elisa kit: 三月 2016

2016年3月31日星期四

Gene therapy can improve the cardiac function of patients with heart failure

A new study shows that gene therapy appears to improve the patient's heart function, which is undoubtedly an excellent news for millions of patients with heart failure.

"The end result of gene therapy is: reconstruction of damaged heart tissue, which can help patients restore mechanical function of the heart," Dr. Justine Lachmann explained. She worked at the Ministry of congestive heart failure NewYotMineola Winthrop University Hospital. For heart failure patients, their heart function weakened or impaired pumping function of the heart disorder. The American Heart Association says this deadly disease for more than 570 million Americans had an impact.

Although the disease on many people's lives had an impact, but there has not been effective in the treatment program, Lachmann represented. "We are through drug intervention, has successfully extended the life of heart failure patients, the drug can change the body produces chemical signals on the heart," she said. "But the result is still very serious long-term use, because it can cause permanent damage to the structure of the heart, such as heart attack."

In this study, the researchers recruited a total of 56 patients with heart failure, their heart function declined by 40% in this study, the researchers through the tip of gene therapy to reverse their heart damage. Gene therapy involves "gene transfer" process, i.e. a harmless virus gene to transport fine cells inside the heart. The gene, once in place, it will produce a protein called AC6, the researchers said that this protein can improve the situation of failure of heart cells.

Some patients had been treated in the new study, while others took placebo. Researchers conducted a one-year follow-up investigation for the participants.

The related articles of the research are published online on March 30th in the journal JAMA Cardiology. Studies show that AC6 gene transfer therapy appears to help restore heart function. Researchers found that gene therapy will increase drug treatment effect.

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New nanoparticles are developed to improve cancer treatment

Researchers from the China University of Technology, Emory University and the Georgia Institute of Technology reported that they have developed a stimuli-responsive clusters of nanoparticles to improve tumor penetration and efficacy. The findings were published in the journal PNAS on March 28th.

Professor Jun Wang from China University of Science and Professor Shuming Nie from Technology and Emory University and Georgia Institute of Technology and Nie Shuming are the co-corresponding authors of this paper. Professor Jun Wang is interested in targeted cancer therapy, cancer stem cell research, nanotechnology drugs and drug delivery systems, RNA interference, nano-biomaterials. He has published more than 120 research papers in journals like Science Translational Medicine and Angew Chem Int Ed.

Cancer is a serious hazard to human health, one of the factors that undermine family and social harmony. In China, cancer has become the first cause of death in urban and rural residents, and the incidence of cancer is in a rapid increase of the number of annual cancer incidence of about 2.6 million, 1.8 million people died. In Europe and other developed countries, cancer is also ranked second in the cause of death.

Chemotherapy is traditional for the therapy of cancer, but the treatment is in advanced clinical widely used lack of selectivity. They are widely distributed in the body, especially in some normal organs and tissues may also have more distribution, reducing the use of this aspect of the drug, on the other hand also on the normal tissues and organs cause significant side effects, leading to patient tolerance reduced, weakening the therapeutic effect of the drug. In addition, long-term use of chemotherapy drugs can also cause cancer cells to chemotherapeutic drug resistance, but more difficult post-treatment. In view of this, looking for specific tumor sites, to improve the selectivity of chemotherapy drugs, it has targeted to become one of the key issues in recent years, cancer research treatment.

With the rapid development of nano-bio-technology, nano-biotechnology and disease treatment of combining the new discipline arising from nano - medicine material gradually attracted the interest of researchers. Nano drugs has become an international hotspot frontier areas of nanotechnology and biomedical research. The main objective of the nano cancer drugs is effective to treat cancer cells transferred to the Department within solid tumors. However, there are still a series of obstacles to a biological drug to reach the target cells at the nanometer.

Here the researchers report that they have developed a stimuli-responsive nanoparticles clusters, and confirmed that according to the endogenous stimulate tumor microenvironment adaptations such as size, zeta potential and drug release rate and some physicochemical properties so eventually overcome these obstacles, especially tumor infiltration may become a bottleneck.

Once iCluster accumulation at the tumor site, tumor cells outside the natural acidity will touch discharged polyamide conjugated platinum (platinum) prodrugs - amine dendrimer (diameter of about 5 nm). Such structural changes greatly improve the treatment of tumors and intracellular penetration. Internalized in the dendritic cell molecule prodrug further decomposition in cisplatin to kill cancer cells. Researchers in various refractory vivo tumor models, including the poor permeability of pancreatic cancer and metastatic cancer drug confirmed iCluster superior anti-tumor activity, demonstrating its universal and broad applicability.

2016年3月30日星期三

The Nature publishes the great progress of neurology

Even the simplest neural network in brain is made up of millions of connections, exploring the huge network is vital to understand the operation mechanism of brain.

An international team led by R. Clay Reid、Wei Chung Allen Lee and Vincent Bonin from the Allen Institute for Brain Science, Harvard Medical School and neurological research center Electronics Flanders (NERF) of R. Clay Reid released the largest cerebral cortex neurons connected network by far, revealing several key factors related to the mechanism of brain network organization. Their findings are published in the journal Nature March 28th.

Dr. R. Clay Reid, who a senior researchers at Allen Institute for Brain Science, said, "This is a climax of nearly a decade ago to start a research project. Network brain too big and too complex to understand cannot be fragmented, so we took advantage of some of the high-pass technology to collect the amount of brain activity and brain wiring large data sets. We found that the effort is definitely worth it, and we are learning a wealth of information about the network structure of the brain and ultimately how brain structure and function associated."

The main author of the paper, neural biology instructor at Harvard Medical School, Dr. Wei-Chung Lee said, "Although the study is always worked in a substantive chapters landmark, this is just the beginning. By discovering the circuit wiring and neurons the relationship between network computing, we now have the tools to begin to reverse-engineer the brain."

Flanders Neurological Research Center electronic project leader Vincent Bonin said, "For decades, researchers have been studying the brain activity in isolation and wiring. We have achieved is unprecedented detail for both areas to bridge the electrical activity of nerve synapses with each other nanoscale connection between the link."

Lee added, "We have discovered the first evidence of anatomical structure of the module, as well as the structural basis of the function-specific connection between neurons in the cerebral cortex of the network. Our approach allows us to define the organizational principles of neural circuits. We is now ready to discover the cerebral cortex connection motif (motif), they are likely to be the basic building blocks of the network functions of the cerebral cortex."

Lee and Bonin first identified in response to specific visual stimuli in the mouse visual cortex, such as bars or bars on the screen neurons. Lee then made thin brain slices, captured these cells and synapses millions of detailed images of the target, followed by a three-dimensional reconstruction. American commentators on both coasts at the same time the team through some 3D images to track a single neuron, and locate the connection between individual neurons.

Analysis of this wealth of data generated some results, including the structure of the first direct evidence to support this view: perform similar tasks to perform different tasks than neurons neurons are more likely to connect with each other. And while tangled with completely different functions to perform many other neurons, these connections greater.

Reid said, "This unique study is part of a combination of functional imaging and detailed microscopy. These microdata reached an unprecedented scale and detail. We first learned about the specific function of neurons get some very powerful knowledge then observe how it is similar or different work to complete the connection of neurons."

Reid said, "It's like a symphony orchestra musicians seated randomly. If you just listen to some of the musicians neighborhood, it does not make sense. By listening to everyone, you will understand music; it actually becomes much easier. If you then go to inquiry every musician who he listen to, perhaps you can even figure out how they are creating music. There is no conductor here, so orchestra needs to communicate."

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The new progress of the liquid biopsy technology

High-throughput sequencing of Circulating tumor DNA (ctDNA) is expected to achieve a personalized cancer treatment. However, the cell-free DNA (cfDNA) in blood is limited, limiting the analytical sensitivity. To this end, researchers at Stanford University have developed a method for correcting errors can be detected frequencies as low as 0.004% of the mutant allele.

In the study published in the journal Nature Biotechnology on Monday, the researchers introduced the approach called integrated digital error suppression (IDES). It is based on the Stanford team developed before a ctDNA detection technology called CAPP-seq, and it has been acquired by Roche.

Previously, the limit of detection CAPP-seq technology is 0.02%, but many have the wrong sequencing fragments. To resolve these errors, the research team first devised a molecular barcodes strategy. Many ctDNA detection developers also use this program to reduce the error rate. Single-stranded DNA and double-stranded DNA barcodes strategies exist, but there are drawbacks. Double-stranded DNA barcodes in reducing errors on better, but less efficient than single-stranded DNA barcoding is therefore not suitable ctDNA limited amount of samples.

To this end, they set out to design a hybrid strategy. First, they devised sequencing connector that can be used for molecular barcodes of single and double stranded. Each strand of the double-stranded molecule of the first four-base mark a bar code, bar code called an index. Then they add two dinucleotide barcode on each of the two strands of the joint, called an insertion bar code. After sequencing, the bar code can be inserted into a complementary match to reconstruct the original double-stranded DNA molecule.

The second step, the Stanford team designed a computational tool that can correct sequencing or PCR system error. To achieve this, they first samples of 12 healthy adults carry CAPP-seq detection. The researchers reported that, despite all kinds of SNV has a background error, but the most common is a G → T transversion, and the error C → T and G → A also has.

They found that, G → T error occurs because the Hybrid Capture Process oxidative damage. They used a computational method to suppress these errors. The combination of these two strategies, so that the error rate has dropped by 15 times, which is by 30 healthy control samples and 142 samples of non-small cell lung cancer confirmed.

Researchers are also NSCLS samples on this verification test. First, they examined 41 patients with advanced NSCLS EGFR mutation hotspot. They detected 88 plasma samples to 412 EGFR mutation, all variations have been confirmed by a tumor biopsy sample. In addition, this test did not check out any false positives.

They then assessed the technical limitations in the detection of the reference cell lines. They created a reference cell lines mixture, wherein the frequency of allelic variation at 0.05-1.6%. They found that the bar code policy and calculation methods are complementary correction, combined with better results. Theoretical detection limit of this method is 0.00025%.

Finally, they used this method to monitor the 30 NSCLC patients with mutations; these patients have had tumor genotyping. The researchers found that they could detect the mutation frequency as low as 0.004%. "To our knowledge, this is the minimum amount of ctDNA with deep sequencing detection by far," the authors wrote.

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2016年3月29日星期二

PNAS: the secret of aging is can be revealed by your body metabolin

Metabolites produced during metabolism can provide a lot of information on individual health, disease, diet and lifestyle. Now, they can tell us more. Researchers and collaborators at Japan Okinawa University Institute of Science and Technology (OIST) Kyoto University recently found some particular metabolites associated with aging, and illustrates the process of body aging. Professor Yanagida at OIST led the team and published their results in the journal PNAS.

To find and analyze these metabolites, the researchers obtained blood samples containing red blood cells (RBCs) including 30 healthy individuals: including 15 young adults (29 ± 4 years) and 15 elderly (81 ± 7 year old). In the past, all the studies had ignored RBCs, but because RBCs accounts for nearly half of the volume, the researchers believe it is worth exploring.

Then they used a technology called liquid chromatography - mass spectrometry (LC-MS), identifying metabolites in the blood. Thus, they can calculate the coefficient of variation or standard deviation by dividing average abundance of metabolites to determine the compound which is increased or decreased in vivo in the elderly.

Yanagida said, "We found 14 kinds of age-related compounds. Of these 14 compounds, half of them decrease in the elderly. The study found the reduced compounds are those which are antioxidative or muscular strength related. Thus, the elderly have fewer antioxidants and weak muscle strength.

The other half of the compound is increased and decreased liver and renal function related metabolites. Yanagida said, "This makes sense. Common sense tells us that, as we age, we lose muscle and kidney function ability, but in the past with no scientific way to confirm this is the case." In addition, some occur in the same age-related metabolic signaling pathway metabolites associated changes occurred, indicating the age affect them."

Yanagida said, "Some of the functions related to the compounds show the same tendency to increase or decrease with age, or in other words, they show a similar correlation."

Because of these identified age-related metabolites, antioxidants and muscle strength decrease that consumption of foods high oxides and exercise is very important, especially after 65 years. This can help raise the level of the relevant metabolites in vivo, improve the physical condition. Although still left a lot of longevity and healthy living related unknown composition, the research team will continue to reveal more information about healthy aging.

Yanagida said, "Longevity is a huge puzzle for us. We want to learn how you can make the elderly happy to spend the last leg of life's journey. This is a way we can contribute to human health."

Researchers from Chinese elite school uncovers the roles of miRNA in leukemia

Leukemia is a malignant tumor in hematopoietic system, commonly known as "blood cancer". In this disease, certain types of leukemia cells show neoplastic hyperplasia in bone marrow or other hematopoietic tissues, they can infiltrate the body's different organs and tissues, resulting in dysfunction of each organ and producing signs and symptoms. The leukemia can be divided into acute and chronic categories according to the cell differentiation.

In recent years, people gradually realized that the extracellular microenvironment vesicles (MV) play an important role in the development and recurrence of cancer. Researchers at Chinese Huazhong University of Science and Technology published an article in the journal Cancer Research that the miRNA in micro vesicles will push leukemic transformation of hematopoietic cells. The corresponding author of the article is Professor Guoan Yuan at School of Life Science and Technology of Huazhong University of Science and Technology.

Studies have shown that chronic myeloid leukemia (CML) K562 cell micro-vesicles, to make into leukemia-like cells in normal hematopoietic stem cells. The researchers found that in the early stages of the micro-vesicles hematopoietic stem cell malignant transformation initiated a number of anti-cancer miRNA pathway and defense, but later involved in cell cycle, DNA repair and energy metabolism and carcinogenicity of miRNA genes up-regulated.

Further studies have shown that high levels of expression in micro vesicles miR-146b-5p regulate cancer-related genes, and thereby promote the transformation of hematopoietic cells. This miRNA inhibitor NUMB main function will increase the level of ROS cells, enhancing genomic instability by silencing tumor.

Genes are the blueprint for a protein, while miRNA helps cells decide whether to manufacture these proteins according to the blueprint. miRNA is long non-coding RNA which is 22nt, bearing a crucial function in the regulation of important processes of embryonic development, cell differentiation and organ generation and the like. These short RNAs largely exist in natural cells. They can be paired with the target gene mRNA and hinder its translation and regulate its expression of target genes in the post-transcriptional level.

2016年3月28日星期一

Fluorescence detection technology is applied to track cancer cells

Brazilian researchers have developed a new medical equipment using fluorescence detection, helping to grasp the metastasis route more accurately, improve the operation efficiency and provide patients with a more optimal treatment.

According to local media reports, the device is developed by the San Carlos Institute of Physics of University of Sao Paulo. The main components include two cameras, a group of infrared device used for detecting fluorescence and capturing images and a display. A mobile device is fixed to the bracket, and the doctor can conduct handle operation.

Some substances are irradiated with light of a specific wavelength, and fluoresce after absorbing energy. According to the researchers, the new equipment would deliver fluorescent powder. And using light with specific color to shine the cancer site, then the light send by fluorescent powder with different colors were captured by cameras. Thus surgery experts can determine the location of the sentinel lymph node in real time.

Lymph gland is a very important tissue in the body's immune system. Clinically, the first lymph node metastases must pass through is called the sentinel lymph node.

According to reports, the conventional pathological diagnosis depends on the doctor's subjective judgment on lymphoid tissue slice, but fluorescence detection technology shows higher sensitivity and accuracy and helps to improve surgical safety. Other advantages of this new device include that it can also generate color images and it can record the process of the surgery to be used for subsequent analysis and so on.

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Cells switch its standby mode under different nutrition condition

Under normal circumstances, cells are usually in a highly active state: in the liquid environment inside the cell, ie the cytoplasm, there are numerous metabolic processes; protein and molecular particles frantically from side to side. However, if these cells do not get enough nutrients and cellular energy content decreased, it will result in the conditon that cytoplasmic pH values decreased significantly, i.e., intracellular acidification phenomenon. At the same time, the cells will go into a "standby mode" and this change can help cells survive. A research team from Dresden, Germany, found that changes in the cells of this standby mode, similar to the cell death process that converts from a liquid to a solid state cytoplasm. Thus, sensitive structures inside the cell are protected.

The standby mode of cells is the result of the cells facing with adverse changes such as undernutrition. In this state, the cell metabolism significantly reduced, resulting in the end of the process of cell growth and division. In extreme cases, these cells have little or no differences with dead cells. But they can revive from this state, and when the environmental conditions are improved, they continue to grow and differentiate.

In this study, under the supervision of Simon Alberti, Munder and his colleagues explored the switch of cells' standby mode switch. They mainly studied the yeast cells and observed the response of yeast cells under the condition of starvation. They found that: when metabolic pathways of the cytoplasm lost energy supply, the speed of movement of organelles and molecular particles gradually slowed down, forming a plurality of large protein molecules and these macromolecular structures are clearly visible under a microscope. Cytoplasm showed consistent changes in response to the environment in undernourished condition. Namely: the high sensitivity of the cells were observed by biophysical methods, changes in the material state observation of cytoplasm - from liquid to solid, until the death of the cells into the stiff state. Facts have proved that, pH value of the cytoplasm under starvation condition would significantly reduce, which is a process that plays a crucial role in the process of cellular changes.

It is worth noting that the difference between sleeping cells and dead cells lies: sleeping cell survival can be reversed, while dead cells can not. When the environment is re-added nutrients, cytoplasmic pH value will rise again, the cytoplasm gradually liquefy solid, then the cells will continue to grow and divide. Munder and his colleagues speculated that the key to the switching of cytoplasm's standby mode is: "There seems to have a special control mechanism and in some environments it will produce the material properties of certain provisions to ensure that the cells are survival." Thus, cells seem to be able to control the metabolism of cells by turning off all processes of ways of life to cheat the environment. Whether this mode is shown in human cells will become the focus of future research.

2016年3月23日星期三

Infants get no significant weight after intake of antibiotics

A new study shows that infants don't get the excess weight until they are 7 years old after they received antibiotics within the first six months after birth.

For diseased children, antibiotics are most widely used prescription drugs, but few people understand the impact of long-term antibiotics to health risks. Meanwhile, researchers said animal studies have shown that babies born during the intake of antibiotics can increase the fat content of the body later.

In this study, the researchers studied the relevant data from Delaware, New Jersey and Pennsylvania involving nearly 40,000 children. About 14% of the children were within six months after birth and had intake of antibiotics. Studies have shown that the average age of children receiving antibiotics was only four months.

The researchers also studied the health of 92 pairs of twins. In twins, a child took antibiotics within six months after birth, and the other children not getting the drug. The researchers found that seven years later, the weight of the twin children showed no significant difference.

In this study, the researchers measure the reference weight; body weight is an important sign response and can measure the health of a person. Too thin or overweight is not conducive to health. Standard weight corresponding to the height of an individual's optimum weight value; healthy weight is different from the standard weight and is a range of values. Population within the healthy weight range has lower risk of illness. The articles related to the study were published in the March 22th edition of journal American Medical Association.

"But for the health of children, they still can't intake of antibiotics for no reason at all," said Dr. Jeffrey Gerber, author of the study and came from the Children's Hospital of Philadelphia.

New research on genetic protection factors related to health and longevity

Kongqing Peng group from the kunming institute of zoology Chinese Academy of Sciences collaborated with Hainan Medical College systematically studied genetic protection factors associated with health and longevity, identifying differentially expressed genes associated with longevity. Related achievements have been published recently in the journal Science Report.

Researching and mining the health protection factors of longevity and its pedigree shows great importance for the development of aging-related disease prevention and health policy.

Kongqing Peng cooperation team took Hainan health and longevity as the study population. Through more than 100 samples of health condition and blood biochemical indicators of longevity family’s health, they found: in the aging process, the total levels of triglyceride (TG) and cholesterol (TC) gradually raised high, but they showed a downward trend among the long-lived people. Similarly, although renal function continued to decline with age, the relevant indicators (blood urea nitrogen, creatinine, etc.) had been well maintained in the elderly with longevity.

Cardiovascular disease is the leading cause of death among adults, and the deterioration of blood lipids and renal function is a risk factor for cardiovascular disease in adults. The improvement and maintaining of these indicators among longevity populations may be an important reason that fewer long-lived people suffer from cardiovascular disease. To further define the reasons for improvement in these indicators, the research group conducted transcriptome test on peripheral longevity family members. They successfully identified differentially expressed genes which were significantly associated with these indicators, indicating that the trait did show the base of genetic regulation.

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2016年3月22日星期二

Crohn's disease patients and ulcerative colitis patients show difference of the microbiota

Recently, a study published in the journal Inflamm Bowel Dis reporting that no significant difference in microbiota composition of inflammatory and non-inflammatory mucosa between patients with Crohn's disease (CD) and patients with ulcerative colitis (UC). However, the researchers found the differences between the two diseases in inflammatory and non-inflammatory mucosa.

"This study shows the difference in microbiota bacterium spectrum of CD, UC or inflammatory bowel mucosa," said Dr. Charles N. Bernstein at Inflammatory bowel disease Clinical and research center in Manitoba University.

Bernstein and colleagues compared bacterial communities of IBD patients in inflammatory and non-inflammatory gastrointestinal mucosa. They were collected from 15 patients with CD, 21 UC patients and 7 patients with non-inflammatory bowel biopsies in 166 parts by colonoscopy. Each patient collected 3-4 parts of ileum, cecum, the colon or rectal biopsy. When the internal CD patients with non-inflammatory and inflammatory bowel mucosa were compared, no significant differences were found in any genus door. We have the same results in patients with UC tissues.

However, when patients with CD and UC patients with inflammatory non-inflammatory mucosa were compared, the differences appeared. Compared with inflammatory UC mucosa, the mucosal inflammatory CD Bacteroides door (P = 0.002) and Clostridium (P <0.05) were detected on the door often grade level; Proteobacteria and Firmicutes (P <0.05) regular checks on the inflammatory mucosa of patients with UC.

Between a group of inflammatory CD and UC groups, soft clostridium group (P≤0.05), Bacteroides (P = 0.003), and Pseudomonas (P <0.001) in the number of significantly different genus level. In the CD group and UC group, 13 species abundance significantly different. No inflammatory bowel disease compared to the control group, non-inflammatory mucosa of patients with UC is the most different.

"Our study shows a comprehensive analysis of intestinal microflora, researching on different segments of the intestinal mucosa inflammatory or non-inflammatory," the researchers concluded. "While we have come to this conclusion that mucosal microflora composition doesn't change according to different inflammation, we can find an interesting phenomenon that microbiota of non-inflammatory intestinal microflora of IBD patients shows more diversification than that of inflammatory bowel microflora."

How does RNA editing promote the growth of tumors?

Recently a new study provides new insights for the role which RNA (ribonucleic acid) may play in cancer. The study was published in the journal Scientific Reports, allowing us to learn more about a new mechanism involved in tumor development and progression, and thus may lead to better treatment in the future.

In every healthy human cell, the genetic information connected to DNA is transcribed into messenger RNA and then translated into proteins - important component of all the body tissues and organs. Popular view is that the majority of malignant tumors are caused by mutations in the DNA, which can lead to abnormal activation of the corresponding protein abnormal activation or inactivation, leading to malignant cell growth and uncontrolled proliferation. RNA editing - through this process RNA sequence "mutate" in the transcript after the introduction and it is possible to affect a variety of cellular processes. But the exact mechanism is still unclear.

Previous studies have shown that there are more than one million sites in the genome edited in varying degrees. Although most of these sites belong to the area where proteins are not translated. But according to proof, the difference between RNA editing level tumors and normal tissue is related to the different clinical outcomes. Currently, only a few coding RNA editing site functionality has been characterized. However, whether and how the non-coding region of RNA editing in most things they affect tumor growth, remains a mystery.

In this study, researchers from Boston University School of Medicine (BUSM), analyzed 14 types of cancer, and identified over 2000 genes, RNA editing levels between tumor and normal tissues showed significant change.

The corresponding author, associate professor of medicine BUSM Stefano Monti explained, "This study shows that RNA editing can serve as an important cellular regulation of epigenetic mechanisms beyond genetics / DNA level. An epigenetic effect of components can be offset by change in another genetic component. Therefore, it is very important to have a comprehensive understanding in the change of cancer genomics. Loopholes of appropriate targeted therapy may be found."

2016年3月21日星期一

Neuregulin-1 can start natural repair function after spinal cord repair

Researchers at King's College London and Oxford University identified a signal molecule called neuregulin-1. This molecule can start the natural repair function after spinal cord injury. The study is published today in the journal Brain. The results of this study may be developed into a new therapy someday which can enhance the self-repair mechanisms by manipulating neuregulin-1.

Spinal cord injury has a devastating effect on muscle and limb function, but central nervous system has only a kind of limited ability to repair itself. If scientists can understand this self-repair mechanism, they can help people to develop new therapeutic strategies using existing repair tools of spinal cord to facilitate the ability to self-repair of spinal cord injury.

Researchers at King's College and Oxford University identified one of these tools for the first time - neuregulin-1, which can transmit signals from the surface of nerve fiber damage in the "spontaneous remyelination" in the process. Spontaneous remyelination occurs in spinal cord injury after a few weeks of natural repair process. Spinal cord nerve fibers lose the protective layer of myelin starts the process. Myelin is the key to communication between the brain and the body. However, the nature and insufficient to fully repair spinal cord rehabilitation, may lead to degradation of the surviving nerve fiber function, can affect balance, coordination and ability to act.

The researchers found that mice missing neuromodulation 1 gene self-myelin repair process is completely blocked, the spinal cord nerve fibers still no myelin (If you can’t transmit nerve signals along the spinal cord). Missing neuregulin-1 gene in mice with spinal cord injury repair Results intact protein 1 gene in mice than neuromodulation poor, especially in walking, balance and coordination of movement ability.

Neuregulin -1 spontaneous myelin repair can’t only start, but also as spinal cord nerve cells in the molecular switch can be activated in these cells myelin repair. The researchers believe this is very unusual, because just get myelin repair capacity of Schwann cells usually only repair the peripheral nervous system myelin sheath of nerve fibers, but can’t repair the myelin in the central nervous system.

Psychiatry, psychology and Institute of Neuroscience (IoPPN) neural plasticity and regenerative medicine professor at King's College Medical Research Institute senior researcher Elizabeth Bradbury believes that all people with spinal cord injury can happen at any time, your life may be at the moment it changes, you may lose all sensation and function below the injury site.

Most current treatments are ineffective, it is an urgent need to repair tissue damage and restoring function after injury new rehabilitation therapy. These new findings improve our understanding of the planning body's ability to repair molecular mechanisms. Professor Bradbury adds enhanced by this spontaneous reaction, we can significantly improve the function of the spinal cord after injury. Our study of other central nervous system abnormalities caused by demyelination has value, such as multiple sclerosis.

Dr. Katalin Bartus at king of Medical says, "We hope that this research can raise a platform for future research, which is very important for choosing different Neuregulin-1 levels of testing to improve the functional repair level after spinal cord injury."

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New use of protein has been found to open a new chapter for disease treatment

Researchers at UT Southwestern Medical Center have discovered new uses of RNA binding proteins. The findings reveal potential treatment options for neurological diseases and related disorders (such as autism, epilepsy, and certain types of cancer).

"This discovery enables us to think from the other side: whether our newly discovered RNA binding protein dysfunction leads to these deficiencies," said Dr. Michael Buszczak, who is the author of the study, an associate professor of molecular biology and a senior researcher at UT Southwest regeneration scientific and medical center.

The study article was published in the journal Developmental Cell, and the results showed that: RNA-binding protein (Rbfox) is responsible to oversee the regulation of messenger RNA (mRNA) in the synthesis of protein engineering. Taking drosophila as the objective of study, the researchers found that Rbfox1 protein has a regulatory role during the process.

Gene encoding process, i.e. the process exon splicing of mRNA, Rbfox1 protein plays a key role in the transcription process to make good protein translation success rate doubled. Splicing occurs mainly in the nucleus site, and the study found that the nucleus contains many Rbfox1 proteins. But also found in the cytoplasm of Rbfox1 mutated protein, which is part of the function of proteins that we previously did not know. “We found that cytoplasmic Rbfox1 inhibit the synthesis of certain proteins," Dr. Buszczak representation.

The first author of the study, UT Southwest molecular biology graduate student Arnaldo Carreira-Rosario found that Rbfox1 can bind to specific messenger RNA molecules that block this messenger RNA is translated into proteins. If Rbfox1 protein loss, the mRNA molecules will no longer be suppressed, which may lead to abnormal cell growth or even cancer.

The researchers found that cytoplasmic proteins are Rbfox1 Drosophila germ cell development required. "Without this protein, differentiation of germ cells is blocked in a special stage, it will not be down. They can’t differentiate into mature eggs," Dr. Buszczak representation. Eggs which can't mature will result in sterile fruit fly and in other cases lead to inappropriate cell proliferation which formed a cancer.

Corresponding author of the study, Dr. Mani Ramaswami worked at Trinity College Dublin, Ireland, said the study found a link between Rbfox1 protein function and neuronal development. Rbfox1 protein may have important aspect significance in development of interference with neurological disorders.

"We believe that after the inactivation of Rbfox1 protein, it will affect the expression of certain proteins, ultimately causing disease. But it doesn't affect the process of RNA splicing," Dr. Buszczak said. "If this interpretation is correct, it will affect people on the part of developing regimen of the disease treatment."

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2016年3月18日星期五

British research team firstly discovers the infection mechanism of HIV and Ebola virus

A research team led by the University of Leeds recently observed how the AIDS virus and Ebola virus attach to cells and spread the virus infection for the first time. The latest achievement of this study published in the Journal of Applied Chemistry is hopeful to provide a new method for the treatment of these diseases: blocking the interaction between the virus and cells, rather than eliminating the pathogens.

According to the report of the official website of University of Leeds, the lead author of this research paper, Dr. Yuan at Astbury structure Molecular Biology Center said that so far, the problem that how AIDS virus and Ebola virus attach to cells is still a "black box". Although scientists know that the virus can interact with healthy cells, in which way that they are bound together remains a mystery.

To do this, the researchers used is called "quantum dots" nano-crystals (about the size millionth of a millimeter), mimicking the shape of the virus, as the virus "double" experiment. Quantum dots are fluorescent crystals, color of light emitted depends on the size of its crystals, this property makes quantum dots is applied to a new generation of TV manufacturers, or as an advanced biological fluorescent probes for molecular and cellular imaging.

In order to be able to bind the quantum dot cells, as they must be wrapped in "sugar-coated." Paper co-author, Dr. Bruce Turnbull Astbury structure Molecular Biology Center said that all human cells were wearing "sugar-coated", their interaction with other cells by binding these proteins sugar; virus through the interaction between the protein and sugar attached to the surface of healthy cells, they want to find out what factors control the binding process.

The results showed that the two proteins that interact with the sugar on cell surface ——DC-SIGN and DC-SIGNR, bind with the surface sugar of AIDS virus and Ebola virus in different ways, thus resulting in the spread of the virus. While before this, the two proteins show different personalities like twins and are almost indistinguishable. The study will contribute to the ultimate development of a series of inhibitors designed to bind to specific virus.

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People with high score of coronary artery calcification are more easily to suffer from cancers

Scientists at Johns Hopkins University said that if a person's coronary artery calcium score is high, the risk of suffering from lung disease and kidney disease is relatively high.

According to the report of Associated Press that coronary artery calcium levels are often used to monitor whether people suffering from heart disease and cardiovascular disease, recent research indicates that high levels of coronary artery calcification is a risk of people suffering from cancer on larger. Scientists have determined coronary artery calcium score by using cardiac CT measuring the number and concentration of calcium in the blood vessels, if someone scores high; it means that he is likely to suffer from coronary heart disease and stroke.

Clinical research for the US Johns Hopkins University Ciccarone Preventive Cardiology Center, Dr. Michael Blaha said the coronary artery calcium score is high, it indicates that there are people likely to suffer from cancer, kidney disease, lung disease and cardiovascular disease. Thus coronary artery calcium score can be used to predict non-cardiovascular diseases.

Scientists of 6814 aged 45 to 84 years of the subjects were investigated for up to an average of 10.2 years after the discovery of which 1238 were tested due to coronary artery calcium score high, suffering from diseases such as cancer, kidney disease, pneumonia, blood coagulation disorders, lung disease and other non-cardiovascular diseases. Only 11% did not appear to suffer from coronary artery calcification in subject’s non-cardiovascular disease, coronary artery calcium score greater than 400 subjects 36.9% had non-cardiovascular diseases.

Two-thirds of cancer patients can be measured with calcium. The score of coronary artery calcium score is higher; the risk of suffering of certain diseases is higher. Compared with the normal people, the risk of cancer increases by 53%; the risk of kidney disease increases by 70%; the risk of lung disease increases by three times; the risk of hip fracture increases more than fourfold.

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2016年3月17日星期四

Obesity parents are more likely to have fat daughters than fat boys

Researchers have found that the adverse impact of diet on health can happen through egg and sperm cells to their offspring even it is not under the case of DNA mutations. A mice study recently published in the journal Nature Genetics provides the most powerful evidence for the non-genetic inheritance of organisms' acquired traits by far. Moreover, although previous studies have shown that sperm cells can carry epigenetic factor, this is the first time that such effects were observed in the egg cell.

Scientists have long suspected that parents' lifestyle and behavior choices will affect the child's health through epigenetics. While the DNA or chromosome chemically modified protein can affect gene expression, but it does not change the gene sequence. Therefore, these changes can be inherited remains controversial.

In the latest study, the German Research Center for Environmental Health endocrinologist Peter Huypens and colleagues for 6 weeks to genetically identical mice fed three kinds of food - high fat, low fat or standard laboratory chow - one. Unsurprisingly, eat a high fat diet mice began to gain weight, and damage tolerance to glucose, which are the early symptoms of type 2 diabetes.

Subsequently, the team from the three groups of mice was taken out of the egg and sperm cells, in vitro fertilization and embryo transplantation to get healthy "surrogate" mother's body. Their idea is that if one kind of behavior or physical characteristics can be observed in the offspring, then it can only be transmitted through the egg or sperm cells.

As the offspring of mice subsequently when fed a high-fat diet, obesity has parents who seem to be more likely to gain weight, and glucose intolerance occur, especially if the parents are obese, then. Parents are relatively thin offspring weight gain to a minimum.

Surprisingly, the authors report the difference between the male and female offspring: If the parents are obese, the daughter seems more likely to gain weight, and the son often only shows glucose intolerance. Compared to the father, the mother's diet style seems to have a greater impact on the offspring's metabolism. Huypens said that this is very interesting, because a similar pattern in some human epidemiological studies also appeared.

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Taxol shows its function in biosynthetic pathway

Taxol is the world's leading anti-cancer drug and has proven a significant effect on a variety of cancer since the 1970s. Its molecular structure and mechanism of function is very complex: studies in 1977 showed that paclitaxel could be incorporated into the cell's microtubule assembly, stabilize microtubules, and prevent shrinkage and chromosome segregation associated with the slowdown of cell division.

The researchers believe that metabolic engineering is the production of complex molecules, including drugs, health products, flavors and spices, which are the most promising approaches. Metabolic engineering can produce expected materials by changing the genetic and regulatory system of a single cell - essentially to converting existing cells into a small factory. Taxol is considered to be the most possible candidate of this biosynthetic pathway.

The research results published by an international research team in the PNAS (Proceedings of the National Academy of Sciences) are committed to overcome existing obstacles in metabolic engineering and select a specific precursor Taxol as their target.

An international research team recently published study in on the metabolic engineering is committed to overcoming the existing obstacles, and select a specific pre-paclitaxel body as its goal. Taking into account the new types of chemical metabolic processes including polymerization and cyclization, glycosylation, they tried to use the cytochrome P450 enzymes in Escherichia coli - a high level of oxygenation chemistry to systematic - nature is usually used for molecular oxidation.

Cells use a particular system to construct complex molecules. First, they build bracket by polymerization and cyclization basal metabolic components. Once the stent in place, cut with a portion of the enzyme functional groups modified molecule - basically, the only part of the molecule works - and these functional processes have a hierarchy in oxygenation, which is mediated by the enzyme P450, also very important. P450 is widely present in the natural metabolic chemistry, because it has no selective oxygenation unique ability of activated carbon, which makes it particularly suitable for the synthesis of molecular biology field.

The researchers did not attempt to produce Taxol, because this is a difficult task. Instead, they tried the drug biosynthesis third step systematic. They designed the P450-mediated catalysis in E. coli, and the first time proved that the bacterium is a suitable host plant of cytochrome P450. They wrote, "Ultimately, this work promoted paclitaxel metabolic engineering, and in the past five years the project has been at a standstill."

They also found that high expression of a single passage upstream module can affect the expression of the enzyme, which in turn undermine the overall performance of their molecular systems. Although the exact cause is unknown, they speculate that this may be the results of some resources were exclusive for the P450 enzymes in the later stage. They wrote, "Fully articulated Taxol pathway had not been completed and it appears to be more complex than previously thought. This work laid faster foundation with more efficient expression for P450 enzymes in E. coli. We hope that in the near future, we will see large-scale application of complex biological compounds and valuable natural product."

2016年3月16日星期三

FGF21 regulates the sensitivity of hepatic insulin

Type 2 diabetes is one of the typical chronic disease; insulin resistance plays an important role in the occurrence and development of diabetes. Develop high insulin sensitivity of target drugs; it is currently one of the most effective ways to improve the effectiveness of the treatment of diabetes. Studies show that, FGF21 is produced by the liver and a major hormone secreted by administering FGF21 treatment or overexpression of FGF21 in vivo, can be reduced in obese rodents, monkeys and humans suffering from hyperinsulinemia, insulin resistance, and the risk of hyperglycemia and other diseases. Current research on FGF21 increasing year by year, but about FGF21 in vivo molecular mechanism of action is still not clear.

A recent study by the depth of in vitro and in vivo experiments in mice found that when the liver-specific knockdown of FGF21 receptor βKlotho, insulin sensitivity and blood glucose lowering effect of FGF21 will be reduced; in the mouse liver, primary hepatocytes and human liver cell lines, FGF21 can suppress an increase in mTORC1 activity by insulin resistance caused prove FGF21 is a mTORC1 negative regulatory factor; experiments also found that when over-upon expression mTORC1 downstream key molecule S6K1, FGF21 small insulin sensitizing effect of rat liver and primary liver cells disappear, further studies have shown that, FGF21 is by activating the liver and primary hepatocytes insulin signaling pathway, thereby promoting glycogen synthesis, gene knockout TSC1 activates mTORC1, thereby inhibiting FGF21 the primary role in promoting liver glycogen synthesis right, inferred, FGF21 may be to promote glycogen synthesis by inhibiting mTORC1.

The study reveals the FGF21 in improved hepatic insulin sensitivity and glucose metabolism in balance, the direct effect on the liver, FGF21 may be as complex mTORC1 inhibitor, by inhibiting the activity of mTORC1 complex, increased hepatic insulin sensitivity, promote liver glycogen storage to increase the utilization of glucose, which regulate the body's metabolism of glucose homeostasis.

The study uncovers the role of FGF21 in the liver and liver cells in the molecular mechanism, providing a new theoretical foundation. It also shows that deep discussion on FGF21-mTORC1 signaling pathway will develop new research ideas for exploring new drug targets of treatment for insulin resistance and type 2 diabetes and other metabolic diseases.

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The promising method of anticancer: Immunotherapy

Among a variety of new cancer treatment methods, the best hope is to use the body's own immune system to seek and destroy cancer cells everywhere.

The concept of "Immunotherapy" had come out for a long time. It originated from an accidental discovery of US surgeon William Corley in the 1890s. Corley noted, after neck cancer patients in a severe skin infection, tumor miraculously disappeared. Corley took decades later, the mixed bacteria injected into the patient's tumor, some patients achieved good results.

Corley was not clear the mechanism of his therapy work, but today we know that this is due to the immune system has a continuous monitoring, defense capability of cancer cells, occurs when the body means that a cancerous tumor defense system ineffective. With cancer who occasionally lucky enough to find tumors shrink and disappear naturally, this may be due to their immune system activation delay to detect the tumor's sake.

With Mercury's death, the exploration of immunotherapy in the early 20th century temporarily stopped. Now, as people understand the depth of the immune system, the immune system to achieve the use of cancer therapy ideas rises again. After all, we have the conventional case can be activated by the immune system to treat infectious disease vaccines. However, unlike influenza and measles vaccines against cancer is needed is "therapeutic vaccine", as it is used to treat existing tumors rather than prevention of diseases, which is one of the important reasons for the treatment of cancer obstacles to vaccine. Nevertheless, we can still use the immune system in terms of specificity and memory to achieve the purpose of specifically destroy cancer cells, and the vaccine remains active for a long time after the injection.

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2016年3月15日星期二

New antitumor immune pathway can help mammals fight against the virus' carcinogenic function

Researchers Southwestern Medical Center University of Texas identified a new pathway of innate immunity which can help mammals resist against carcinogenic virus. The study was recently published in the journal PNAS.

Virus-related cancer is actually quite common, "over 20% of human cancers and chronic viral infections," first author Dr. Xiaonan Dong said. Dr. Dong graduated from Tsinghua University seeks to reveal the host - pathogen interaction of molecular mechanisms, in particular autophagy in innate immunity role.

Autophagy is a fairly conservative process, cell by autophagy to clear damaged proteins and organelles. Studies have shown that autophagy-related protein beclin 2 can promote the decomposition of oncogenic viral proteins, inhibit cancer and viral infections caused.

Improve beclin 2 expression, Kaposi sarcoma-associated herpes virus G protein-coupled receptor (GPCR) degrade rapidly, reducing signal transduction promote tumorigenesis. Reduce beclin 2 expression, GPCR virus persists, promote tumorigenesis. This response is part of the endosomal lysosomal transport, and bacterial protein is fed to the lysosome through this process.

"We have a better understanding of the immune system against cancer-causing virus mechanism," who led the study, Professor Dr. Beth Levine said. "Help identify new therapeutic targets and develop new anti-viral therapy."

EB virus (EBV) is a ubiquitous herpesvirus type 4, is closely associated with many tumors, including Burkitt's lymphoma, Hodgkin's lymphoma, stomach cancer, nasopharyngeal carcinoma, and so on. According to statistics, more than 90% of the adult body have lurked virus. EBV infected B cells process has been studied extensively, but it is the mechanism of EBV infection of epithelial cells is still poorly understood. Sun Yat-sen Cancer Center and Harvard Medical School research team found that, NMHC-IIA nasopharyngeal epithelial cells is an important factor-mediated EBV infection.

HPV is one of the most common sexually transmitted viruses and HPV-induced head and neck cancer is increasing year by year. People need to understand molecular changes HPV-positive head and neck cancer, and the development of new therapeutic strategies based on this. Nature magazine published by far the most comprehensive head and neck cancer genome sequencing analysis. Cancer Genome Atlas Program (Cancer Genome Atlas, TCGA) scientists revealed the human papillomavirus (HPV) and the impact of smoking on the head and neck cancer, head and neck cancer compared with other cancers of the similarities and differences, for the diagnosis and treatment of head and neck cancer provided new direction.

Cervical cancer is the second leading cause of cancer in women, especially common in developing countries, where early screening is not common. It found that almost all cervical cancer is the human papillomavirus (HPV) infection. Scientists have long thought that estrogen is the main factor driving the growth of cancer. However, a study published in the journal PNAS shows that the estrogen receptors in cancer cells almost all disappear.

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A RNA binding protein that plays an important role in the process of cancer growth

Recently, a study on gene expression in leukemia cells shows that a kind of RNA binding protein plays an important in promoting the development of cancer in rats. The proteins are usually active in the fetal tissue in the adult body is closed, but it was re-activated in a number of cancer cells. This expression pattern makes it an attractive anti-cancer drug target, because blocking its activity is unlikely to cause serious side effects.

The new study, published in the March 14 of the "Journal of Clinical Investigation" magazine, with a focus on a particularly aggressive B-cell acute lymphoblastic leukemia (ALL) - in children and adolescents, the most common type of leukemia. From the University of California, Santa Cruz (UC Santa) and the University of California at Los Angeles (UCLA) scientists led by a research team found that an RNA-binding protein (referred to as IGF2BP3) in this group of patients with B-ALL cancer cells It is excessive.

In this paper, co-author, UC Santa Cruz molecular, cellular and developmental biology associate professor Jeremy Sanford said, "This protein --IFG2BP3, with many types of cancer and the prognosis is poor exciting about this study is that it goes beyond. We first demonstrated that abnormal expression of this protein is sufficient to induce disease."

Such studies have identified by RNA binding proteins directly regulate genes; many of the genes are shown to be associated with cancer oncogene. In particular, the improved protein has a full understanding of the gene (called MYC) expression, which in turn has a large number of the regulation of the expression of genes associated with cell proliferation.

Compared with other proteins involved in the regulation of gene activity, RNA binding proteins have not been well studied. When a gene is turned on or "expression" of an RNA copy of the DNA sequence of the gene is composed, then, this "messenger RNA" carry the genetic code is translated into a protein, the exercise of some of the cell function. Many factors are involved in the regulation of gene transcription into messenger RNA which and when transcribed, but the RNA binding protein interaction with messenger RNA itself to the post-transcriptional regulation of gene expression has occurred. Scientists are just beginning to uncover the gene expression of post-transcriptional regulation of complexity.

Sanford said the case IGF2BP3 B cell leukemia, RNA binding proteins overall effect is that by altering the expression of numerous genes, and promotes the proliferation of B cells.

Leukemia begins in the bone marrow hematopoietic stem cells; it will cause all the different types of mature blood cells. A wide variety of genetic changes will occur resulting in abnormal proliferation of white blood cells, side by side out of normal blood cells. Sanford at UCLA collaborators Dinesh Rao, is research involving chromosome mixed lineage leukemia (MLL) gene rearrangements in B-ALL cases, this type of leukemia accounts for 5% of B-ALL patients with poor prognosis increased risk of early recurrence after treatment.

In Rao's lab will determine one of these cases IGF2BP3 most deregulated gene, they began working with Sanford laboratory to find out which genes are directly regulated by the IGF2BP3. Sanford and Rao is a friend since college when, Rao know, Sanford laboratory is to use a small number of "capture RNA binds to a specific protein molecule," one of the laboratory technology. This technique is known as single nucleotide resolution crosslinking immunoprecipitation (iCLIP), so that Sanford laboratory capable of identifying hundreds of RNA transcripts in IGF2BP3 binding sites in both B-ALL cell lines. They also found that, IGF2BP3 enhance MYC and other oncogenes in hematopoietic stem cell expression.

By studying this effect in mice, the researchers found, IGF2BP3 overexpressed in bone marrow, can lead to the proliferation of hematopoietic stem cells and B cell progenitor cells, resulting in B-ALL MLL- rearranged some of the features.

Sanford said, "Understanding its mechanism of action, for the exploration of treatment of 'can interfere with the proteins' function in the disease'. There is an important possibility that RNA-based therapies can isolate the protein and prevents it from binding to RNA transcription. This will be one method among the gene expressions related to cancer cell proliferation."

2016年3月14日星期一

Inhibit the development of lung cancer by silencing a gene

Scientists believe that the discovery of the like from bacteria to plants, insects and human organism "conservative" genes among species play an important biological function. Previous limited research on these genes in a gene --Nitrilase 1 (NIT1) showed that it can inhibit the development of cancer. However, the researchers Thomas Jefferson University Sidney Kimmel Cancer Center found that compared with normal cells, Nit1 in common lung cancer cells is a significant overproduction. When Nit1 silenced, lung tumor growth was inhibited.

Their findings are published in the journal Oncotarget, the first description of the growth and progress Nit1 non-small cell lung cancer role. Senior researcher of the study, radiation oncologist Thomas Jefferson University School of Medicine, Sidney Kimmel Lupo (transliteration, Bo Lu), said these findings strongly suggest that, Nit1 may be a new target for drug treatment required.

Dr Lo said, "Now, in the majority of patients with lung cancer, cancer of the existing therapy is becoming increasingly resistant, making lung cancer as the most important cause of cancer death in the world. Therefore, urgent need for new drugs, Nit1 inhibitors may represent a new drug policy. "Dr. Sidney Kimmel Thomas Jefferson University school of medicine, Radiation Oncology, Pharmacology and experimental Therapeutics Professor Adam Dicker noted that the study is a good example of "aimed at understanding the basic mechanisms of lung cancer Research on how to determine possible new drug targets".

Dr. Lu and his colleagues have prepared a mouse model, when the mouse genome in the presence or absence of Nit1, due KRAS mutations and to develop lung cancer. Using a mouse model lacking Nit by researchers Dr. Jianke Zhang prepared scientists will cross these mice and found that due to the lack of Nit1 tumors, tumors than the mice carrying the gene active Nit1 formed five times smaller. They also found that, Nit1 in human lung cancer tissues and cell lines are highly expressed in cancer cells and silence Nit1, you can reduce the survival of cancer cells.

The researchers then tested the "suppression Nit1 whether to increase cisplatin (a commonly used cancer chemotherapy drugs) in mice with lung cancer in effect". Dr Lo said, "When Nit1 is silenced, the cancer becomes significantly more sensitive to cisplatin. This is the story of discovery - a false assumption brought a possible new drug strategy."

Currently, Dr. Lu and his colleagues are continuing to study Nit1 expression and inhibitory mechanisms behind its potential impact on the development of lung cancer in immune surveillance.

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CRISPR tells us that gene editing is just the beginning

On March 7th, the website of the journal Nature published an article entitled article "CRISPR gene editing is just the beginning", pointing out that gene editing is only a starting point of CRISPR technology application. The real ability of this biological tool in these feature stories in Nature is to explore the operational mechanism of the genome. And it introduced technological achievements and applications published on Nature, Science, Cell and their sub-journals recently.

Epigenetic modification on DNA is not the only genome code to be cracked. Over 98% of the human genome does not encode proteins. But the researchers believe that a considerable part of such DNA doing important things, they are adopting CRISPR-Cas9 to clarify what it is.

Some DNA encoding such as microRNAs and long non-coding RNA molecule of a class - people think they have a function other than protein synthesis. Other sequences can be required to enlarge the gene expression "enhancers." Most common risks associated with the DNA sequence located in the genomic region containing the non-coding RNA and enhancers in. But before CRISPR-Cas9, researchers were difficult to figure out the function of these sequences. Boston Children's Hospital hematologist Daniel Bauer said, "We do not have a good way of these non-coding genomic annotation from the feature is now more sophisticated in our experiments."

University of Southern California molecular biologist Peggy Farnham and colleagues used CRISPR-Cas9 delete mutations in prostate cancer and colorectal cancer genome research found enhancer region. Sometimes the findings surprised her. In an experiment not released, her team deleted a past that is important enhancer, not its one million bases in a gene expression changes. "It happened when we usually classify a regulatory element influence the way you remove the element and does not match."

When possible use of CRISPR-Cas9 researchers to explore the large fragment of DNA regulation will be more surprises. From the Massachusetts Institute of Technology (MIT) genetic David Gifford and Brigham and Women's Hospital research team led by Richard Sherwood advantage of this technology in the base sequence of some 40,000 manufacturing mutation, then examined whether each change would near fluorescent protein coding genes affected. Thereby resulting in a DNA sequence to enhance gene expression profiles, including several based on characteristics such as gene regulation chromatin modification is not predicted sequence (CRISPR NEW, Looking for gene regulatory elements, High-throughput mapping of regulatory DNA.Nature Biotechnology 34, 167-174 (2016) doi: 10.1038 / nbt.3468).

In-depth study of this dark matter is faced with challenges even using CRISPR-Cas9. Cas9 wizard RNA cleavage enzyme will inform its site, but only if there is a specific and near the common DNA sequence cleavage site. Researchers who want to silence the gene is not difficult, because these important sequences are almost always exists somewhere within the gene. But for those who want to complete a short non-coding RNAs are very specific changes for the limited choice. Netherlands Cancer Institute researcher Reuven Agami, said, "We cannot get any sequence."

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CRISPR tells us that gene editing is just the beginning

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2016年3月11日星期五

The incidence of chronic diseases for MS patients is higher than that of normal people

New research shows that compared with other chronic diseases, multiple sclerosis (MS) patients the probability of no higher than people suffering from neurological disorders.

The study included 23,400 newly-diagnosed MS patients and 116,600 ordinary people who don't have MS. Common chronic diseases include: hypertension, diabetes, high cholesterol, heart disease, chronic lung disease, epilepsy, fibromyalgia, colitis, depression, anxiety, bipolar disorder and schizophrenia. For these chronic diseases, there is a higher incidence of MS patients, except high cholesterol. 19% of MS patients and 9% of people without MS have depressive disorder.

The research results have been published in the on-line edition of March 9 of Neurolog. It was reported that many chronic diseases show gender differences. 22% of the male MS patients suffered from high blood pressure, 15% of the males without MS suffered from high blood pressure. Female rate of high blood pressure were 14% and 12% respectively. The incidence of Diabetes, epilepsy, depression, anxiety for male MS patients is higher than that of female. However, the incidence of female MS patients with chronic lung was higher than that of males.

Dr. Ruth Ann Marrie is the director at Tony Manny University Multiple Sclerosis Clinic. She said that the findings are very significant with some reasons. The study questioned whether MS has the common risk factor problems with these chronic diseases. If there is, can we find ways to reduce the risk of these diseases and MS. In addition, the study found that MS develops faster on patients with chronic diseases, so doctors and patients must be aware of this and find ways to control it. However, this study doesn't prove that MS are actually are associated with these chronic diseases.

William Grant from nutrition and health research center in San Francisco sunlight believes that a possible reason is that MS and these diseases have common risk factors. Smoking, obesity, lack of VD and omeg-3 fatty acids all can cause deterioration of MS. These factors in various combinations can also cause deterioration of those chronic diseases. Doctors should recommend people with MS pay attention to correct these problems.

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Microbial distribution location decision lifespan

We already know that the composition of intestinal microflora changes will affect our health. For example, there are some specific microorganisms may lead to the occurrence of certain human cancers; or alter the normal metabolism of people; some microbes may even accelerate human aging.

Metazoan gastrointestinal health is very important to the district. Each region of intestine and stomach has various gastrointestinal specific microorganisms. If ecological imbalance of these microorganisms happens, it can cause gastrointestinal disorders.

And the link between the phenomenon that gastrointestinal followed with microbial imbalance and gastrointestinal partitions is still unclear. Recently in Drosophila, scientists found that the change of venue of their gastrointestinal microbial composition and distribution will shorten its life.

In a recent article published in Cell Host & Microbe, scientists found that after further study, the microbial distribution and formation of young flies have relevance with distribution of intestines and stomach. While in the Drosophila stomach of elderly flies, since the inflammatory signals lead to cell aging stomach wall and status is changed, the emergence of metaplasia stomach, gastrointestinal partition declined. The presence of a particular region also will be distributed prior to microbial disorder. JAK / activation associated with aging Stat signaling pathway leading to the inner wall of the stomach tissue deformation. If the stomach tissue and suppresses JAK / Stat signal can prevent microbial imbalance, thereby extending the life of fruit flies. This suggests that microbes on human health, their specific location in the stomach tissue is critical!

Their findings explain the physiological mechanism that chronic inflammations associated with age cause the decrease of gastrointestinal partition, thus resulting in the regional microflora imbalance, ultimately limiting animal life.

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2016年3月10日星期四

New finding: amino acid is the biggest material source of cancer cells

Cancer cells maintain their mad proliferation primarily by consuming glucose. Scientists have always thought that most of the constituent materials of cancer cells come from glucose. MIT researchers recently found that although cancer cells consume relatively less amino acids, they are the largest source of materials of cancer cells. The study was published in the journal Developmental Cell on March 7th.

We all know the capacity way of cancer cells is different with normal cells. Human cells decompose glucose through a series of complex chemical aerobic reactions, while the tumor cells need to switch to fermentation process without oxygen. This metabolic strategy has lower efficiency and the energy it generates is much less. Some researchers believe that cancer cells use this inefficient metabolic strategy for the new cells to produce basic materials.

Researchers developed several different types of cancer cells and normal cells in vitro, providing them with different marker nutrients of carbon and nitrogen and traced the ultimate fate of these molecules. The researchers also measured the cells mass before and after the division of the cell mass to calculate the proportion of each nutrient in the newborn cell mass.

Studies confirm that the majority of glucose is decomposed by cells and generates lactic acid, thus it becomes useless for cells. Although the speed of cells consuming glucose and glutamine is quite quick, the quality of both molecules contributes little to new cells' quality: glucose contributes 10-15% carbon; glutamine contributes about 10% carbon. Other amino acid besides glutamine has greatest contribution to cells. The carbon atoms coming from this source account for 20-40% of the total cell mass. This study provides a new way for people to study cancer cell metabolism and helps to develop new drugs to block the ability of cancer cells to grow and divide.

Phosphofructokinase 1 (PFK1) glycolysis "gatekeepers" responsible for a key step in the catalytic glycolysis pathway, so that the fruit-6-phosphate into fructose-1,6-diphosphate. Metabolites and hormone signaling through activation and inhibition PFK1, glycolysis is adjusted to meet the energy needs of cells. The research team of the University of California and Columbia University won the first mammal PFK1 tetramer (human platelet-type phosphofructokinase PFKP) high-resolution texture. Research indicates that the target PFK1 active treatment is expected to control the disease in disorders of glycolysis.

Tumor growth requires cancer-associated fibroblasts (CAF) to provide key metabolites. These cells undergo reprogramming to support metabolic glycolysis. However, it is the molecular mechanism of this change is still poorly understood. Shanghai Jiaotong University and the research team at the University of Kentucky found that, IDH3α down CAF is a key metabolic reprogramming switch capable of making the transition from oxidative phosphorylation to aerobic glycolysis. The results are published in the journal Cell Reports, the corresponding authors of the article are Huabing Zhou from Shanghai Jiao Tong University School of Medicine and Mi Army from the University of Kentucky.

New precursor cells are found to be able to produce new HSPCs

Recently, researchers at the Icahn School of Medicine at Mount Sinai found some cells in mouse embryos based on previous work. These cells are hematopoietic stem cells or precursor cells of hematopoietic stem cells / progenitor cells (HSPCs). In previous studies, they reprogrammed mouse skin cells as HSPCs in the laboratory. Now, they have identified progenitor cells in a mouse embryo and placenta and the cell can mature and produce HSPCs in the laboratory. Their findings were entitled "Hematopoietic Reprograming in Vitro Informs in Vivo Identification of Hemogenic Precursors to Definitive Hematopoietic Stem Cells" and published in the journal Developmental Cell on March 7th, indicating that this reprogrammed process can repeatedly function during blood cell development. These results may eventually prompted researchers to prepare patient-specific HSPCs and bring more differentiation of blood products for cell replacement therapy.

Patients who suffer from blood diseases (such as leukemia, lymphoma, and multiple myeloma) and people with compromised immune systems are in great demand for transplantable stem cells. Researchers are exploring an approach that can produce large amount of HSPCs in the laboratory and the method of preparing patient-specific HSPCs. The reprogramming process developed by the researchers at Icahn School of Medicine at Mount Sinai seems to mimic the normal blood's function of cell production or developmental hematopoiesis - from precursor cells eventually become HSPCs cells. This technology shows the potential to provide a different source of stem cells and alleviate the needs of transplant.

The research team analyzed the embryo and placenta of mice to explore whether there are certain cells which has a similar phenotype as precursor cells do and confirmed that they can mature into HSPCs in the laboratory.

Senior author of the study, associate professor at Mount Sinai School of Medicine, Developmental and Regenerative Biology Icahn Kateri Moore pointed out, "In the long run, in order to cure the disease, we need to be able to transplant something which can continue to produce new blood cells but not rejected by the patient's body. We are excited about the results of this study. In the laboratory, these precursor cells can grow to HSPCs which can be portable. Our reprogramming process can inform the development of hematopoiesis, and vice versa."

Other members of the research team include Dr. Ihor Lemischka Developmental and Regenerative Biology professor, author, former postdoctoral researcher at Mount Sinai School of Medicine, Icahn Biology Dr. Carlos-Filipe Pereira. He is currently an assistant professor at the University of Coimbra.

Dr. Lemischka said, "Direct reprogramming research could improve the applications of regenerative medicine. We have 20 years of research and experience in the field of hematopoietic stem cell biology. Our ultimate goal is to prepare into blood cells in the laboratory and increased productivity of patient-specific blood cells. This study makes us closer to achieving this goal."

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2016年3月9日星期三

Blood test can be used to detect Chronic Traumatic Encephalopathy

According to a study published in the Journal of Alzheimer's Disease, blood tests would be used to detect chronic traumatic encephalopathy (CTE).

Chronic traumatic encephalopathy (CTE) is a tau disease caused by previous repeatedly head hit, such as repeatedly hit on the head occurring in American football and other sports. CTE can be diagnosed by neuropathological examination. Many clinical features of the general population in the CTE are very common, regardless of whether there is the history of the impact head. Thus clinical diagnosis of CTE is quite difficult. Now it is common in the diagnosis of other neurodegenerative diseases such as Alzheimer's disease, therefore an objective biomarker is needed to diagnose CTE. This study was designed to detect whether plasma tau protein can be used as a positive diagnosis of CTE biomarkers.

This study included the 78 National Football League (NFL) players and 16 reference objects. The extracellular vesicles came from the plasma of all subjects. Fluorescent nanoparticle tracking analysis was to determine the number of vesicles tau staining.

It was found that the extracellular tau of NFL group is higher than reference objects group. There are extracellular tau differences between the two groups, with a sensitivity of 82%, a specificity of 100%, and positive predictive value of 100% and a negative predictive value of 53%. In NFL group, the higher extracellular tau is related to poor memory and slower thinking speed.

In conclusion, these preliminary findings show that plasma extracellular tau protein may be a marker which is accurate non-invasive and can be obtained for the diagnosis of CTE.

It is not suggested to use Vitamin D to relieve pains and cartilage loss caused by knee osteoarthritis

A recent study reveals that supplement of vitamin D for the patients who suffer from knee osteoarthritis and 25-hydroxy vitamin D levels does not reduce knee pain or relieve cartilage loss.

In males and females who aged 60 years or older, the percentage of osteoarthritis symptoms were 10% and 13%. There is no treatment to alleviate bone arthritic disease at present. Vitamin D can reduce cartilage degradation and bone turnover, thus it may prevent the development and progression of knee osteoarthritis. Observational studies suggest that vitamin D is related to benefits brought by osteoarthritis, but the evidence from clinical trials is conflicting.

Changhai Ding, Australia University of Tasmania, Hobart, Tasmania, MD, Ph.D., And colleagues randomized 413 patients suffering from symptomatic knee osteoarthritis and 25-hydroxy vitamin D concentrations assigned to receive low monthly oral vitamin D3 (50,000 international units; n = 209) or identical placebo for the treatment of up to 2 years. The study was conducted in Tasmania and Melbourne in Australia.

In the recruitment of 413 research participants (average age is 63 years old; 50% are females), and 340 (82%) completed the study. The researchers found that in the course of two years, comparing with placebo, vitamin D supplementation did not cause any significant difference between MRI detected tibial cartilage volume and knee pain detection. Two groups of patients tibial - femoral or tibial cartilage defects - femur bone marrow lesions also showed no significant difference. In the course of two years, the concentration of vitamin D in patients with vitamin D group had no more improvement than the placebo group.

The authors wrote, "These data suggest that, to slow down the progression of vitamin D or structural changes of knee osteoarthritis disease lack for supporting evidence."

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2016年3月8日星期二

Organic foods may not be as healthy as you think

A new study shows that organic milk may contain high ω-3 fatty acids. But it doesn't mean it will be more suitable for you. One study showed the conclusion that the ω-3 fatty acid level of organic milk is higher than that of the general aquaculture products, but a professor made a strong opposition. No other studies cause controversy like the study on whether organic food has a significant advantage does. The study published by Professor Seal last week in the British Journal of Nutrition the (a study on meat, showing that meat also contains high ω-3 fatty acids) certainly has its critics.

The study used meta-analysis of research methods, analysis of 196 papers (36 studies on the meat) milk. The study found ω-3 fatty acids in organic grass-fed cows milk contains output, 50% higher than ordinary cows. These fatty acids help to reduce heart disease. However, 50% sounds like a lot, but in fact only 4% of whole milk fat (semi-skimmed 2%). In other words, organic milk contains very small amounts of fatty acid is. Professor Seal believes that if you add organic cheese and butter, fatty acids will increase. However, it was pointed out to eat more fruits and vegetables than eating organic dairy products to get more nutrition.

There is no evidence that eating organic food for your health much sense. Professor Seal in 2009 and 2012, two meta-analyzes in the paper reached a different conclusion, and therefore found no organic link between food and health. Seal said the professor, his research more fully, there is a significant statistical significance - and its clinical significance is not the same. To prove that the consumption of organic food is wholesome, we will have to study population were randomly divided into eating organic foods and eating non-organic food groups, but they will have to eat the same food for several months. Even so, you can only by measuring the level of some of the physical signs of disease, such as cholesterol levels or weight, to speculate whether healthy.

So please don't be surprised. People say they buy organic foods because they have fewer pesticides, antibiotics and additives. They also think it is better for animals and soil. However, a 2012 Stanford University meta-analysis results, although there are pesticide residues on non-organic food, but the amount is safe. It boils down to whether you believe this security number - you can avoid them under the premise. So far, this study suggests that the traditional healthy foods and organic healthy foods have the same benefits.

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Changing the use of some virus residue can help fight against virus

About 8% of human DNA originates from viruses. They are residue of ancient struggle between our ancestors and infectious virus. These so-called endogenous viruses are often considered as junk DNA without clear biological significance. But scientists from the University of Utah School of Medicine confirm in a new study that evolving and changing the functions of some viruses can making it as a weapon against the virus itself.

In the paper published on March 4 in the journal Science, scientists reported to have found that some viral DNA fragments embedded in our genome regulate some genes which are basic elements of our innate immune system. The innate immune system is the first line of defense which helps the body fight against a number of pathogens including viruses. When using the experimental method to remove some of the exogenous sequence fragments, the defense system will be seriously damaged.

Co-senior author Dr. Cédric Feschotte, associate professor of human genetics said, "We have confirmed that some of the endogenous viruses shape our biology. In mammalian genome, viral DNA repository promotes the updates of innate immune system."

Human capacity of the innate immune system to fight foreign invaders depends on a coordinated response. When infected, cells release interferon to issue a silent alarm. This molecular signal will trigger adjacent cells to activate arsenal consisting of hundreds or thousands of genes to fight against the invaders. By analyzing the public and available genome datasets of human cells, the authors found that interferon seems to activate thousands of endogenous retroviruses (ERV). Since these retroviruses were inserted urgently into our genome millions of years ago, they lost the ability to generate infectious viral particles long ago. Their location in the genome provides clues information about this interferon inducing element of modern functional potential. Not randomly distributed, they are concentrated in some of the nearby genes known to function in immunity.

Feschotte said, "This is the first evidence shows us, some elements really involved in the immune genes turned on." Feschotte and associate professor of human genetics Nels Elde co-senior author of the paper, the paper is postdoctoral Edward Chuong the main author.

To test the viral DNA fragment is indeed vital to the immune, scientists are using gene editing tools CRISPR / Cas9 delete one by one in a number of cell culture virus sequences which are located in the vicinity of the known immune genes. In the absence of exogenous sequence mutant cells cannot respond to interferon immune genes adjacent to properly open, it confirmed that they serve as a switch-borne virus. In addition, when infected with virus AIM2 cell immune response to viral DNA near the gene deletion element, which significantly reduced the effective implementation of the immune response capabilities. In summary, the results show that the ancient viral DNA is essential for virus infections start against contemporary right defense.

Due to the similarity of the virus-derived switch is embedded in the vicinity of many immune genes, suggesting that they work together to help coordinate our cellular defense. "Cellular interferon response is like an alarm system. We found that the most important in this system some of the switches from the actual ancient virus," Chuong said. The study also found other endogenous retroviruses their "connections" and other mammal’s clues interferon response, which may indicate a wide range of species-specific immune response mechanisms.

Elde said, "the transformation of the innate immune system in which some residual virus was likely not accidental." Rapidly evolving and changing pathogen invasion strategy continue to challenge the immune defense. To keep up with its evolution in the past simply recombinant virus genetic material provided. Many viruses originated as an integral part of the virus replication process into our genome. Evolution reverses the situation and we can benefit from it."

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2016年3月7日星期一

Making use of a genetic code to reconstruct neurons

There are different types of neurons in our brains, each of which has its own genetic tags that define their functions. Neurons all originate from progenitor cells - these specialized stem cells have the ability to divide and produce neurons.

Now, neuroscientists from the University of Geneva Medical School clarify the mechanism of progenitor cells generating neurons. By developing a new technology called FlashTag, researchers isolated and developed the neurons at the special moments and decoded the genetic code which makes it possible to construct neurons.

The study published in the March 3 journal Science found that not only allows researchers to understand the developmental mechanisms of our brain, but also know how to use the genetic code to make stem cells to reconstruct the neurons. Now researchers will be able to better understand the underlying mechanisms of autism and schizophrenia and other neurological diseases.

Under the leadership of Medicine Department of Neuroscience based neuroscientist Denis Jabaudon the University of Geneva, Switzerland, the researchers developed a technique called FlashTag developing them at that moment neurons generated. With this method, in progenitor cell division at the moment, it is marked on a persist in progeny cells fluorescent marker. Scientists can then be isolated and developing new neurons dynamically generated observation gene in their first few hours of expression. Over time, researchers can study their evolution and changes in gene expression.

"In the past, we can only get a few pictures to reconstruct the history of neurons, leaving a lot of space to carry out their own speculation. Thanks FlashTag, now full genetic movie show in front of us. From the beginning of each moment can be seen, so that we can understand the development of the situation, identify the main features of their mutual and incentives for, "Denis Jabaudon said. A study in mice cerebral cortex, scientists have revealed the neuronal differentiation indicates the sequence of events, new neurons to guide early transcription wave ultimate cell fate, identified key genes neuronal development, confirming their expression dynamic crucial for normal brain development.

Access by neurons formed the original password; this study found that helps us understand the function of neurons in the adult brain mechanisms. Neurodegenerative diseases seem some of these genes with the primitive neural development and many years occurred about. This indicates that the moment generated neurons may show a tendency after some environmental factors may influence the occurrence of subsequent disease. By understanding the genetic choreographer neurons, the researchers were able to observe from the outset of these genes show, predict disease identified potential anomalies.

After successfully reading the genetic code, scientists will be able to rewrite it in newborn neurons. By changing the expression of certain genes, they can accelerate the growth of neurons, thereby changing the script development. With FlashTag, now isolated from newborn neurons in vitro reconstruction of brain circuits become possible, which allows scientists to test their capabilities and develop new therapies.

Developed a powerful tool for the study of neurological brain research has important significance. On the same day in the journal Cell, researchers from Columbia University two articles to demonstrate a new method to fully identify the type of neurons. This approach will help people to quantitative analysis neuronal diversity in all regions of the brain.

In November 2015, Stanford University research team recently in Science magazine published a technological breakthrough. They develop imaging tools electrical activity of individual neurons in conscious living animals, so that people understand the neuronal activity reached unprecedented depth.

In October 2014, researchers from the University of California, San Diego constructed a new type of cell with a fluorescent dye. This dye can respond to specific neurochemical and changes color. These researchers transplanted cells into the mammalian brain in vivo, thus they could observe how the nerve signals change a food reward learning process. The research results were published in the journal Nature Methods.

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