New risk calculator can evaluate the risk of developing a psychosis of the individual

New risk calculator can evaluate the risk of developing a psychosis of the individual -

A new risk calculator can predict the risk of developing psychotic disorders such as schizophrenia of an individual, according to a new study published today in the American Journal of Psychiatry . The research involved collaborators from nine sites, including Beth Israel Deaconess Medical Center (BIDMC) and may help researchers test treatments to prevent the onset of full psychosis.

Psychosis is characterized by hallucinations and delusions. The new calculator assesses the risk of developing a psychosis after experiencing early warning signs of schizophrenia, such as hearing voices of an individual

"Until now, clinicians may give patients only a rough estimate of how their condition may progress. - What about 15 to 25 percent of people who experienced early warning symptoms will be to develop a more serious condition, "said Larry J. Seidman, PhD. D., a psychologist at BIDMC and Professor of psychology at Harvard Medical School. "With this new risk calculator, clinicians can now give patients an individual risk assessment. More specific information allows people to have a more realistic sense of what is happening, which can reduce anxiety. "

In more stressful life events, trauma and family history of . and schizophrenia, the calculator takes into account five factors to determine the risk level of an individual These factors include: age of onset, levels of unusual thought content and suspicious; social functioning; powers verbal learning. and mental processing speed

Seidman and her colleagues analyzed data from interviews with 596 subjects, aged 12 to 35 who were diagnosed with attenuated Psychosis syndrome, a condition in which patients may experience hallucinations and / or develop unusual thoughts but acknowledge their perceptions are not based in reality.

the research team, led by Tyrone Cannon of Yale University, PhD, then developed the risk calculator that analyzes risk factors for schizophrenia. After following with the subjects every six months, the researchers found that 16 percent of patients diagnosed with Attenuated Psychosis Syndrome had converted to psychosis within two years.

The symptoms of unusual thought content and suspicion have contributed most at risk of developing psychosis. A decline in social functioning, less verbal learning and slower processing speed were also important factors. People who were younger (in their teens or early twenties) when their symptoms began, also have an increased risk. Stressful life events, trauma and family history of schizophrenia found to have a lower impact on the risk profile of an individual

"The risk calculator does not account processing or other potentially favorable environmental factors that can reduce the risk. this is a direction for future research, "said Seidman, adding that the power of the computer lies in the development perspective of the symptoms for patients and their families. "Having hallucinations, he is, does not add much weight at all predictive Maybe that person has good cognitive function and has not decreased socially - .. This profile would lead to a good score of treatment can result, potentially with less fear. "

Innovative treatment nanobubble detects and destroys cancer cells in mice

Innovative treatment nanobubble detects and destroys cancer cells in mice -

The innovative technology developed by researchers funded by the NIH was able to find and to facilitate the killing cancer cells in mice without harming surrounding healthy tissue. A treatment using this technology in humans could reduce the cancer recurrence rate or metastasis.

The cancer cells that can not be removed by surgeons often cause tumors to metastasize or return. In a study published in Nature Nanotechnology in February, Dmitri Lapotko, Ph.D., and his team at Rice University (now with Masimo Corporation, CA) describe a new way to fight against these residual cancer cells. In this new approach, the tiny gold particles have specific cancer antibodies attached to their surface, which allow particles to be swallowed up in high concentrations and cluster only in cancer cells. These gold clusters, when exposed to a short wide laser pulse, heat and the surrounding liquid evaporation, producing a "nanobubble plasmon." This nanobubble produced a "pop sound" that reveals the cancer cell and causes an explosion that destroyed from within

The researchers examined gold nanoparticles to treat cancer in the past, but the particles were missing specificity. they were unable to differentiate between healthy cells and cancer cells. Lapotko and his team are the fight against this problem by combining the use of gold particles coated with antibodies to the nanobubbles generation created with a short laser pulse.

The gold particles can be injected prior to surgery so they can go to and gather in cancer cells. After a tumor is removed in surgery, laser (near infrared) energy pulse is weak, that can move safely through a centimeter of fabric is applied. The laser pulse does not cause the damage induced in nanobubble remaining cancer cells with gold particles and which are only destroyed. This unique approach may be able to reduce the amount of unintentional damage done to the patient, especially if the tumor is located in a sensitive area like the brain, head and neck, breast or prostate cancer.

"This is a creative and innovative approach that combines an understanding of heat transfer basic biophysics with exquisite specificity and chemistry of targeting antibodies," said Rosemarie Hunziker, director of the tissue engineering program the NIBIB. "This could become a powerful tool in our arsenal to fight against cancer."

When surgeons have injected these gold particles to mice with cancer before surgery, initial results have been impressive. While 80% of operated mice group that did not receive the treatment of gold particles died due to tumors returning within 10 days after surgery, none of the mice that received tumor regrew treatment nanobubble further in the next two months.

researchers hope to begin clinical trials in humans in the coming years.

UCLA researchers develop a new combination therapy to activate the immune response against glioblastoma

UCLA researchers develop a new combination therapy to activate the immune response against glioblastoma -

UCLA researchers have developed a revolutionary new combination treatment that uses a vaccine to activate a response immune against advanced brain tumors. The therapy uses an antibody blockade to prevent cancer of the brain to protect the patient's own immune cells so they can recognize the brain tumor and attack it.

The diagnosis of glioblastoma multiforme (GBM) is associated with an extremely poor prognosis in most people with the disease. median survival is estimated that follows traditional treatments, such as surgery, radiotherapy and chemotherapy, is generally 14 to 18 months.

The new results are published online in the journal JCI Insight.

The new three-year study led by Drs. Robert Prins, Linda Liau and Timothy Cloughesy, all members of UCLA Jonsson Comprehensive Cancer Center, showed for the first time a vaccine to dendritic cell, in combination with the antibody blockage of a cell surface receptor immune known as PD-1 of the name, produces a more effective response immune response against GBM beyond the use of either treatment alone.

"These results are the first to accurately describe the mechanism by which an effective immune response can be seen in tumors in the brain," said Prins, an associate professor in the Department of Neurosurgery at UCLA . "We found that the effective anti-tumor immunity for glioblastoma must have a significant infiltration of killer T cells and blockaded major checkpoint axes that make these killer T dysfunctional cells within the tumor."

Prins and his team added that the combined treatment is effective to remind the immune system that the WBG is a foreign invader, which essentially prevents brain cancer to recur or more.

administration PD1 / PD-L1 antibody blockade alone may not be successful in glioblastomas that do not have a significant infiltration of T cell vaccination of dendritic cells allows the infiltration of cells in brain tumors T, while the PD-1 (mAb) antibody blockade removes the shield of active tumor to hide from the immune system.

The methodology differs from previous research in metastatic melanoma cancer and non-small cell lung cancer because it shows that activation of an immune response using vaccination of dendritic cells may be necessary in tumors that do not respond to / PD-L1 checkpoint inhibitors only one PD.

the next step of the research is to understand how the signaling mechanism of the PD-1 pathway / PDL1 integrated into other potential means of immune suppression are currently being investigated.

Scientists reveal how common asymptomatic condition can develop in the myeloma

Scientists reveal how common asymptomatic condition can develop in the myeloma -

Researchers from Birmingham University and hospitals across the West Midlands revealed how a condition asymptomatic town can develop myeloma blood cancer.

They found that changes in the bone marrow needed for the cancer to grow have already taken root in the previous condition, raising the possibility that early medical intervention could prevent this type of incurable cancer to take root.

research, which was funded by the blood cancer charity Bloodwise, is published today in the journal leukemia .

Myeloma affects the plasma cells, a type of white blood cell that originates in the bone marrow. Diagnosed in more than 4,000 people a year in the UK, less than half of patients survive more than five years after diagnosis. Symptoms often include debilitating and painful bone damage, anemia and nausea

Myeloma almost always progresses in a seemingly benign condition called "MGUS", which is especially common in the elderly -. As much as 7% of people aged over 85 have MGUS. Only about one in 100 patients with MGUS develop myeloma each year and there is currently no way to accurately predict which patients do and when.

Myeloma will spread to other organs, suggesting that the myeloma cells depend on the support of other cells in the bone marrow environment to survive. The researchers showed that Birmingham early in the development of MGUS, the cells that make up the connective tissue of the bone marrow change their behavior and become more favorable to the growth of cancer. They discovered that a key gene, called "PADI2" becomes particularly overactive in these connective tissue cells, which leads to overproduction of a signaling molecule known as interleukin-6 (IL-6).

conjunctiva release of IL -6 cells in the bone marrow, where it binds to receptors on the surface of malignant plasma cells, asking them to multiply rapidly and to resist cell death signals . It is already known that the presence of elevated levels of IL-6 in bone marrow of the patient significantly reduces the effectiveness of a key chemotherapy drug called bortezomib.

The researchers believe that drugs designed to target the gene PADI2 in MGUS and myeloma patients can significantly reduce the support signaling that myeloma cells are dependent, and can increase the effectiveness of current treatments.

significantly the PADI2 gene has also been linked to the development of other types of cancer, rheumatoid arthritis, Alzheimer's disease and autoimmune disease, and any drug developed could have wider applications beyond myeloma

Dr. Daniel Tennant, who led the research at the University of Birmingham, said :. "It is now clear that the bone marrow of patients with MGUS, traditionally considered a benign condition, is significantly different from that of healthy individuals. Environmental bone marrow in these patients seems to be able to support the growth of cancer even though the majority of patients will not progress to myeloma.. While this research is in the early stages, it offers the exciting possibility that early intervention could delay or even prevent the development of cancer "

Dr Alasdair Rankin, director of research at the blood cancer charity Bloodwise, said: "There is an urgent need for new treatments for myeloma, which, while largely incurable, can have a devastating impact on quality of life. with a population over more, MGUS and myeloma will only become more frequent. drugs designed to eliminate the myeloma support system used to develop could be an effective way to treat the disease, or even prevent completely. "

CNIO study shows pro-inflammatory molecule IL-17A can be a key factor in the development of NASH and HCC

CNIO study shows pro-inflammatory molecule IL-17A can be a key factor in the development of NASH and HCC -

NASH (NASH) is a serious liver conditions above hepatocellular carcinoma (HCC) and is currently incurable. A study in search of the Spanish National Cancer Centre (CNIO) shows that a pro-inflammatory molecule IL-17A, is a key factor in the development of this pathology, and stresses that blocking IL-17A or inhibiting cells that secrete IL-17A with drugs such as digoxin (antiarrhythmic agent) may be useful for preventing NASH in patients predisposed to develop HCC.

HCC is the most aggressive liver tumor and a major cause of morbidity in cancer. Several risk factors have been associated with this cancer and its early stages, but the molecular mechanisms underlying the carcinogenic process remain unclear.

non-alcoholic fatty liver disease (NAFLD), characterized by the accumulation of excessive fat, is prevalent among obese people, patients or people infected with the virus-diabetes, and it is a important risk factor for HCC development. However, all obese people are changing at the most severe form NASH, which has a significant inflammatory component.

"The fat accumulation (steatosis) by itself can not explain the occurrence of NASH. In contrast, inflammation determines the progress and results of the disease, since only 10% 20% of obese patients with fatty liver disease will eventually develop NASH, "said Nabil Djouder, leader of the study. That Djouder and colleagues found that NASH, which is currently incurable, is the result of several "hits" and that "the first step is DNA damage to promote inflammation caused by excess nutrients" .

working with different mouse models, the authors demonstrate in the latest issue of Cancer Cell how excess nutrients stimulate the expression of an oncogene called URI in the liver. URI -which is also upregulated in viral hepatitis- leads to DNA damage in hepatocytes, which triggers systemic inflammation and crosstalk between white adipose tissue and the liver that ends ultimately in NASH.

Where DNA damage occurs in hepatocytes, immune cells infiltrate the liver, especially Th17 cells which release pro-inflammatory molecule IL-17A. This molecule, which is a cytokine induced neutrophil infiltration of adipose tissue which leads to insulin and the release of fatty acids resistance, resulting in non-alcoholic steatohepatitis. "Type 2 diabetes seems to precede NASH and HCC," said Djouder.

The researchers also treated healthy mice with injections of IL-17A and observed how the first signs of NASH appeared after four weeks, which confirms its crucial role in the development of the disease . Moreover, Djouder and his team blocked IL-17A using various methods -antibodies and digoxin among others- and prevented the development of NASH and HCC.

In addition, the URI of expression and IL-17A were positively associated with nonalcoholic stetatohepatitis and HCC in obese, HVB and HCV patients. This finding should pave the way for a new prevention strategy for NASH and HCC in high-risk patients, particularly diabetes or infection with viral hepatitis.

"HCV treatment is a socio-economic challenge of our society that blocking IL-17A [...] with digoxin may provide a cheap and effective prophylaxis for hepatitis B and C infected patients with high risk for NASH and HCC, "concludes the newspaper.

Scientists discover new and unexpected features of collagen

Scientists discover new and unexpected features of collagen -

WHAT: Scientists from the National Institutes of Health show unexpected new details about the fundamental structure of collagen, the most abundant protein in the human body. In laboratory experiments, they showed that collagen once considered inert forms structures that regulate how certain enzymes decompose and reshape the body tissues. The discovery of this regulatory system provides a molecular view of the potential role of physical forces at work in heart disease, cancer, arthritis, and other processes related to the disease, they say. The study appears in the current online issue of Proceedings of the National Academy of Sciences .

Scientists have known for years that collagen remodeling plays an important role in a variety of biological processes ranging from wound healing to cancer growth. In particular, researchers know that collagen is broken down by a certain class of enzymes called matrix metalloproteinases (MMPs), but exactly how they did it remained somewhat of a mystery, until now.

In the NIH study, the scientists isolated individual, collagen fibrils of nanoscale rat tail tendons. They then exposed the fluorescence labeled collagen fibrils human MMP enzymes. Using video microscopy, scientists have followed thousands of enzymes that move along a fibril. Unexpectedly, the scientists observed that the enzymes have preferred to fix in some places along the fibrils, and over time these binding sites moved slowly, or disappeared and reappeared in other positions. These observations revealed collagen fibrils have defects that form spontaneously and heal. In the presence of voltage, such as tendons stretching, defects are probably eliminated, which prevents collagen decomposition enzyme which is responsible for the physical strength, the researchers suggest. In short, they have identified a possible mechanism of the sensitive strain to regulate tissue remodeling.

medical journalist describes slow journey to healing traumatic brain injuries

medical journalist describes slow journey to healing traumatic brain injuries -

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Eleven years in the New England Journal of Medicine, medical journalist Susan Okie, MD, introduced the two readers veterans of the US military who have suffered traumatic brain injuries in Iraq and the challenges they face in the recovery period after return. In the July 14 issue of the NEJM, Okie describes its follow-up interviews with the soldiers, and the slow journey to recovery that continues more than a decade later.

"A visit with [Jason] and Pepper [David] ... Emme. I observed many healing evidence, not only in the way they sound and what they are able to do, but in how they seem to have feelings and dreams, "Okie wrote in the NEJM article medicine and society," long-term Monitoring of TBI. - slow progress in science and recovery "

Okie details the personal journeys of each man through the years and when they did not have health care. It explores how each symptom encountered so often associated with TBI and PTSD: insomnia and nightmares, irritability, depression, guilt and anxiety

The recovery of each man is "slow "- Pepper only received comprehensive TBI evaluation VA. hospital this year - but both continue to make progress, Okie said, and she attributes the resilience of the two men to a common factor

"Although the surgical and medical treatment was crucial to Emme and pepper to departure , close personal relationships have suffered. them during the last decade, "she wrote.

Okie observed that Emme survived a critical distance probably because a longtime friend reached out for him just in time. and she said to Pepper, it seems that marriage and devotion to the family "helped to survive periods of sorrow for what he had lost."

"in men, courage, proud to have served in the military, and loyalty to their comrades were other sources of strength, "she said.