The risk of liver cancer may still exist even after liver viruses are cleaned

The latest study completed by researchers from the US Centers for Disease Control and Prevention (CDC) and Anchorage, Alaska Native Tribal Health Association was published in the Journal Digestive Pharmacology and Therapeutics.

Hepatitis B is infected with a liver by the hepatitis B virus (HBV) caused by the human body into another body fluid from an infected person spread occurs in vivo, such as in the sharing of needles and other injection equipment, mother to child transmission at birth. According to CDC, HBV chronic infection the risk of age-related; 90% of children are infected become chronically infected, compared to only 2-6% of adults as chronic.

Since 1991, when the United States launched a national strategic approach to eliminate hepatitis B virus infection, and for the first time recommended routine vaccination of children, emerging in HBV infection has declined by about 82%. CDC estimates that in 2013, the number of newly infected with hepatitis B virus in the United States is 19,764 people, the highest infection rate of adults, especially men aged between 25-44 years. However, the presence of chronic infection very large number of Americans. CDC estimates that in the United States about 700,000-1,400,000 people have chronic HBV infection die of the disease each year is estimated there are about 2,000-4,000 people.

Development of children are chronically infected with approximately 25% of cases, 15% of adult cases of death from cirrhosis or liver cancer, and in most cases, they did not show symptoms until the occurrence of these serious diseases. Worldwide, about 240 million people suffer from chronic hepatitis B, an estimated 786,000 people each year die from hepatitis B-related liver disease.

In their study, the researchers selected subjects were 1,346 cases of patients with chronic HBV infection from Alaska native, they 1982-- followed up in 2013 between. They chose during follow-up of chronic hepatitis B virus infection has been resolved in patients with 238 cases, and 435 are still infected persons (control group) and its match. Patients were matched for age, sex, hepatitis B virus strains aspect. The team found that hepatitis B virus clearance seems to be no significant difference in the risk of developing liver cancer.

The researchers noted that, although we do not know why the clearance of hepatitis B virus does not seem to affect the risk of liver cancer, they think it is probably due to a number of factors. For example, one reason may be in the early stages of infection, hepatitis B virus has been integrated into the genome of liver cells, and can clear the virus persist in the blood traces.

The authors point out in their study that the HBV DNA levels are still detectable in "a significant proportion" of patients with the disease after traces of the virus (anti-viral antibodies) have been cleared from the blood. This increases the possibility of the host "low level of ongoing HBV replication along with the continued integration of" the of liver cells, causing liver cancer risk of the virus from the blood after being cleared still persist. Lead author Prabhu Gounder said, "As adults obviously still have risk of liver cancer after the infection is treated, they may still need close follow-up."

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Statin drugs may not lower the risk of colon cancer

A new study shows that long-term use of cholesterol-lowering statin drugs seems unable to reduce the risk of suffering from colon cancer, but it can affect the body's cholesterol levels.

Previous studies have shown that statin drugs and lower cholesterol levels can reduce the risk of colon cancer. "But in fact, we still don't know whether it is statin drugs or lower cholesterol levels that can reduce the risk of colon cancer," researchers from the University of Pennsylvania explained. Therefore, the researchers designed experiments to compare the effect of statins and lower cholesterol levels on the risk of colon cancer. In the study, participants included more than 22,000 patients with colon cancer and more than 86,500 non-colon cancer patients.

The results were similar results to previous studies: taking statins can reduce the risk of colon cancer. But the researchers also found that for those who didn't continuously take statin drugs had no significant change in the risk of colon cancer when compared with people which had been taking statins. The researchers also found that the population with higher cholesterol levels had lower risk of colon cancer, which had nothing to do with the use of statin drugs.

The researchers also found that no matter for statin users or users of non-statin drugs, both of their body cholesterol levels would fall within a year before they were diagnosed with cancer, which has always been a phenomenon that we can't be very understandable.

However, the study doesn't prove a causal relationship between lower cholesterol levels and the increase of risk of colon cancer. The study just found a link between the two aspects.

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Scientists have developed a new technology to joint DNA barcode in a single cell

According to the latest issue of Molecular Systems Biology, Canada researchers have developed a new technology that can joint DNA (deoxyribonucleic acid) barcode in a single cell to search interaction among millions protein pairs.

In recent years, DNA barcode technology enables scientists to carry out high-parallel test (many different types of cells in the same test tube) possible, and develop next-generation DNA sequencing technology, to further improve the counting and the barcode reading results of efficiency.

However, the number of tests carried out in the same test tube, but is limited by the number of cell type-coded. All along, DNA barcodes are one-dimensional, which is a bar code can only do one test. Allow barcode together in the cell, which means scientists can now break this barrier. The new technology can significantly increase the number of experiments carried out in a single test tube, under the same conditions can cost 10 times more efficient.

Widely used in yeast two-hybrid (Y2H) method, carry a "bait" proteins in yeast cells and carry a "prey" proteins in yeast cells mate. After Y2H manipulate the system, only the "bait" and "prey" protein cells stick together to survive, so that scientists can observe the correlation between what each protein. It is named "Fusion barcode Genetics - yeast two-hybrid (BFG-Y2H)" new technologies, carrying thousands of "bait" and "prey" protein pair in the same cell culture dish.

The novelty of the method is that the BFG-Y2H by cells programmed from the "bait" and "prey" DNA barcoding cells connected together to form a "fusion barcode", then use the next-generation DNA sequencing methods for fusion barcode testing.

The researchers said the ultimate goal of this study is to establish a three-dimensional view of protein interaction network rather than a static map. By establishing effective protein interaction maps contain richer information, BFG-Y2H method can extend the researchers' understanding of the mechanism of cells, proteins and show interaction among proteins which only take place under certain environmental condition, thus accelerating the understanding of gene functions and human disease.

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Anorexia is not a purely psychological illness

In all mental disorders, the mortality rate of anorexia is the highest. However, the etiology and treatment of this disease are poorly understood. Now scientists believe that we may have been in wrong direction.

British researchers said that anorexia may derive from bacterial infection rather than just a purely psychological illness - perhaps psychological reasons are important, but they are not convincing as a primary or underlying cause of the disease. In addition, chronic fatigue and irritable bowel syndrome may also have the same causes. So far, this is just a hypothesis to be tested. But once the hypothesis can be verified, it will be able to bring new treatments for anorexia, providing new hope for patients with anorexia, irritable bowel syndrome and chronic fatigue.

The researchers believe that the bacterial infection, the patient's immune system to secrete antibodies against. But then, these antibodies become confused and start attacking its own nerve cells. This "autoimmune attack" could explain the symptoms that occur in patients with the three diseases, can also explain the huge difference in the incidence of sex - we all know that women are more prone to autoimmune diseases, and the incidence of the three diseases in women rate is 10 times that of men. Therefore, nerve cell autoantibodies may be part of the cause of these diseases.

Bacterial hypothesis could also explain some special anorexia symptoms, and many people will associate it with the influence of fashion and model for young girls. The role of autoantibodies in the limbic system of the brain may lead to extreme emotions, including fear and nausea. These adolescent girls will be emotional and socio-cultural standard ideal body type linked to food and obesity lead to further nausea and fear.

If anorexia is really from a bacterial infection, then it means it might be infectious. However, researchers believe that social factors may still have an impact on whether people sick. For example, childhood suffered physical and sexual abuse may be more likely after the bacterial infection prevalence. Social factors can affect the disease symptoms, but it is not the only causes.

Today, researchers are testing their hypothesis on laboratory animals and trying to identify the specific bacterial species that confuse the immune system. If they can isolate the culprit, then it is possible to restore the normal balance of bacteria - by transfusing healthy blood to eliminate bacteria that induce autoantibodies and the autoantibodies.

Read more: http://www.cusabio.com/ELISA-Kit/Human-anti-caudate-nucleus-CN-autoantibody-ELISA-kit-1080385.html

Pain can accelerate the speed of kidney failure and increase the risk of death

A study published recently in the Journal AJKD explored the relevance of pain with renal dysfunction and the development and risk of death of chronic kidney diseases. The results showed that moderate-severe pain can accelerate the rate of decline in kidney function, increasing risk of death.

The retrospective cohort study included 2,360,056 American veterans, nearly 60% of which had pain problems and common paregoric for them are opioid analgesics. The estimated baseline of glomerular filtration rate (eGFR) is ≥ 60 mL / min / 1.73 m2. Pain rating: None (0), mild (1-4 points) and severe (5-6), and severe (≥ 7 points). Endpoint: eGFR declines and incidence of eGFR <60 mL / min / 1.73 m2 or all-cause mortality.

After adjustment for baseline eGFR level, demographics, comorbidities, cardiovascular risk factors and depression, use Cox proportional hazards regression model with pain (1) eGFR decreased rapidly; (2) eGFR <60 mL / min / 1.73 m2 occurred or all-cause mortality rate correlation.

It was found that the risk of eGFR rapidly decline in patients with moderate and severe pain was much higher than that of those without pain or with mild pain. The ratio of patients with moderate pain was 1.11 (95% confidence interval 1.09-1.14); the radio of patients with severe pain was 1.17 (95% confidence interval 1.13-1.21). Patients with moderate and severe pain had the risk of eGFR <60 mL / min / 1.73 m2 or risk of death 30% higher than those without pain. The risk radio of patients with moderate pain was 1.30 (95% confidence interval 1.28-1.31), the risk ratio of patients with severe pain was 1.30 (95% confidence interval 1.28-1.32).

Although this study has several limitations (a lack of detailed data on the types of pain and pain location), it still shows that pain is associated with the increase of incidence rate of eGFR <60 mL / min / 1.73 m2, the speed of decline in renal function and mortality.

More details: http://www.cusabio.com/Recombinant-Protein/Recombinant-Escherichia-coli-O6:H1-strain-CFT073--ATCC-700928--UPEC-Inner-membrane-transport-permease-YbhS-11106397.html

The therapy of nanoparticles may be effective for the treatment of acute myeloid leukemia

A study published this week in the journal Nature - communication indicated that nanoparticles carrying a class of non-code RNA small molecule miR-22 which can regulate gene expression shows the therapeutic potential of mice model with acute myeloid leukemia.

Acute myeloid leukemia is a cancer of blood cells, and it will still take away people's lives in five years even after intensive chemotherapy. While we have a lot of information about the characteristics of acute myelogenous leukemia genomic variation, the drive progenitor cells into cancer cells, the molecular mechanisms that we know very little.

Chen Jianjun and his research team analyzed 62 samples of cancer patients and found that individual class in acute myeloid leukemia express miR-22 is reduced. Using a variety of mouse models of acute myeloid leukemia, the study indicates that the recovery of the expression level of miR-22 can inhibit specific cellular pathway, hinder the development of acute myeloid leukemia and cancer cells is maintained. Researchers followed by nanoparticle transport miR-22 short-chain RNA into two kinds of leukemia mouse model, a mouse leukemia cells containing GM first model, the second model from mice containing human leukemia cell line to assess the power of miR-22 therapy. In both models, the use of miR-22 treatment has brought a prolonged survival time and delays the progression of cancer.

Further tests are needed to verify the possibility of treating acute myelogenous leukemia using nanoparticles carrying miR-22 before the start of clinical trials. In addition, researchers have suggested that the combination of this therapy and chemotherapy drugs should also be effective for the treatment of acute myelogenous leukemia.

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Upper respiratory tract infection increase otitis media of child before the age of 1

A study recently published in the Journal Pediatrics noting that the respiratory viral infections, bacteria colonization and lack of breastfeeding increase the risk of acute otitis media among children before the age of 1.

This study evaluated the upper respiratory tract infection (URI) and the incidence of complications, including acute otitis media (AOM) and lower respiratory infections (LRI), evaluated the bacteria - viruses affect the reaction, as well as genetic and environmental risk factors for the development of acute otitis media.

The researchers followed up from birth to age 1 AOM Development 367 healthy babies. Collection 1 year old, 6-month and nine-month-old nasopharyngeal samples valuation bacteria and PCR studies. In any diagnosis of viral URIs when samples are collected nasopharynx.

Data show that 305 subjects occurs 887 times URIs, 143 babies occurred 108 cases AOM. Baby occur an average of 4.7 times per year occur AOM URIs, without the AOM infants per year and 2.3 URIs (P <0.002). The study found children with AOM pathogens value higher than that of children without AOM (P <.005). The results also show that breastfeeding can reduce the risk of children URIs and AOM (P <0.05).

The author, pediatrics and pathologist Chonmaitree and her colleagues from Medicine Department of Pediatrics and University of Texas wrote that moraxella catarrhalis with or without other bacteria all changed the risk of URI (HR = 6.1; 95% CI, 4.04-9.23) and AOM (HR = 1; 95% CI, 0.62-1.6). Whether with viral infection or not, Moraxella catarrhalis infections increase the risk of URI. "These complex viruses - bacteria reactions may provide clues of pathogenesis of URI and AOM, which requires a larger study sample." David Costill wrote.

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IL-33 protein can reverse the decrease of cognitive function for mice with Alzheimer's disease

A study led by scientists at the Hong Kong University of Science and Technology and the University of Glasgow, UK found that a protein called IL-33 can reverse the symptoms and decrease of cognitive function for mice with Alzheimer's disease. The study was published in the Journal PNAS on April 18th.

Professor Nancy Y Ip at Chinese Academy of Sciences and Hong Kong University of Science and Technology and Professor Eddy Liew at Infection, Immunology and Inflammation Research Institute of University of Glasgow are the co-leaders of the study. Professor Nancy Y Ip mainly studies on relationship between neurotrophic factor and neuronal development.

Functional integrity of the cerebral neocortex, dependent on the correct amount of excitatory neurons and inhibitory neurons. But it is not clear, new abnormal cortical neurons during the development of production will lead to consequences. Nancy Ip research team found that neurons in the neocortex upper overproduction will lead to similar autistic behavior. They then confirmed, S- nitrosylation (S-nitrosylation) proteasome-dependent degradation of p35 inhibits Cdk5 activity, regulation of hippocampal synaptic strength. The findings published on Nature Communications magazine.

Alzheimer's disease is a devastating disease, and there is no effective treatment currently. It is the most common cause of dementia in the UK affects about 85 million people mostly aged 65 or older. It affects people between the ages of 1/14 with the positive growth of our aging population. It is estimated that there will be 65 million people worldwide suffering from Alzheimer's disease till 2030.

Professor Eddy Liew said, "Alzheimer's disease is currently in urgent unmet clinical needs. We hope that our findings may ultimately translate to humans. Organism in various cell types can be produced by IL-33, the protein in particularly abundant in the central nervous system (brain and spinal cord) in. we formed a mouse strain progressive disease like Alzheimer's disease (APP / PS1) of age to carry out experiments. we found that injection of IL-33 to senescence APP / PS1 mice, can rapidly improve their memory and cognitive function in a week to normal levels in mice of the same age."

Some signs of Alzheimer's disease include the presence of extracellular deposits of amyloid protein plaques, neurofibrillary tangles in the brain is formed. In the course of the disease, 'plaques' and 'tangles' accumulation, leading to the loss of connections between nerve cells, eventually neuronal cell death, loss of brain tissue.

IL-33 appears to be to work through the mobilization of microglial cells surrounding the amyloid plaques, absorb and digest them, to reduce the number and size of plaques. IL-33 is a known degradable soluble amyloid by inducing enzyme neprilysin to do this. In addition, IL-33 therapy may be acting by inhibiting inflammation of the brain tissue, the researchers confirmed earlier inflammation promotes the formation of plaques and tangles. Thus, IL-33 not only helps clear amyloid plaques have formed, but also the first stop of the plaques and tangles deposition.

Professor Liew added, "is not clear that the current findings associated with human Alzheimer's disease, but there are some encouraging clues. For example, some previous studies confirmed the genetic mutation of IL-33 in Europe and China the association between Alzheimer's disease population. in addition, the brains of patients with Alzheimer disease than non-Alzheimer's patients contain less IL-33."

"Despite the excitement, there is a certain distance between laboratory studies and clinical applications. In the medical field, there are enough false 'breakthrough' warning us that before the completion of rigorous clinical trials, we should hold our breath. We just enter the phase I clinical trials in tests of toxicity produced by a dose of IL-33. However, this is a good start."

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We may open our cellphone with skull recognition in the near future

According to foreign media reports, at present, it has become more and more common to unlock the mobile device using fingerprint scanning technology, and iris and facial recognition technology to unlock is also under intense research and development. But next major biological unlock device may come from our skulls. Recently, a research team composed of researchers from the University of Stuttgart, Germany, Saarland University, Max Planck Institute for Informatics developed a system called the SkullConduct, namely using the unique sound of skull to unlock the device.

Firstly, the research team adapted the Google Glass. They put a bone conduction speaker and a bone conduction microphone inside the glasses so that users can be able to wear the two key components of the system on the head.

After uses wear the device, it will play one-second audio. It is learned that this audio can't be detected by human's ear. After that, the microphone on Glass would identify and record the skull voice. Since the skull structure of each person is unique, so the reflected sound is unique, too. Moreover, this authentication method doesn't require user to write down anything or make a physical action. Research team said that the success rate of SkullConduct is as high as 97%.

Now, SkullConduct is still in the early stages of development, so it has to be faced with some limitations, such as the impact of the surrounding environment noise on pickup of skull voice, changes in body weight which would change the skull echo of the users.

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How do the genes of brain dopamine system play an important role in prolonging life?

Researchers at research institute of University at Buffalo found how the genes of brain dopamine system play an important role in prolonging life.

The study was led by a senior researcher Panayotis(Peter) K. Thanos at the Royal Irish Academy. He and his research team studied the dopamine gene in mice to assess their impact on the life and behavior. Dopamine is a neurotransmitter in the brain to help to control rewarding and pleasure center, helping to regulate body mobility and emotional reactions.

The researchers found that the dopamine D2 receptor gene (D2R) significantly affects lifetime, weight and activity, but it only have a role when the environmental compatibility (including social interaction, sensory and cognitive stimulation, etc.). The key is to be combined with exercise. Thanos said, "Exercise is an important part of enriching environment, which is an important factor that gene shows effect on brain function and behavior."

It was found in the research that, relying on the expression and regulation of D2R gene, the survival time of mice living in a good environment was increased by 16% to 22% compared with mice living in the general environment. Thanos said, "These results are the first to show that D2R gene and environment reciprocally affect survival time and aging. This research decipher the individual differences of longevity at the level of genes and environment."

The results are very meaningful for the exploration of the effect of the interaction between inheritance and environment on lifetime and activities of people.

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Gene editing technology may be helpful to treat Alzheimer's and breast cancer

A study reported the method of locating and modifying single DNA base without random insertion and deletion of genome. This new "base edit" method uses a modified CRISPR / Cas9 protein to make it other two kinds of protein. It is more efficient than the existing method of repairing a single base mutation has been used to culture cells, successfully reversing the single base mutation associated with the diseases including late-onset Alzheimer's disease and breast cancer. The results of recently published in the journal Nature.

Most genetic diseases come from single nucleotide mutation (point mutation). Currently widely focused gene editing technology CRISPR / Cas9 involves cutting two chains of DNA to form a double-strand breaks in the DNA target sequence. However, when a single nucleotide correction for the standard CRISPER / Cas9 method is often inefficient, and frequently introduced randomly inserted into the target location / shear genome, which is mainly the result cell response to DNA double-strand breaks.

In order to improve the efficiency of correction point mutation, while reducing the insertion / deletion frequency, Cambridge, Massachusetts, Harvard University David Liu and colleagues modified Cas9 protein, it no longer cut double-stranded DNA, but still able to bind to the target DNA sequence. By installing bases on Cas9 modifying enzymes (APOBEC1), researchers can directly cytosine (C) is converted into uracil (U), and consistent uracil and thymine (T) base pairing methods. In order for an edited permanent base pairs present in the cell, the researchers used a third protein in normal cells repair DNA to manipulate the process, so that the target C: G base pairs converted to T: A base pairs. Studies have shown that the system can effectively correct the base edit various point mutation associated with human disease in mouse and human cell lines exist, and the introduction of insertions / deletions are extremely low volume.

The other two-year study published in the journal Nature provide new information about Cpf1 enzyme mechanisms and structures. Cpf1 enzyme can be used as a substitute for Cas9 in gene editing CRISPR-mediated. Berlin, Germany Max Planck Society, Institute of Biology infection Emmanuelle Charpentier team has proved the difference between Cpf1 and Cas9. It can perform two activities of RNA processing and DNA cleavage in targeted gene editing, which may open new way of editing and scilenting a specific sequence genome. In another study, China Harbin Institute of Technology research team reported the crystal structure of the RNA Cpf1 attached to the protein and described how the shape changed during the attachment.

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Better understanding of how some drugs affecting cognitive impairment and dementia

According to a new study published in JAMA Neurology, many over-the-counter drugs contain anticholinergic drug, such as nighttime cold medicine, and the occurrence of anticholinergic drugs and cognitive dysfunction related to the elderly.

Previous studies have found that anti-cholinergic drugs can increase the body's cognitive impairment and dementia risk. The study included a total of 451 cognitively normal older (average age 73.3 years), these subjects from the US National Research Program: Alzheimer's disease and neuroimaging studies Indiana memory and aging research. In which 60 (13%) subjects taking at least one of the high activity of anticholinergic drugs. By analyzing brain scans, the researchers explored the potential mechanisms associated with both.

Cognition and memory tests showed that compared with patients not taking anticholinergic drugs, patients taking these drugs lower short-term memory and executive function test, the average score. Taking anticholinergic drugs in patients Wechsler Memory Scale revised logical memory immediate recall test average score was significantly lower than patients not taking anticholinergic drugs for their executive function composite score as well.

Results positron emission tomography (PET) showed that patients taking anticholinergic drugs reduce their glucose metabolism, glucose metabolism is a biomarker of brain activity. Regional activity in the hippocampus and memory-related also reduced, previous studies have confirmed that this was an early manifestation of Alzheimer's disease occur.

Magnetic resonance imaging (MRI) showed great correlation between brain structure and use of anticholinergic drugs. Compared with patients not taking anticholinergic drugs, patients taking anticholinergic drugs full leather smaller, but larger and ventricle.

"These findings led us to a better understanding of how these drugs affect brain which increases the risk of body's cognitive impairment and dementia," the study's lead researcher, chief researcher, from Indianapolis, Indiana University Health Sciences Center shannon Risacher said, "based on these findings, for elderly patients, doctors should start to think about alternative medicine anticholinergic drugs."

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Scientists find the mechanism behind telepathy

Recent study finds that the human brain appears to be rewriting history, so that people choose to make after an event seems precedes events. In other words, people would add "loop" psychological timeline so that they feel able to predict what actually happened. Related achievements recently published in journal Psychological Science.

From Yale University's Adam Bear and Paul Bloom volunteers who carry out some simple tests. In one trial, participants observed a white circle, and quietly to guess which will turn red. Once the circle change color, they have to report on their prediction was correct.

Expected accuracy rate is 20%, but in many trials, the rate accuracy reported by subjects was much higher than this. This suggests that volunteers may have telepathic abilities, or unwittingly playing a psychological trick on him.

The study is designed to help explain what is actually taking place. Researchers in the white circle appear and become one of setting different delay between the red, ranging from 50 milliseconds to 1 second. When the shortest delay, participants reported the highest accuracy rate - more than 30%.

In fact, a red circle appears the ongoing impact of the decision. Mechanism behind this behavior is unclear. The researchers said it might be the sequence of events correctly perceived - before actually making forecasting a circle has changed color, but then people will subconsciously remember the sequence permutation, therefore appears to be a first predicted. This may be caused by sudden changes in sensation-driven control lust for life.

Another possibility is that, due to the inherent limitations of the perception process, people do wrong perception of the current sequence of events. In other words, human brain is not trying to deceive people to believe themselves in a commanding position. It's just trying to follow the correct sequence to deal with an event sequence that happens rapidly.

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Longevity genes have maintenance effect on hematopoietic stem cells

Professor Ju Zhenyu research group at Hangzhou Normal University revealed the important role of longevity gene Sirt6 in maintenance of hematopoietic stem cell homeostasis. The related findings are recently published in the Cells - Stem cells.

Sirtuin is widespread in the body of a class-dependent histone deacetylase, by acting on different substrates, widely involved in stress response, steady state regulation of fatty acid oxidation, energy metabolism and other physiological processes. Sirtuin expression levels gradually decrease with age. It has been found that over-expression of Sirtuin can extend the life of lower organisms, but its specific mechanism of stem cell homeostasis remains unclear.

Ju Zhenyu group found that Sirtuin family members SIRT6 Caused by Lack of activity regulated Wnt signaling pathway, forcing the hematopoietic stem cells into the cell cycle proliferation, and ultimately led to the hematopoietic stem cell depletion; and the use of Wnt pathway inhibitor ICG001 could reverse Sirt6 knockout hematopoietic stem cells hyperproliferative and depletion.

The results in delaying stem cell aging and disease prevention and treatment of bone marrow failure has important scientific significance. At the same time, the study for the first time revealed the SIRT6 from the level of epigenetic regulation of hematopoietic stem cell development and the aging process is an important pathway, which is of great significance for in-depth understanding of SIRT6 on adult stem cell homeostasis and aging regulation and exploration of stem cell aging-related diseases intervention.

Read more: http://www.cusabio.com/Polyclonal-Antibody/BMP-2-Polyclonal-Antibody-11106185.html

The level of vitamin K1 is linked with coronary artery disease

According to a study published online on Apirl 8th in Journal of Thrombosis and Haemostasis shows that there is a relation between gene-decided vitamin K1 levels and coronary artery disease as well as myocardial infarction.

From New York, CUNY School of Public Health, C. Mary Schooling evaluates the risk of coronary artery disease or myocardial infarction in accordance with the level of vitamin K1 genetically determined.

She uses CARDIoGRAMplusC4D (64374 patients and 130,681 cases of control) by independent samples diversity of acquired vitamin K1 with coronary artery disease or myocardial infarction in association estimates, in addition to the use of global lipid genetics research group (196,475 cases of participation researchers) to estimate the association between lipids and vitamin K1.

Schooling observed a positive association between vitamin K1 single nucleotide polymorphism and coronary artery disease or myocardial infarction (odds ratio, 1.17 / unit forecast vitamin K1 levels of gene log transformed), but did not find it and non-transformed normal LDL-cholesterol, high-density lipoprotein, and the positive correlation between triglycerides. With a disease or myocardial infarction, coronary artery more relevant now that the only gene rs2108622, which is functionally closely related to the level of vitamin K1 (odds ratio 1.21).

"Vitamin K may lead to coronary artery disease or myocardial infarction, or whether vitamin K and other coagulation substance decided early prevention of these diseases are related, this may be worth considering," Schooling wrote.

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New enerated anti-cancer drugs to promote research of drug development and pharmaceutical chemistry

A team of researchers led by Professor Pauline Chiu at the University of Hong Kong chemical cortisol have generated stable protein A, a molecule capable of slowing the growth of cancerous tumors in laboratory. They published the results in the journal Chemistry-A European Journal.

Cancer is a disease with an abnormal and unregulated cell growth. Nevertheless, the tumor does not grow more than 2 millimeters unless accompanied by angiogenesis - to nourish tumors and allowed to spread to other parts of the body vascular development. Thus, inhibition of angiogenesis molecules can slow the growth of cancer.

Cortisol stable protein A is a natural product extracted from the sponge in Indonesia, there is a low-dose anti-angiogenic activity. In addition to being the main substance of anti-cancer therapy, in which cortisol stable protein a derivative is a potent anti-HIV agents. However, natural resources obtained from cortisol stable protein A is difficult, therefore, to generate laboratory is another way to get used for future research and drug development quantities.

The impressive complex structures and biological properties of the protein a stable cortisol inspired many of the world famous chemist to produce this molecule. The research team through a (4 + 3) cycloaddition reaction of cortisol generated successfully stabilized protein A, the reaction Chiu Labs research and development and optimization, to generate seven ring centered structure.

"Inventing new chemical reactions is extremely important area of research, as each new reaction is enabling tool, opened the door to generate a number of important molecules," Chiu said. "In this case, the cycloaddition reaction of our research and development is an important step in our strategy, which allows us to generate stable protein A cortisol can effectively complete."

The efficient path Chiu developed can load up the known largest stable protein A generation amount of cortisol. Its production surpasses that of half production path developed by Scripps Research Institute, and seven times the total amount generated from Harvard University. Through this way, cortisol stable protein A and its analogues can be more efficient generation to promote research and the future of drug development pharmaceutical chemistry.

Read more: http://www.cusabio.com/ELISA-Kit/Rat-Adrenocorticotropic-hormone-receptorMC2R-ELISA-kit-1081318.html

A new model is developed to show how brain produces consciousness

According to the report of Swiss Federal Institute of Technology in Lausanne (EPFL) website, the school in collaboration with other university researchers proposed a two-stage model to explain how the brain processes unconscious information and turns the unconscious information into the conscious. According to this model, consciousness does not continuously arise but every once in a while. There is up to 400 milliseconds between the unconscious state and consciousness. There is no sense of time in this compartment.

The researchers published the paper in Public Library of Science • Bio recently, pointing out that people feel the world around is seamless and smooth, but it is an illusion. Some recent experiments show that the information is not the outside world into the conscious awareness continuously, but the brain collects such information in discrete time points, after treatment rendered. Like every second of film 24, as too fast and let us put mistaken continuous.

The researchers studied data previously published experimental psychology and behavior, with a two-stage model describes the information processing consciousness. First stage of the unconscious: the brain processes certain characteristics of things, such as color, shape, duration, etc., in the unconscious state with high time-frequency analysis of them, during this period no sense of time, but also feel not change the characteristics of things, time, wherein the digital signature is encoded, as color coding, as shape. Then the stage of consciousness: unconscious after processing is complete, the brain and gives all the characteristics of the final "picture", i.e. the brain and finally presented the things that make us aware of this information.

The whole process from the outside to stimulate awareness of cognition, the duration of up to 400 milliseconds. From a physiological point of view, this delay is quite long. First author, EPFL psychophysics lab Michael Herzog explained, "Because the brain want to give you the best, most clear message, which spend a lot of time for you to realize that it's no good unconscious processes because it will make people very confused."

The researchers noted that this was the first two-stage model of how consciousness arising, providing a more complex explanation for how the brain manages consciousness. It also provided new insights on for the relation between brain processes information and how we recognize the world.

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Making use of transgenic technology to increase the cadmium tolerance of plants

Soil heavy metal pollution is one of the major global environmental problems. The heavy metal contaminated soil can be absorbed into the food chain crops, seriously affecting food security and endanger human health. Phytoremediation genetic engineering is important ways to solve the heavy metal pollution, which find and discover withstand heavy metal poisoning and excess accumulation of heavy metals in the regulation of key genes and to elucidate its mechanism of action, from the source of the genetic engineering of plants to be successful and repair agricultural food safety control key. Recently, relevant research group of Professor Explorative Hefei University published online in the International Botanical renowned journal Plant Physiology.

The way forward genetic screening study, identified a mutant of Arabidopsis resistance to cadmium, the use of biotechnology cloning the corresponding gene mutation, found that the gene encodes a transcription factor ZAT6, it can be specifically incorporated directly into the control glutathione GSH synthesis plant precursors ie chelate pigment, a key promoter of synthetic genes on and coordinate related gene expression of glutathione-dependent activation of the plant hormone synthesis pathway on chelation, thereby increasing the plants chelate pigment synthesis, and ultimately improve plant Cd accumulation and tolerance.

"Therefore, the use of overexpression ZAT6 transgenic technology to increase the Cd accumulation and tolerance of plants, providing new genetic resources and technical means for heavy metals contaminated soil phytoremediation genetic engineering." Cao Shuqing said the application of this gene in remediation of Cd contaminated soil has gained intellectual property rights. It can be extended in other large biomass plants.

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Conserved gene translocation protein plays a role in regulating sleep and metabolism

The sleep time of drosophila and human is the same, and caffeine will affect their sleep. If not sleeping well at night, their memory will be affected. Recently, a study on drosophila has shown that there is a link between lack of sleep and metabolic disorders (including abnormal diabetes, obesity and blood sugar levels). The study firstly identifies conserved gene translocation protein plays a role in regulating sleep and metabolism.

Human severe insomnia and increased appetite, insulin resistance, and long-term insomnia are more likely to suffer from obesity, metabolic syndrome, type 2 diabetes and cardiovascular disease. In contrast, the metabolism of the human body clock and regulate sleep has a huge role.

The researchers said the human sleep and diet are closely related, and any of them as pathological problems and metabolic disorders. While there is considerable evidence that insomnia and associated metabolic disorders exist, but we do not know the specific connection between them it is like.

When the flies hungry, they will reduce the sleep time, sleep time as they use for food. Drosophila researchers link between sleep and feeding conducted research, you want to find out exactly what kind of genes affecting their sleep. The results found that when neurons decreased translocation of protein, fruit flies will be like hunger satiation sleep as well.

After the addition, the researchers measured sleep, glycogen, triglycerides and blood sugar levels in the fruit fly, Drosophila designed for the specific diet and the starvation response of Drosophila divided into two separate mechanisms of hunger and insomnia. The researchers said that many genes may regulate sleep and metabolism, and the study indicates the translocation of the protein plays a role in the integration of these processes. Also, insomnia caused by hunger is not due to the increase of body's nutrient storage. Thus, translocation protein is regardless of hunger or hunger-induced behavior, but it can cause insomnia when hungry.

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Be careful about the use of antioxidant on cancer patients

Daily goods which are rich in antioxidants such as beauty skin care products, coffee, tea, red wine and vitamins may be double-edged sword under certain conditions. A research team led by Professor and director of endocrinology Zheng Hongting at Xinqiao Hospital of Third Military Medical University published a latest study confirming that antioxidants in everyday life and the clinical may promote tumor metastasis. This article entitled "pathway activation NRF2 antioxidant anti-diabetic drugs accelerated tumor metastasis" was published on April 13th in top international academic journals Science series journal - Science Translational Medicine. The researchers proposed that physicians should be more cautious when in the development of hypoglycemic treatment regimen for some patients with both diabetes and cancer.

It is understood that the correlation between diabetes and cancer had been come up at as early as in 1910 by some scholars, and a growing number of epidemiological evidence showing that diabetes is closely related with the tumor. With the rising incidence of diabetes, diabetic patients with cancer patient population are increasing. The past five years, Zheng Hongting team used mice to carry out the test, liver, colon and healthy mice antioxidant drugs were found by comparing antioxidant drugs in vivo mouse tumor lesions has shifted. After further study confirmed that some drugs can increase the antioxidant activity of the tumor cells, which will accelerate the invasion and metastasis of tumor lesions.

The findings overturn the conventional simple understanding of antioxidant and have important implications for the choice of diabetes mellitus patients with cancer hypoglycemic drug and antioxidant. They also send a warning that people should be cautious about antioxidant use in cancer patients. The journal Science - Translational Medicine said in the allotment of reviews, "Previous dietary antioxidants elements are commonly used in cancer prevention, but this study shows that antioxidant may be a double-edged sword and even has no benefit. So antioxidants should be used with caution, especially for patients with diabetes and tumorigenesis.

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The journal Science finds the blocker of cancer

Researchers from Massachusetts General Hospital (MGH) found that immune cells seemed to prevent the development of melanoma and other cancers in animal models. These film lymphatic sinus (SCS) macrophages form a protective film in surrounding of the lymph nodes, blocking the entrance of delivering tumor tissues and the tiny structures which help the cancer growth and metastasis. However, such SCS macrophages barrier appears to be temporary, and it will collapse when the tumor makes progress and or responses to certain cancer therapies. These important findings were published in the journal Science on April 8th.

The study's lead author, Pittet Dr. Mikael MGH Center for Systems Biology, said: "People often think that the tumor inside macrophages by helping the formation of new blood vessels to deliver nutrients to the tumor cells to promote cancer growth in our laboratory. We have been studying the mechanism of tumor throughout the body to communicate with the immune system, especially for our understanding of the tumor and whether it's away from the macrophage interaction of interest occurs."

CANCER a potential signal to the molecules of immune cells is the use of tumor-derived extracellular vesicles (tEVs), known TEVS can bind to and activate a number of different cell types. Although it is possible to predict the level of detection tEV treatment response and survival, but it is very difficult to assess the impact tEVs in live animals. The MGH research teams in a new way with a combination of genetic and imaging methods to track the tEVs their targets.

In genetically engineered tumor cells can be generated in mice tEVs with light markers, the researchers confirmed that tEVs can leave the tumor, migrate to the body, and found that most of them are highly concentrated in the vicinity of the lymph nodes, which are tEVs conveying pipe through the lymphatic to here. In another group carrying different receptor protein of melanoma in mice, the research team found tEVs mainly SCS macrophage interaction, SCS macrophages in the lymph nodes surrounding the formation of a fibrous capsule direct cell layer.

In order to determine the observation that mice with human disease is relevant, the researchers examined from 13 patients with non-melanoma cancer sentinel lymph node - which is closest to the tumor, the tumor is expected early diffusion point. Although these lymph nodes has confirmed itself is not melanoma, but researchers lymph nodes in 90% of patients around the SCS macrophages found in melanoma-derived substances. Tumor-derived substance is present in those macrophages did not reflect the primary tumor progress.

Further experiments found that, SCS macrophages play a tumor inhibitory effect in melanoma and lung cancer in a mouse model. This is usually within the tumor-promoting macrophages in stark contrast. Although the current study showed that, by limiting the SCS macrophage suppressing proliferation of cancer tEVs, with the density of SCS macrophage tumor growth begins to decrease around the lymph nodes. Some chemotherapy and immunotherapy drugs have been found to destroy the SCS macrophages barrier. Once tEVs into the lymph nodes, they will bind B cells, followed by B cells to produce some antibodies accelerate tumor growth.

Pittet said, "because of the current people to develop some treatment methods to deplete tumor inside the tumor-promoting macrophages interest to determine whether these treatments also affect the protection of SCS macrophages may be valuable. The best the results may be removed within the tumor macrophage tumor-promoting activity, while retaining the activity of inhibiting tumor SCS macrophages. strengthen SCS determine whether to block macrophage tEVs enter lymph nodes transmit, and a better understanding of the activation tEV B promote cancer cell growth mechanism will also be useful."

Macrophages are phagocytes present in blood, lymph tissues and all tissue types of mammalian. They play many different roles in normal development, homeostasis, tissue repair and the immune response to pathogens. Their diversity means that they are involved with almost every human disease. They are also a major treatment goal, because their function can be enhanced or inhibited to change the outcome of the disease.

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Why are the sizes of bacteria limited?

The size of the bacteria can be different in eight orders of magnitude - if the smallest bacteria is as large as human hands, then its giant "relative" can hold 4000 tractor trailer. However, despite that the growth and reproduction of large bacterial is faster, there is a limit in how big these microorganisms can grow.

To clarify the reason, computational biologists proposed a computer model to predict how bacteria metabolism and cellular components change with the different size of cells. They used the principle of how much a bacteria need make it "assembly" --the normal operating details of DNA, protein and molecule factory which is called ribosome.

The researchers recently published a study in the Journal of the International Society for Microbial Ecology, reporting that space limitation simultaneously controls the maximum and minimum size of bacteria. Bacteria won't be smaller than their same kinds whose size has reduced. Because if so, there is not enough space for essential DNA and proteins. And they can't change much larger, because the larger species need a lot more energy requirements with its increased size. Therefore, they need more ribosomes, while bacteria which try to keep those records larger than the existing bacteria can't hold additional ribosomes it needs.

The researchers said that the understanding of the minimum size of bacteria can help life biologists who are looking for extraterrestrial life exclude too tiny life signs. At the same time, with understanding of the maximum size of bacteria, biologists can more conduct careful study on how other microorganisms like unicellular eukaryotes deal with this limit.

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Single-cell technology is expected to cure cancer

Targeted therapy can block tumor growth pathway, but these cells are often able to take a detour and develop resistance to drugs. Caltech research team recently used single-cell analysis to fully draw the circuitous route of cancer. The study was published in the journal Cancer Cell on April 11th, providing precious information for developing more effective combination therapies.

Studies have shown that single cells phosphoproteomics technology can reflect the internal activities of individual cancer cells and signal transduction. "We see the growth of cancer cells to other path, you can find ways to put them all blocked," the article's corresponding author, Caltech James Heath said.

Glioblastoma is the most lethal kind of brain tumor. Although it has been developed for cancer mutations targeted therapies, but their effect is usually very short. Combination therapy targets while more mutations may be better ways to combat this disease. Heath and his colleagues conducted in-depth study of glioblastoma tissue obtained by surgery. They found that glioblastoma within 48 hours of drug targets mTOR pathway produces resistance.

Research indicates that before we found any clinical change, glioblastoma began to grow again choose the path, to find ways to circumvent the anti-cancer drugs. Single cell phosphoproteomics technology can help people to develop a more effective combination therapy of glioblastoma. The technology for personalized treatment of other cancers also makes sense, such as analysis of melanoma cells to BRAF inhibitor resistance.

Researchers University of Houston and Huazhong University of Science and Technology published an article in the journal PNAS, demonstrating a single-cell research in nanotechnology for people. They use magnetic carbon nanotubes to extract biological molecules from living cells. This nano materials can be slipped into the cell molecules smuggled out, it had no effect on cell viability. Researchers can use this technology to extract information from a single cell basis.

Zhejiang University and Harvard University researchers on the embryonic stem cells were single-cell mRNA-seq analysis. They found that these cells exhibit heterogeneity is caused by serum-free culture. The researchers identified a high degree of variability in which the gene cluster, and a unique chromatin state. The study, published in the journal Cell Reports, 80 Zhejiang University professor Guo Ji, etc. is corresponding author of this article.

In recent years, single-cell sequencing technology is developing very rapidly and widely used in epigenetic research. Scientists recently wrote a detailed description of the genetics of unicellular apparent in some key technologies. These technologies can help us detect the epigenetic modification of DNA, histones, and chromatin level in a single cell.

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Does Zika virus only cause one brain disease namely microcephaly?

According to the recent news of American Academy of Neurology, a small-scale study report from Brazil Recife Rehabilitation Hospital said that in addition to microcephaly, the Zika virus may also with another type of brain myelin lesions caused by autoimmune For encephalopathy type, similar to multiple sclerosis. The researchers will report this finding found that at the 68th annual meeting of the Society in Vancouver, Canada from Jan. 15th to 21th.

The authors, Brazil Recife Rehabilitation Hospital Feirui La Maria said, "Although this is a small-scale study, we can provide evidence to prove the impact of the virus on the brain is different from the previous situation. Of course, further research is needed, in order to explore whether there is a causal link between the Zika virus, and some brain problems."

The researchers tracked Recife from December 2014 to June 2015 to the hospital, and exhibit the same family have Zika virus in symptomatic patients, and in December 2014 to December 2015 period observed 151 neurological symptoms of patients, and they have a fever accompanied by rash, there are some severe itching, muscle and joint pain, red eye. They were infected with the Zika virus, Dengue fever, Chikungunya fever virus tested negative. After examination of which 6 people neurological symptoms consistent with autoimmune disorders, some time, some symptoms, some 15 days after the onset of symptoms.

In these six people, two of them developed acute dissemination encephalomyelitis (ADEM), which is a sudden swelling of the brain and spinal cord lesions lead to one kind due to the myelin sheath. The scan showed signs of white matter damage. Four people develop Guillain - Barre syndrome (GBS), which is a peripheral nervous system and myelin-related disorders, and previous reports showed that the disease is related with Zika virus. When they are discharged, five of them still showed motor function problems; one had vision problems; one had memory and thinking problems.

Scientists obtain more knowledge of the mechanism of type 1 diabetes

In type 1 diabetes, immune system attacks the insulin-producing cells in the body. Assistant Professor at Harvard Medical School and the Joslin Diabetes Center immunology department researcher Stephen Kissler said that scientists clearly understand this process of autoimmune attack, but they don't understand what trigger this attack and how to stop this process.

Dozens of small mutations significantly increase the risk of disease, researchers are careful to explore the contribution of each gene. Now Kissler Laboratory has discovered a way in which a gene called RGS1 may help promote their own immune attack.

During the attack, the immune cells are called T cells infiltrate the pancreas and destroy insulin-producing β cells. Another immune cells called B cells to produce antibodies, and may also participate. In a mouse model of type 1 diabetes, RGS1 affect one type of T cell, called "T follicular helper cell", which is essential for B cells to produce antibodies, Dr. Kissler and his colleagues "genes and immunity" recently reported.

"In short, we found that the gene acts on the frequency of these T follicular helper cells, which is important for B cells, and the disease appears to be also very important", Assistant Professor at Harvard Medical School Kissler said. The found particularly striking because clinical studies have found those patients with type 1 diabetes, the blood, the higher the number of these cells.

"Overall, T follicular helper cells for B cells is very important in patients with type 1 diabetes, the body of these T cells are more their disease seems to be very important, and why have the gene involved RGS1 the new interpretation, "Dr. Kissler concluded.

"We will continue to test a number of other genes to see whether there is a very potential modification of type 1 diabetes," he adds. "We understand more information of pieces. It is easier to find the best way to intervene in the disease. When we know more about other genes, this piece of information about RGS1 could become valuable information, because it may help us open this mystery."

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New method of storing data by DNA

According to the University of Washington (UW) official website news, research scientists from the university and Microsoft in terms of DNA data storage goes a step further: they passed the 1's and 0 transcoding adenine, guanine, cytosine, and thymine this DNA nucleotide sequence of the four kinds of constitution, and the success of the pictures and videos stored in the DNA fragment, and a lossless data is read, the latest research will revolutionize computer or storage.

According to a report from the British Daily Mail recently, the amount of data of humanity "digital universe" is expected to reach 44 trillion GB in 2020. At that time it will exceed our storage capacity. In order to compensate for the lack of storage space, scientists are trying to store data information into DNA. UW associate professor of computer science and engineering Luis Sezi said, "Life creates the amazing molecule of DNA, which is capable of efficiently storing various data which are related with human genes and life systems. It is very compact and durable."

In the latest study, researchers converted 0 and 1 long sequence from the digital data of images and video into four basic components of DNA sequences. Subsequently, the digital data is divided into pieces and stored by being synthesized as a large number of artificial synthetic DNA molecules. Such molecules can be dehydrated and stored for a long time. Moreover, with the use of DNA sequencing technology, the researchers were able to "read" the data and convert it into original form, and a lossless image reading can be achieved. This study compresses digital data which can fill the entire Wal-Mart to the size of a lump of sugara.

Sezi said, "We used a series of molecular biology experiments to demonstrate the feasibility of our system design. We have succeeded in the data storage in the DNA and performance of random can read back to the original value."

The researchers explained that compared with the current digital storage technology, DNA molecules improves the tightness of data storage by hundreds of times. At the same time, the data storage devices we currently use such as flash memory, hard disk, magnetic disk and optical storage media would be damaged in a few years, but the new method can save the information for centuries.

However, the researchers said they are also facing a huge challenge, namely, to enhance the cost and efficiency of the new method so that it can be applied on a large scale.

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HIV shows its resistance to gene scissor

There is new evidence showing that HIV is fickle and difficult to cure. Chinese and Canadian scientists published an article in the American journal Cell Report on the 7th reporting that the HIV now can also soon show resistance response to the popular "gene scissors" therapy, but this therapy is still expected to be improved to continue to be anti-AIDS.

Scientists discovered that bacteria can obtain partial DNA (deoxyribonucleic acid) fragment and integrate it into the genome to form memory after a virus infection. When invaded again by this time, bacteria will transcribe corresponding RNA (ribonucleic acid) and use the "location information" therein to guide the locating and cutting of Cas protein complexes, thus destroying the invading virus DNA.

In recent years, the popular "gene scissors" therapy - genome editing technology CRISPR just uses this principle, using a customized RNA to lead Cas9 enzyme which acts as a role of scissor responsible scissors effect. Scientists cut the DNA viruses imported by HIV into host cells according to presupposed sites, thus preventing the proliferation of HIV replication.

But according to these new reports, their experiments confirmed that HIV can escape under gene scissors rapidly. The sequencing of the genome with HIV escape indicates that this virus had changed the DNA target sequence identified by CRISPR technology.

Liang Chen pointed out that the appearance of HIV's escape or a "resistance" is not accident. What surprised them was that further analysis showed that the changes of HIV were mostly not caused by virus reverse transcriptase which was generally considered by the scientific community. He thought the changes happened when host cells were trying to restore the cracked DNA because of cutting after Cas9 enzyme cut the DNA of HIV. "In other words, the therapy also helps in the escape of the virus when inhibiting the proliferation of HIV."

The researchers proposed two improved schemes to treat AIDS using gene scissors: one is to attack multiple HIV genomic sites to increase the difficulty of escape for virus; the second one is to use scissors enzyme except Cas9.

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The increase of fat content may be linked to iron overload

Recently, Liang Bin research group at the Kunming Institute of Zoology of the Chinese Academy of Sciences found that iron overload can lead to the increase of expression of ferritin in C. elegans and fat content. The study has been published online in the journal Genetics.

Numerous clinical studies have found that the content of the body's iron and serum ferritin (dynamic iron storage protein) is highly associated with obesity-related diseases (such as diabetes and fatty liver), and reduce the iron and ferritin content can alleviate these metabolic disease symptoms. However, the molecular mechanism of fat accumulation of iron overload cause is unknown.

Model organism C. elegans life cycle is short, easy to carry out large-scale genetic screening, the researchers found, and mammals, iron overload can lead to increased expression of ferritin in C. elegans, increase the fat content.

The study found that nematode causes serum iron overload - increase glucocorticoid-induced kinase SGK-1 expression, the role of fatty acid transport protein ACS-20, a large number of lipid transport food into the cells by intracellular lipid droplet protein will lipid transported to the lipid droplets in the store, a lot of accumulation of fat leads to obesity nematodes. Meanwhile, the family of cytochrome P450 CYP-23A1 played a role in fat metabolism and balance iron metabolism, CYP-23A1 gene knockout nematodes cause more susceptible to iron overload, more fat accumulation in the cells.

The study showed that serum - glucocorticoid-induced kinase SGK-1 is a core gene of new regulation of iron metabolism and lipid metabolism. The mouse with SGK-1 knockout showed no other obvious phenotype, therefore SGK-1 is expexted to be a potential target to treat obesity and obesity-related metabolic diseases which are led by iron overload.

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Scientists firstly use fluorescent probe to analyse the mystery of cytomembrane

Recently, scientists from Japan, the United States and India firstly observed the raft domain in cytomembrane in live cells, namely the active site carrying special molecular community in cytomembrane. Related study is published in the international journal Nature Chemical Biology. A researcher Naoko Komura said in the study that the speculation of the raft domain with special cell membrane structure domain has gone for more than 25 years, but scientists had never really observed into the structure in living cells, while the researcher made major breakthrough in this study.

In the study, researchers observed the behavior of ganglion monoglyceride. Ganglion monoglyceride is a special kind of lipid molecules, which plays an important role in a variety of biological processes in the body, including the formation of lipid raft domains, the entrance of toxins into cells and receiving chemical signals. However, scientists are still not exactly sure about the working mechanism of ganglioside, so researchers lack for probe to accurately track the movement of ganglioside till now.

In the previous study, researchers were not able to simulate the behavior of a natural ganglioside in artificial model systems, while researchers adsorbed a fluorescent label on a ganglioside in this research, then they took advantage of adsorption fluorescent markers which were absorbed in specific sites synthesized to compound four holistic ganglioside; using this new type of fluorescent analogs and with the combination of unique high-resolution fluorescence molecular imaging technology, researchers have achieved the record of special ganglioside in living cells for the first time.

Researchers reveal how to form ganglioside CD59 protein carry cholesterol and lipid raft region, CD59 GPI-anchored receptor proteins belong to the family of one; Dr. Kenichi Suzuki said the technology is difficult to observe the use of normal fat cells the dynamic behavior of mass raft region, and in this paper we use fluorescent probes ganglioside achieve this purpose, many scientists now can begin to conduct in-depth studies to reveal how toxins, bacteria and viruses invade to cells.

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The brain of people with a long-term insomnia lacks for special nerve cells

Sleeping is one of the most important activities for the brain in a day. Recent studies have shown that when we fall into a deep sleep, our brain will start to do logistic work to clean up the debris of all-day work and help us reset the neural network, ensuring that it can run efficiently again when we wake up again. But lack of sleep would deprive the important rest part of brain, leading us to a tired condition during the daytime.

According to the report in US Times on April 5th, a group of researchers from China and Europe carried out a detailed analysis on insomnia, the study of how insomnia affects brain cognitive, perceptual and emotional part.

Brain imaging study compared the results of 23 normal sleep insomnia staff and personnel. Researchers focused on the brain's white matter volume. White matter volume can reflect what is called myelin specific proteins on nerve cells attached, which can improve the ability of nerve cells to transmit signals between cells. Early brain imaging studies show that differences in a specific part of the brain people insomnia may be due to a lack of myelin due.

The researchers found that compared with normal people, people with insomnia (refers to more than one month's time sleep problems, daytime sleepiness and sleep disorders people) show significantly less link of white matter, particularly in the area of controlling sleep and wakefulness. Presumably, the signal interference between these regions resulted from the reduce of myelin around neurons, thereby the degree of activity and association between them reduced.

Scientists have found that in fact, insomnia people would lose 83% (that is 5/6) of the nerve diameter, most of which are located on the right side of the brain, that is the area which controls emotion, thinking function and perceptive functions like sense of light, smell and touch. In the future, more research is needed to explain what might cause the differences of brains among people with insomnia.

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CRISPR tool shows new potential in gene editing

Accurate DNA / gene replacement is a promising genome editing tool and can be easily extended to molecular engineering and design breeding. Currently, CRISPR / Cas9 system can be well used as a tool for plant gene knockout. For instance, Chinese Academy of Agricultural Sciences CRISPR achieved soybean genome editing; Anhui Academy of Agricultural Sciences made use of CRISPR to edit rice genome; applying genome editing technology in plant genes functional identification and crop breeding. However, gene replacement in plants has been rarely reported.

A simple method for precisely targeted genome editing could have important applications in terms of functional identification and genetic improvement of plant genes. In recent years, meganuclease 1, zinc finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs), has been developed as a sequence-specific nuclease, for targeted double-strand breaks (DSBs) introducing DNA, in order to let us conduct gene editing through endogenous DNA damage repair pathways.

Recently, researchers have associated nuclease based CRISPR system, developed a new guide RNA gene editing tools. CRISPR / Cas9 nuclease system, can be a chimeric RNA (a so-called single guide RNA, sgRNA) targeting a particular genomic locus, as compared with protein targeting tool guide, have a higher degree of flexibility targeting selection sex. CRISPR / Cas9 system has been proven to promote genome editing different species, including mammals (including humans), microorganisms and plants.

Use CRISPR / Cas9 achieve knockout, it represents the first application of this system, because the Cas9 induced DSBs, can be connected via a non-homologous end (NHEJ) mechanism to repair, which is an error-prone repair pathway, may be introduced in the DNA repair process short deletion or insertion. HDR (homology-directed repair), is an alternative method for repair of DSBs chromosome, the genome of the plant engineering more attractive, because it can achieve more subtle modifications of the DNA sequence, including DNA correction, replacement or targeted gene knock , or any type of mutation.

HDR-dependent target gene replacement or knock provides an unprecedented opportunity for genome editing, but also more challenging because the targeted DSB (s) must be a recovery template coexist. Using a pair of the sgRNAs Cas9 TALENs or nucleases can generate targeted genomic deletion mutation. Dual-induced DSB damage or deletion mutation, targeted gene replacement is also a necessary step.

Stable transformation CRISPR / Cas9 of, and a vector genome editing necessary element contains (by Agrobacterium-mediated transformation), by identifying "non-transgenic" organism easily screened. About HDR-mediated gene targeting, Fauser et al demonstrated that nuclease and nicking enzyme systems are effective tools. When paired sites near each other, the precise design paired sgRNA / Cas9 nicking enzyme neighbor - which may have enhanced specific method can be used for targeted gene insertion, gene stacking and Knock. However, to date, no study in vivo targeted gene replacement event created in plants, but also has a lower risk of GM contamination.

In this study, the researchers targeted two MIRs (AtMIR169a and AtMIR827a) two flanking region through a pair of passing sgRNAs. They first designed a double sgRNA / Cas9 carrier composition (construct # 1), successfully removed the miRNA gene regions --MIR169a and MIR827a. By PCR and subsequent sequencing, the researchers validated these shortcomings, so MIR169a and MIR827a sites generate 20% and 24% deleted efficiency.

Then, they achieved the targeting switch of a target gene through the stable conversion between CRSPR / Cas9 and a donor template DNA donator templater, in which the same point of the sgRNA target plant is designed to remove the target gene and remove DNA donator which promotes HDR. These findings demonstrate an alternative strategy which uses CRSPR / Cas9 system for genome editing by gene replacement.

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How do plant meristemoid cells regulate organ size?

Plant meristemoid cells are a class of cells which have activity of stem cell and they are distributed between the leaves epidermis cells with differentiation and expansion. According to statistics, about half of leaf epidermal cells are derived from the meristemoid cells, but the molecular mechanism of how plant meristemoid cells determine organ size is hardly known. Li Yunhai's Research Group and Wang Yingchun's Research Group at The Chinese Academy of Sciences Institute of Genetics and Developmental Biology collaborated with Dirk Inze's Research Group in Belgian and other cooperation and discovered an important mechanism of the plant meristemoid cells' regulation function in organ size.

Li Yunhai's Research Group has identified a number of key factors in organ size regulation. Wherein, DA1 encoding a receptor protein ubiquitin, da1-1 mutation produced a large body organ. The latest study found that, da1-1 suppressor mutant sod3-1 limits meristemoid cells proliferation, thus affecting the size of the organ. Genetic analysis showed that this gene DA1 acting on different genetic pathways. SOD3 gene encodes a transcriptional regulator SAP. Overexpression of SAP have a big organ, organ size indicates that SAP is a positive regulatory factor. Further studies showed that SAP is an F-box-containing proteins WD40 repeat domain. SAP may interact with SCF complex member ASK1 / 2 and CUL1 to form SCFSAP E3 ubiquitin ligase complex. SAP is capable of interacting transcription factors PPD and PPD ubiquitin-mediated degradation. Genetic analysis showed that SAP and PPD function in the same genetic pathway through the regulation of plant meristemoid cells proliferation to decide the organ size.

The study revealed the F-box protein transcription factors PPD SAP and interaction, and mediates ubiquitination and degradation of PPD, thus regulating the molecular mechanisms meristemoid cells proliferation and organ size. The study not only finds the new mechanism of plant meristemoid cells regulation of organ size in theory, but also provides theoretical basis and genetic resources for breeding high-yield plant.

The study results were published online April 6 in Nature Communications. Doctoral candidate Wang Zhibiao in Li Yunhai's Research Group is the first author of this paper, paper and Li Yunhai is the corresponding author. The study was funded by the National Natural Science Foundation of China and transgenic major projects.

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The gene insertion technology of Sleeping Beauty transposon is greatly improved

"Sleeping Beauty" transposon is widely used in the transformation of the genome, and it shows great potential in clinical trials leukemia and lymphoma. EMBL scientists have recently solved the key structure of "Sleeping Beauty" transposon, and they greatly enhanced the efficiency of this transposon inserting genes by making improvements based on the structure. The study was published in the journal Nature Communications on March 31th.

In the treatment of leukemia and lymphoma, "Sleeping Beauty" transposon is used to insert genes to a patient's T cells. After transformation of these T cells back to the patient later, the ability to search and destroy cancer cells. This method is simpler than rely on viral vector gene therapy is much more, the cost is relatively low. For this reason, "Sleeping Beauty" transposon attracted many pharmaceutical companies, will soon enter clinical trials.

Therapeutic T cell transformation and selection takes time, which is a major bottleneck in gene therapy. T cell transformation and migration faster, better patient prognosis, treatment costs are lower. However, to date only people on the "Sleeping Beauty" transposon is modified based on speculation. To this end, EMBL researchers determined the structure of "Sleeping Beauty" active region.

Inserting gene therapy includes "Sleeping Beauty" transposon and CRISPR / Cas9 advantage. CRISPR / Cas9 cleave specific sites in the genome, is the ideal way to remove the genetic error. However, CRISPR / Cas9 cannot be directly inserted gene fragment, relying instead on cell repair mechanisms. "Sleeping Beauty" transposon can simply bring own fragment inserted into the genome, and its efficiency has been improved significantly. "We designed a variant of 30% higher efficiency than the existing version," who led the study Orsolya Barabas said.

Scientists have found that in May last year, were high hopes that gene therapy may not completely solve the problem as people expected. Two clinical trials leading medical journal "New England Journal of Medicine," published show that gene therapy to restore vision will fail within a few years.

In July last year, researchers at Harvard Medical School and Boston Children's Hospital by gene therapy, the success of genetic deafness in mice restored the hearing. The results are published in the journal Science Translational Medicine for the treatment of hearing loss due to mutations basis.

RNAi makes the cells degrade corresponding mRNA by introducing siRNA or shRNA and conducts genetic screening according to loss of function phenotype. However, RNAi is relatively prone to error. UCSF research team largely overcame the off-target effects of RNAi for genome-wide screening through the establishment of a complex mix of ultra-shRNA library. They further enhances the activity of the shRNA by improving the system to showcase a new generation of shRNA libraries which is targeted the human and mouse genomes. The results were published in the journal PNAS. Studies have shown that a new generation of RNAi library's performance in the test is equally compared with CRISPRi.

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The mechanism of two new drugs for treating basal cell carcinoma

In an article published in the journal Cell, the leading scientists from the United States transformed Genomics Research Institute (TGen) and the Mayo Clinic detailedly describe the mechanism of two relatively new drug helping patients with basal cell carcinoma.

Basal cell carcinoma is the most common type of skin cancer in the United States with nearly 2.8 million new cases in each year. The sunny Arizona has the world's highest incidence of skin cancer. Anti-cancer drugs and Sonidegib Vismodegib inhibit a component of Hedgehog cell signaling pathway - a protein called the Smoothened (SMO). According to this article published in the journal Cell on February 25th, unchecked SUMO sends a signal to other proteins along the Hedgehog signaling pathway, resulting in the activation of cancer.

The journal Cell specially invited Dr. Daniel Von Hoff and Aleksandar Sekulic made the report. Dr. Von Hoff is a famous professor and chief physician in transforming Genomics Institute. He is also the chief scientist in clinical trials cooperated by HonorHealth and TGen and Clinical medicine Professor of Mayo. Dr. Aleksandar Sekulic is an associate professor of dermatology and deputy director of the Department of Dermatology as well as deputy director of the Mayo Clinic Personalized Medicine Medical Center.

In the latter an FDA Phase I clinical trial led by TGen and Mayo Clinic-led Phase II clinical trial, in 2012, approved Vismodegib as a first line treatment of basal cell carcinoma. This is at TGen-HonorHealth cooperation test; get the first drug approved by the FDA, and the FDA-approved treatment inoperable basal cell carcinoma of the first drug.

In 2009, "New England Journal of Medicine" (NEJM) Journal, Dr. Von Hoff recorded some initial findings described Vismodegib effects in dealing with some of the Hedgehog signaling pathway gene mutation.

Dr. Sekulic led to the subsequent stage Mayo Clinic Vismodegib pivotal clinical trials, so that in 2012 Vismodegib received FDA approval. Published in 2012 in the second article in NEJM, Sekulic study has found Vismodegib (trade name Erivedge) in 43% of patients with locally advanced basal cell carcinoma and 30% of patients with metastasis in patients with reduced basal cell carcinoma tumors.

It received FDA approval in 2015 of a second SUO inhibitor Sonidegib (trade name Odomzo) in patients with locally advanced basal cell carcinoma in the response rate was 44%. It is not approved for treatment of metastatic cancers.

Basal cell carcinoma (BCC) is the most common form of cancer, 90% of people there is risk, especially in older people, UV radiation and more. Although this cancer is common, it is not very deadly. So far, the understanding of the BCC is still very limited. To this end, the University of Geneva (UNIGE) of geneticists sequenced these skin tumors DNA, which identified the oncogene. The study published in the March 2016 Nature Genetics magazine for new personalized therapy foundation.

SMO inhibitors have in clinical studies for the treatment of various cancers. Although the majority of patients receive Vismodegib after treatment, access to significant clinical benefits, but some patients often develop resistance. Published in the journal Cancer Cell 2015, two papers discussed basal cell carcinoma drug resistance mechanisms.

Basal cell carcinoma is the most common cancer in the population of European. Although it is not as fatal as other skin cancers, it can be disfiguring. Researchers reported in 2009 in the journal Nature Genetics that they had identified two new variations associated with basal cell carcinoma.

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Promoting and applying the multiple gene detection

The 21th National Comprehensive Cancer Network (NCCN) Annual Conference was hold from March 31-April 2 in 2016 in Hollywood. The conference added several new gene mutation detection for the hereditary risk management of breast and ovarian cancer.

Recent studies have found PALB2 gene mutation associated with breast cancer invasiveness, and RAD51C, RAD51D, BRIP1 gene mutations increase the lifetime risk of ovarian cancer. Dr. Tuya Pal American Cancer Research Center in Moffett said, "In the past year, more and more data indicate that these new genes are associated with ovarian cancer risk. Salpingo oophorectomy recommended or considered by NCCN guidelines in the past which reduce risk are greatly limited by BRCA1、BRCA2 and Lynch syndrome."

She said, "With the presence of BRCA1 gene mutation, the lifetime risk of ovarian cancer reaches 44%; With the BRCA2 gene mutation, the risk reaches 27%; with Lynch syndrome, the estimated risk reaches about 10%. Based on the current multiple studies, we believe that the evidence of which is similar to BRCA1, BRCA2 shows that the mutations of BRIP1, RAD51C and RAD51D increase the risk of ovarian cancer."

Dr. Pal noted, NCCN guidelines do not incorporate these new mutations as tubal oophorectomy recommended indications. She said, "This is a recommendation that can be considered, but we can discuss it and I will not therefore strongly recommend salpingo-oophorectomy, but the situation should be to communicate with patients if their bodies have these mutations, then. prophylactic oophorectomy is a reasonable choice "have a family history of ovarian cancer population should understand this information, Dr. Pal added:." family history is an important reference, if we find a strong risk family history of ovarian cancer, it should be based on new mutations recommended preventive cancer risk control. "Given the current ovarian cancer are not better screening methods, gene mutation is particularly important.

PALB2 has become a high-risk breast cancer gene mutations in one, and other related genes in breast cancer risk as well as BRCA1, BRCA2, PTEN and PT53. When To reduce the risk of cancer and prophylactic removal of the breast, to refer to these genetic changes.

The risk of breast cancer PALB2 mutations female life is about 35-40%. Studies have shown that breast cancer gene mutation associated PALB2 aggressive form. "If individuals carrying BRCA1 mutations develop into breast cancer, perhaps no big deal, because the vast majority of patients are diagnosed early. But when accompanied PALB2 mutation, in view of such strong invasiveness of cancer patients, and therefore need to carefully consider whether to take prophylactic mastectomy. "said Dr. Pal.

Genetic testing for breast cancer treatment has important significance. Once diagnosed with breast cancer patients by detecting understand their genetic predisposition, and accordingly decide what kind of treatment. If the tumor is detected before the genetic risk of breast or ovarian cancer can be proactive and prevent these cancers.

With the popularization and application of multi-gene detection, the gene diagnosis in the field of breast cancer has undergone many changes. But the development of technology can't change the role of the physician. The reasonable and appropriate interpretation of test results is essential. The physician should fully inform the patient whether it is positive or negative results, and the significance of these results for cancer management should be fully explained.

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Researchers confirm the key mechanism of tau protein preventing the formation of memory

As we all know, twisted tau protein fibers would aggregates in the brain cells of Alzheimer's patients, but their exact role in this disease remains unclear. Now, a study in mice conducted confirms how human memory formation tau hinder key mechanism - strengthening connections between neurons.

In healthy cells, tau protein to help secure microtubules, while microtubules act as the surrounding cells transport substances track. However, in Alzheimer's patients, the protein becomes toxic, but the important question is what form of outstanding tau toxicity.

In the latest study, from San Francisco's Gladstone Institute of Neurological Disease Li Gan and colleagues found that the brains of patients with Alzheimer's disease possess a higher level of special tau. It is with a particular change and is known as the acetylated tau.

They then studied the acetylation of tau in a mouse model of Alzheimer's disease role. The study found, it will accumulate in the synapse connections between neurons. When people form memories, synaptic cell membrane by insertion of additional receptors can be strengthened, and this enhances their response. However, acetylated tau depletion of another protein called KIBRA, and KIBRA essential for synaptic strengthening this mechanism.

"We are very excited because now we have learnt the link between tau and memory." Gan said, "We are very cautious, because we know that this may not be the only link in understanding this mechanism, we are still in early stages."

In the trained neurons, restore KIBRA levels can reverse the effects of acetylation of tau and restore its ability to strengthen connections. Gan believes that this provides a strategy for the treatment. "If we provide more of these proteins into neurons, we can repair generally-observed loss of synapses enhancements."

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Learn gorilla genomes more accurately

Latest Advancement of gene sequencing technology, researchers have significantly improved the previous assembly of the gorilla genome. To better understand human biology and genetic variation, with a complete, high-quality data is quite important and we have recently relatives of non-human primate genome.

The first complete genome of a gorilla was sequenced in 2012. However, the genome contains more than 400,000 blank gene sequences, and the previous method of assembling genome has led to some inaccurate gene structure. To this end, David Gordon and others used long read sequencing technology along with a unique combination of algorithms to reconstruct an accurate much of the gorilla genome. The DNA they used was isolated from the body of a western lowland gorilla called Susie in Lincoln Park Zoo in Chicago. The comparison between Susie3 with the previous gorilla genome assembly (gorGor3), this new assembly (Susie3) contigs decreased 96% contigs refers to a short sequence may lack information about its location in the genome.

Similarly, the authors say, for gorGor3 genome sequence 433 861 blank, they have filled 94%. To better understand the genetic variation in these species, the team used a short read sequences from six other Western lowland gorillas. The Susie3 and compare the human genome assembly revealed a total of 117 512 and 697 insertion and deletion mutant inversion. These events have more than 86% of previously undiscovered.

The result of our species and our non-genetic variation between human cousins provide a better understanding, but also demonstrates to other mammalian genome sequencing more accurate method.

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Scientists identify that change of DNA can decrease 3 years of human life

Scientists identify that change of DNA can decrease 3 years of human life. Scientists have found that the differences between the two independent DNA regions of human chromosomes may affect the person's life. These two changes, called variant, relatively common in humans. There are more than two thirds of humans would inherit a single copy of a variant from father or mother.

The study found there is a variant of the single-copy might reduce human life expectancy of up to one year, about two-thousandths people inherit two copies of the variant of the research team predict the average person's life may be reduction of 3 years. One variant associated with increased lung cancer risk and a serious respiratory disease associated genes. Another variant occurs in a gene associated with high cholesterol and Alzheimer's disease.

The study also found that the impact of these variants for male and female life expectancy is different. Genes associated with Alzheimer's disease a greater impact on women, and lung disease associated with a greater impact on men variability.

Researchers at the University of Edinburgh, by analyzing more than 152,000 people have the information they found that these people were involved in UK Biobank study, which is a long record of thousands of volunteers, health information projects. The study has been published in Nature Communications and is funded by the Medical Research Council.

Peter Arthur Population Health and Information Sciences Institute of the University of Edinburgh, Dr. Joshi said that although the impact of these big people life mutation on a little surprised, but remember this is only part of the situation, it is very important. The greatest impact on life is our way of life, which we can control.

Jim Wilson from Arthur Population Health and Information Sciences Institute of the University of Edinburgh said the finding is just tip of the iceberg. With the accumulation of this data, we expect more discoveries. What is exciting is that some may be beneficial to health.

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