Here's a cool "hi-tech" commercial from 1977 of the Sony Betamax system. It's cool to see how much we've gone forward in 30 years. Probably the best invention in this time was and is the Internet, and will be until someone finds a cure for cancer or AIDS. Until then, enjoy this 1977 Sony Betamax Commercial.

This video clip shows how an infrared x-ray machine can work, without the actual harmful effects of x-rays (like cancer also known as mesothelioma to some). An Infrared X-ray Machine displays your vessels and muscle directly on top of your skin by just moving your body under the beam. Enjoy this cool video clip.

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).

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.

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.

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.

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 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. "

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!

Three hours of jogging or 13 of walking per week: according to a U.S. study moderate exercise reduces the risk of breast cancer Being fit, as we know, is not only an aesthetic issue. And now it seems that it is also useful for the prevention of breast cancer. A study of about 65,000 women by researchers at Washington University School of Medicine in St.. Louis and from Harvard University in Boston, just published in Journal of the National Cancer Institute, points out that women practicing sports have a 23 per cent lower risk of developing cancer before the menopause. In particular, it may be important to regularly exercise between the ages of 12 and 22 years. "We have prevention strategies for breast cancer pre-menopausal, but our research shows that physical activity during adolescence and youth, between 12 and 35 years, may be important in the long term reduction of the risk of cancer", said Graham Colditz, professor of Prevention and Control and co-director at the Siteman Cancer Center, Washington University School of Medicine and Barnes-Jewish Hospital. "This is just one more reason to encourage young women to exercise regularly."

At the Ifom-Ieo Campus, a study began on the operation of a molecule which opens new avenues of research for less toxic treatments in chemotherapie. The study in Cell magazine. Developing new chemotherapies able to kill cancer cells without harming healthy ones: This is the goal that's still far away but we can see the light. Thanks to an international study to which has substantially contributed a team of Campus Ifom-Ieo (Foundation Institute of Molecular Oncology - European Institute of Oncology) in Milan, in fact, it was possible to identify a molecule - called Ndc80 - which could be the ideal target of new chemotherapeutic drugs, because it's active only when the cell reproduces (mitosis). The research, led by Andrea Musacchio in collaboration with Peter De Wulf, was published in the journal Cell. One of the problems with current chemotherapies is that, in addition to attacking the cancer cells, in part it also kills healthy cells. This is because the drugs (for example, taxolo) affect proteins that, although mostly engaged in the process of cell proliferation (typical of tumor masses), they are also involved in other processes with other cells that are not sick. A molecule found only in reproducing cells would be the ideal target.

Three studies have demonstrated for the first time a genetic cause for this type of cancer. Perhaps also responsible for nicotine dependence A gene variation on a region of chromosome 15 is related to the risk of developing lung cancer. At this same result came three independent studies, two published in Nature and one in Nature Genetics, and is the first time that there is a genetic cause for lung cancer, in addition to environmental factors among them, of course, smoking. Between cancer and smoking is perhaps the most obvious cause-effect relationship in epidemiology. And here lies the point: a region of chromosome contains objected to three genes which in turn contain the instructions to produce a very particular protein: the nicotinic receptor for acetylcholine. As the name implies, this receptor has a strong affinity for nicotine and a change in its structure could cause cancer in itself and, affect dependence on smoking (according to the second one of the three studies)

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.

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.

A study analysis conducted over the past 27 years by British researchers, suggests that some Fans can reduce the risk of developing cancer. A review of studies published over the last 27 years suggests that the anti-inflammatory non-steroidal pharmacy drugs (Fans) such as aspirin could reduce the risk of breast cancer by as much as 20 per cent! In support, some experts of Guy's Hospital in London appeared in a publication of International Journal of Clinical Practice. According to Ian Fentiman, Fans could play an important role not only in prevention, but also as a therapy for women who have developed this type of cancer, combining their use with a hormonal treatment and using them as analgesics.