by providing a better quality.

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 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 study conducted by an Italian and published on Pnas shows that healthy cells, if required to "diet", have an increased resistance to stress caused by the drugs compared with those ill. Fasting can be a weapon against the heavy effects of chemotherapy. Just as the fight against cancer concentrates its efforts on the so-called magic bullets, drugs capable of selectively target diseased cells from laboratories of the University of Southern California shows a new paradigm: protect healthy cells and then go furiously only against those sick . A team led by biologist Italian Valter Longo, which involved the United States laboratories and the hospital Gaslini of Genoa, has discovered a kind of magic screen that healthy cells (as a result of caloric restriction) have as a defense against chemotherapy. The results of the study appeared on Pnas Early Edition (here a link to the video.)

Robo4, present in the cells of the blood vessel wall, may improve or prevent the consequences of eye diseases The age-related ocular degeneration is the leading cause of blindness in people over 65 years old, and retinopathy lead to total loss of sight in most of the patients of diabetes, about 21 million in the world. In particular, the degeneration and the destabilization of the vessel wall causes many times a loss of liquid and, consequently, severe inflammation that can lead to blindness. A new protein, named Robo4, identified in cells in the wall of blood vessels, may prevent these anomalies and help reduce or even prevent various vascular diseases related to an increase. The study, conducted by Dean Li and colleagues at the University of Utah, in the United States, was published in Nature.

Muliple mutations of a single gene lead to the accumulation of a protein in motor neurons that causes death. Mutations in a single gene could be the basis of amyotrophic lateral sclerosis (Sla), the neurodegenerative disease that leads to progressive paralysis and that affects every year in Italy 1,500 people, mainly men of average or advanced age. The discovery, the result of years of studies conducted by international team in which the names of Emanuele Buratti Baralle Francisco and the International Centre for Genetic Engineering and Biotechnology (Icgeb) in Trieste, and guided by Christopher Shaw of King College London, appeared in Science.