Well, smoking is not good for your health, but you already know that. However, if you'll be smoking anyway, then it could be an opportuniy to learn some very cool tricks. For example, this guy has some amazing skills, and it's a miracle that he didn't yet light his hair on fire! Enjoy the show!

Well, if you're like me, you don't. But some Asian cultures have insects on their regular menus. And it gets me thinking...if they taste like chicken (like you hear), and they are good for your health (virtually no fat, only proteins), why do we prefer Big Macs and other types of unhealthy foods?

A tree can have a pretty negative impact on your health. That is, if it hits you when falling. Proof of concept, is this video, where 2 dudes try to down a tree. Unfortunately for them, the tree fought back hard

If you've watched the movie "Super size me" then you know what McDonald's food can do to a human in a month of non-stop eating. Further proof of this is this video, in which the Frech fires don't seem to wanna decompose! It's amazing!

The particles of cobalt-chromium can cause DNA damage even if they do not come physically into contact with the cells. The nano-particles manage to damage the DNA of cells protected by a barrier made up of cellular membranes, without physically entering into contact with the cell, but rather through a multitude of chemical signals. This was found in a study coordinated at the Bristol Implant Research Center, proving that it brings out a new risk associated with nanotechnology, but also the opportunity to exploit this behavior in an innovative way. Nano-particles are now widely used. In surgery, for example, are an integral part of prostheses and implants. The research conducted so far on the risks of nanoparticles, however, relates mainly to the effects of direct exposure, while very little is known about what can cause the indirect exposure. In the new study, researchers have wondered if a barrier device was able to protect cells from the effects of nano-particles consisting of chromium and cobalt in the tissues of the clothes and orthopedic implants. The researchers interposed a barrier between nanoparticles formed out of multilayer chromium-cobalt (in quantities thousands of times greater than those with whom we come in contact normally) and a culture of human fibroblasts (connective tissue cells). Although nano-particles have not managed to cross the membrane, the fibroblasts had DNA mutations which were ten times more than the control fibroblasts. According to scholars, the effect is due to chemical signals between the cell membrane and fibroblasts. If the lines of communication between them are broken, the rate of DNA damage returned to normal.

This study researched killing cancer cells with nano-magnets, with the same principle as a microwave oven. The study of nano-particles applied to biomedicine continues to give interesting results, as research is still in its infancy. Through their work, the chemists from the university of Cagliari are now investigating some of the possibilities opened by this field. One is to use magnetic particles to convey the drugs only to the diseased cells, the other is to drive up the tumor and then force them to oscillate under the control of a variable magnetic field, thereby heating the target cells, just like a microwave oven does with the water molecules contained in food. This second mechanism exploits hyperthermia. It appears that cancer cells can be destroyed by beeing brought to a temperature of 42.5 degrees Celsius for about half an hour. In order arrive at the place desired, the particles must be incorporated into liposomes, hollow microspheres formed by lipid bilayers (for which reason they are called "magneto-liposomes"), which are able to overcome the barrier of cells. They must have a diameter of about 20 nanometers. Larger could indeed block blood vessels, while smaller particles may be "eaten" by macrophage cells which are in charge with the elimination of foreign bodies. Currently, the research team is working on the synthesis of particles and study of their structural and magnetic properties. Currently these are being built in oxide of iron or iron cobalt. The latter are more manoeuvrable, because their magnetic properties depend strongly on the direction along which the field is applied to (property known as magnetic anisotropy).

Can we act on stopping the process of infection, without the risk to develop strains resistant to antibiotics ? Small molecules that interrupt the chemical signals by which bacteria communicates by blocking the process of infection have been identified. The discovery, published in Molecular Cell, as well as representing a new option in the treatment of infections, reduces the risk of growth of bacteria strains resistant to antibiotics. Bacteria will exchange information with a system of intercellular communication, called quorum sensing, which allows them to perceive and respond to changes in density and to coordinate actions of the group. As soon as the conditions are favorable to population growth, for example if they are within a host, the bacteria sends chemical signals to molecules that bind to receptors inside: LuxR-type proteins or proteins of the type LuxN, located on membrane of each cell. In this way the infection proceeds without hitches. " Blocking the communications of the enemy has always been a winning weapon. The researchers searched the key to succeeding, and found in an old acquaintance. In a previous study Bassler and colleagues had discovered that a class of molecules called lactose acilomoserina (AHL), is able to compete with the signals acting on LuxN proteins, preventing them from binding to the receptor. In the recent study, researchers have realized that the AHL can also bind to proteins of the LuxR type. In this way was brought into light the AHL the ability to bind to both receptors, although the two proteins have two completely different structure and location mechanisms.

Cancer threatens the conservation of some wild species because it represents one of the top causes of death. This was also recently featured on the Discovery Channel. Cancer affects some animals with the same effect as in human beings, and could be the cause of extinction of some wild species. The researchers say the Society of Preservation of Fauna and Flora of New York have found an increase in cancer cases in wild animals in recent years. According to their findings, published in Nature Reviews Cancer, the species most affected are those at risk of extinction, like the Tasmanian devil, a small marsupial carnivore, already decimated in the late nineties by a rare form of transmissible cancer (the devil facial tumor). The cause is unknown, but it has been shown that malignant cells are able to spread among the samples and through bites during fights. To save the species, biologists are now isolating infected animals in zoos or reserves. Denise McAloose and Alisa Newton, authors of the study, have investigated the possible causes of cancer in different species, and have found a correlation between cancer and pollution. For example, for the living beluga in the estuary of the St. Lawrence River (Canada), a form of bowel cancer is the second leading cause of death. The culprit could be an organic compound (a polycyclic aromatic hydrocarbon that is found in oil, but also in municipal waste), already known to be carcinogenic for our species.

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.

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.

The habitual consumption of alcohol reduces the size of brain mass. This suggests a study in Neurology magazine. The more we drink, the more our brains will decrease. To suggest this is a report of Wellesley College, Massachusetts, published in the journal Archives of Neurology (a publication of Jama) and this week the American Academy of Neurology. We know that the volume of the brain decreases with age (about 1.9 percent every ten years). This physiological reduction is accompanied by an increase in white matter lesions and both factors - reminiscent of the authors - are related to cognitive problems like memory. While some scholars have suggested a possible positive effect of alcohol on reducing the normal volume of brain mass, this new study suggests just the opposite. Data was collected on a sample of over 1,800 individuals aged between 55 and 64 years, most consumers of alcohol or ex-drinkers, which carried out magnetic resonance (participants in the Framingham Offspring fall Study, a study of the cardiovascular problems started in 1971, for which it was collected information on weekly consumption of alcohol, sex, body mass index and other physiological parameters). The results show that there is a significant correlation between alcohol intake and reduction of brain volume, especially in women which usually consume less alcohol than men.

Npas4: This protein regulates the formation of inhibitory synapses between neurons. The inhibitory activity of neurons is regulated by a particular switch. This is a protein involved in the formation and maintenance of synapses in regulating selectively switching the electrical signal between nerve cells. Its name is Npas4 and was discovered by researchers from the Children's Hospital in Boston this week to publish their study in Nature. In particular, the protein in question is a transcription factor, that is a molecule that can activate or deactivate specific genes. Those which would be linked to Npas4 are more than 270. When the protein is produced in large quantities, we are seeing an increase in the number of inhibitory synapses on the surface of nerve cells. But what induces the production of high levels of Npas4? According to the researchers this is a reaction to excitatory synaptic. "It is as if the same excitement triggers a program to rebalance the brain with inhibition," says Michael Greenberg, coordinator of the study, which continues: "The mice in which the protein is suppressed, in fact, have neurological problems: are anxious, hyperactive and more subject to seizures. " The discovery could help researchers in studying these disorders. Inhibition, in fact, plays an important role in brain development.

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.

The mutation of the gene Alk would be responsible for inherited forms of cancer. Neuroblastoma is a childhood cancer more widespread and aggressive: it attacks the autonomic nervous system during development, forming frequently in tumor masses or into the chest. A study, published in Nature and coordinated by the Children Hospital of Philadelphia (USA), indicates that mutations in the gene anaplastic lymphoma kinase (Alk) would be responsible for inherited forms of the disease. The international group of researchers, including some of the Italian Institute for Cancer Research in Genoa, have collected genetic information of 20 families where the disease was presented in more than one occasion, by analyzing the DNA of 176 people ( of which 49 with neuroblastoma). Eight families, in which at least three individuals suffering from the disease were closely analyzed, possessed the changed Alk gene. The normal role of this gene, which expresses a transmembrane receptor, is not yet understood in depth but, according to previous studies, its alterations increase the risk of developing lymphoma or lung cancer.

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. "

The ventral striatum, a part of the brain already known to be associated with rewards and unexpected stimuli, is the center of our desire for adventure. The research in Neuron. A group of researchers from the Wellcome Trust Centre for Neuroimaging at the University College of London has identified the area of the brain directly linked to our desire for adventure. Or, more precisely, our propensity to live new experiences and to experience what we do not know. For the study, published in Neuron, researchers have developed a test: the participants were presented a series of images associated with different sums of money put into a premium, and were asked to guess which of the sums was higher. Although the volunteers easily could identify the image associated with richer rewards, when it was introduced a new figure, all of them tended to choose the latter rather than those already known with secure profits. Through magnetic resonance imaging, neuroscientists have noticed that the area of the ventral Striatum (an area of the brain already known to be associated to receive a reward and unexpected stimuli) was particularly active when participants opted for the novelty.

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.

For the first time a molecule of genetic material was observed in real time, that is able to correct damage in its structure The repair of a damaged DNA molecules is a mechanism well known in genetics, but so far no one had given testimony in real time. Researchers of the Kavli Institute at the University of Delft, the Netherlands, were able to document at the level of a single molecule of DNA, the homologous recombination, one of the mechanisms of repair frequently put in place by the cells. The work was published in the journal Molecular Cell. The rupture of the molecule of DNA can be caused, for example, from ultraviolet rays or X-ray, but it can also happen during normal cell division. The type of damage can affect a part of the structure internal molecules, but the cells are equipped with various mechanisms to repair it. If these damages were not immediately corrected, they could lead to changes in functional levels!

An experimental study opens a way for gene therapy as a possible treatment for cases that do not respond to medicines in cases of Epilepsy. Research on Brain. Almost one third of people suffering from epilepsy don't respond to prescription drugs. To date, the only possibility for many of them is to undergo an operation to remove the area affected by the disease in the brain, but an alternative to surgery could rise by gene therapy. An experimental study of the Department of Neuroscience of Mario Negri in Milan, led by Noah, has shown that it is possible to induce the sick cells to produce a protein with anticonvulsant properties. And what this substance does is significantly reduces the recurrence of seizures. The research, conducted in collaboration with international groups led by Gunther Sperk University of Innsbruck (Austria), Asla Pitkanen University of Kuopio (Finland), and Matthew During dell'Ohio State University (USA), was just published on Brain magazine.