Heavyweight research Top10
December 26, 2016 Source: Bio Valley
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];[1] Neurology: Heavy! It is first discovered that bacteria directly affect the disease progression of Alzheimer's disease.
Doi:10.1212/WNL.0000000000003391
Recently, a research report published in the international journal Neurology , researchers from the University of California, Davis Institute of Neurology and Brain Research, discovered for the first time in the late-onset (late-onset) Alzheimer's Higher levels of Gram-negative bacteria are present in brain samples of patients with cerebral lipopolysaccharide and E. coli K99 pilin levels in brain samples of these patients, and the researchers also found that These lipopolysaccharide molecules are able to accumulate in amyloid plaques, which is directly related to the pathology and disease progression of patients with Alzheimer's disease.
Researcher Xinhua Zhan said that we tested all 18 aging brain samples by immunohistochemistry and found the cell components of Gram-negative bacteria: lipopolysaccharide and E. coli K99 pilin, compared with Western blot analysis. As a result, k99 is significantly increased in the brains of patients with Alzheimer's disease, and lipopolysaccharide is also able to accumulate on the amyloid plaques and in the blood vessels of the patient's brain. Researchers are not sure whether the bacteria caused Alzheimer's disease or the result of the disease.
[2] Cell: Heavy! Scientists propose new strategies for cancer
Doi:10.1016/j.cell.2016.11.005
Previous studies have found that the Hippo pathway kinase LATS1/2 can act as a tumor suppressor, but a recent study published in the internationally renowned journal Cell , scientists from the University of California, San Diego Medical School revealed the kinase through research. LATS1/2 has a special role in inhibiting cancer immunity, and related research or hopes for developing new strategies to improve the efficacy of immunotherapeutic drugs.
Researcher Dr. Toshiro Moroishi said that before our study, no one knew that the Hippo pathway could regulate immunogenicity, and the elimination of the kinase LATS1/2 in cancer cells could improve the immunogenicity of tumors, thereby enhancing immunity against tumors. React to destroy cancerous cells. The Hippo signaling pathway regulates organ size by regulating cell growth, apoptosis, and stem cell turnover, but abnormal regulation of the Hippo signaling pathway triggers cancer.
In in vitro studies, the researchers found that the deletion of the Hippo signaling pathway kinase LATS1/2 promoted cancer cell proliferation and tumor survival, while the mouse model of lack of immunity found that the Hippo pathway can support the function of tumor suppressors. However, when the researcher Moroishi and colleagues knocked out the LATS1/2 kinase in mouse cancer cells and tested the growth of tumors in the healthy immune system model, they found that the mouse's body's immunogenicity improved, and the mice The body can successfully destroy cancer cells, the researchers said, the immune response of the mouse model is different from the immune response of the human body, so the response of the two is not the same, and further research is needed later.
[3]Science: Peking University, China found that developing a live virus vaccine is feasible
Doi:10.1126/science.aah5869
In a new study, researchers from Peking University in China developed a new vaccine. They claim that this may provide a new way to produce live virus vaccines, and as they imagine, the vaccine may be suitable for any type of virus. They outlined their method of modifying an influenza virus to cause it to elicit an immune response without the risk of infection. The results of the study were published in the December 2, 2016 issue of Science , entitled "Generation of influenza A viruses as live but replication-incompetent virus vaccines."
Currently, most vaccines contain a virus that has been killed or has been impaired to the extent that it is unlikely to cause infection when injected into a healthy person. If similar viruses are found in vitro, and before they have an opportunity to proliferate and cause infection, these vaccines work by causing the immune system to target these similar viruses. Unfortunately, in some cases, people with weaker immune systems find themselves infected after vaccination. In this new study, the researchers took a new approach to building a vaccine—modifying an influenza virus and modifying it in a way that does not allow any patient to become infected.
[4] Nature: Major discovery! Identify cells responsible for initiating and promoting multiple tumor metastases
Doi:10.1038/nature20791
In a new study, Spanish researchers identified metastasis-initiating cells through a specific marker called protein CD36. This protein found in the membrane of tumor cells is responsible for the uptake of fatty acids. CD36 activity and dependence on lipid metabolism can distinguish metastatic initiating cells from other tumor cells. The relevant research results were published online in the Nature Journal on December 7, 2016, and the title of the paper is "Targeting metastasis-initiating cells through the fatty acid receptor CD36."
The researchers found metastatic CD36+ cells in samples from patients with oral cancer with varying degrees of invasiveness. In the analyzed oral cancer, a small number of cells were found to have the ability to initiate metastasis. Tumors that do not metastasize express CD36 such that they are metastatic.
Furthermore, the researchers confirmed that the effect of CD36 on metastasis is the same for melanoma cells and breast cancer cells. Similarly, statistical analysis of patient samples revealed that ovarian cancer, bladder cancer, and lung cancer metastasis are also dependent on CD36.
[5]Nature Supplement: Heavyweight discovery! Telomere too long may not be a good thing
Doi:10.1038/nsmb.3335
From the past to the present, scientists have been linking telomere shortening to body aging and disease. Now scientists are beginning to study the factors that regulate telomere length. A recent study published in the international journal Nature Structural & Molecular Biology In the report, researchers from the Salk Institute found that telomeres of appropriate length are important for maintaining the health of stem cells. Research is to deepen scientists' understanding of stem cell biology and help develop stem cell-based Therapies, especially those related to aging and regenerative medicine, offer new research clues and hopes.
Researcher Professor Jan Karlseder said that this study shows that the optimal length of telomeres can be finely regulated between the two extremes. We all know that shorter telomere lengths induce cell damage, but let us be incredible. Yes, this damage effect also occurs when the telomere length is long. Telomere is the DNA structure of the terminal repeat of the chromosome, and its length can be increased by telomerase. As the cell replicates and the telomere at the end of the chromosome is reduced, the chromosome itself decreases with the decrease of the telomere length. It is increasingly affected by damage and eventually causes cell death.
[6] Nat Med: God! Hungry to treat childhood leukemia?
DOI: 10.1038/nm.4252
Researchers from the Southwestern Medical Center recently discovered that intermittent hunger can inhibit the development and progression of a common childhood leukemia. But this strategy has no effect on another type of blood cancer that is common in adults. The relevant research results were published in the international academic journal Nature Medicine .
The researchers found that for both subtypes of acute lymphoblastic leukemia (ALL), B-cell ALL and T-cell ALL, hunger can both inhibit disease progression and reverse disease progression. The same method has no effect on acute myeloid leukemia (AML), which is common in adults.
Current methods of treating ALL are very effective for children, but relatively poor for adults. ALL and AML originate from different bone marrow-derived blood cells, ALL affects B cells and T cells, while AML targets other types of white blood cells such as macrophages.
[7] JMC: New cancer-targeted chemotherapy technology or expected to be introduced into human clinical trials
Doi:10.1021/acs.jmedchem.6b01470
Recently, a research report published in the International Journal of Medicinal Chemistry , scientists from the University of California, San Francisco (UC San Francisco) developed a new and diverse targeting system for research on chemotherapy drugs. Based on the abnormally high level of free iron in many cells, which is different from the protein-bound iron commonly found in living cells; after studying with mice and cancer cell lines, the researchers succeeded in selectively killing cancer cells while still It avoids the side effects of chemotherapy caused by healthy cells, and it also increases the tolerated dose of healthy cells by 50 times.
This new approach envelops potential chemotherapeutic drugs into a protective chemical framework that releases the drug when it encounters a high-iron environment in the tumor, and it also provides oncologists with valuable new tools to help them take advantage of Higher doses of chemicals target cancer cells, while also significantly reducing the side effects of the drug on patients. Researcher Dr. Alan Ashworth said that because chemotherapy plays an important role in cancer treatment, we must find new ways to reduce the side effects and improve the efficiency of the treatment. This study makes us very excited because it can Help us to deeply analyze the weakness of the tumor, while also inhibiting the recurrence of the tumor and the emergence of drug tolerance.
[8]Cell: Revealing the anticancer mechanism of diabetes drug metformin
Doi:10.1016/j.cell.2016.11.055
A considerable amount of evidence has shown that metformin, a drug used to treat type 2 diabetes for more than 50 years, can also prevent or delay the growth of certain cancers; however, the mechanism behind its anticancer effects is unknown. Now, in a new study, researchers at the Massachusetts General Hospital (MGH) have identified a pathway that appears to be the basis for metformin to block the growth of human cancer cells and prolong the lifespan of C. elegans, suggesting this Genetic pathways play an important role in a variety of organisms. The results of the study were published in the December 15th issue of Cell , entitled "An Ancient, Unified Mechanism for Metformin Growth Inhibition in C. elegans and Cancer."
Dr. Alexander Soukas, author of the paper and author of the Human Genetics Research Center at Massachusetts General Hospital, said, "We found that metformin reduces the influx of molecules into and out of the cell's 'information center'. The decreased nuclear transport translates into this drug blocking cancer growth. The ability, and notably, is also the reason why metformin can prolong life. By revealing the health effects of metformin, these results provide us with a potential new way to think about treating cancer and increasing healthy aging."
[9] OncoTarget: Heavy! Traditional Chinese medicine therapy system can effectively treat cancer!
News reading: Chinese herbal treatment shows signs of effectiveness in bone marrow recovery
Recently, a research report published in the international magazine OncoTarget, researchers from the University of California, Los Angeles, found that a traditional Chinese medicine therapy system called TSY-1 (Tianshengyuan-1) can increase telomeres in normal blood cells. Enzyme activity, but at the same time it reduces the activity of telomerase in cancer cells; telomerase is a key enzyme responsible for telomere production, which plays an important role in the regulation of normal cell division, and related research results show that Telomerase therapy plays an important role in the treatment of blood cell loss and cancer.
More than 80% of cancer patients have increased telomerase activity in the body, and other medical conditions associated with decreased or abnormal telomerase function may occur, and increased and decreased telomerase activity may result in insufficient blood cell count. Cancer is of great importance; when the bone marrow of an individual cannot maintain the supply of healthy blood cells, it triggers the failure of bone marrow transplantation, and the annual bone marrow transplant failure affects 7/100,000 individuals.
[10] Nat Genet: Identifying potential HIV therapeutic targets using CRISPR
Doi:10.1038/ng.3741
In a new study, researchers from the Whitehead Institute, the Lagan Institute, and the Broad Institute in the United States used CRISPR-Cas9 gene editing technology to identify three new targets that are expected to be used to treat HIV infection. They described how to use CRISPR to screen for HIV infection but not the human genes necessary for cell survival to identify five genes—three of which were not identified in earlier studies using RNA interference (RNAi). . Their methods can also be used to identify therapeutic targets for other viral pathogens. The relevant research results were published online in the journal Nature Genetics on December 19, 2016, and the paper titled "A genome-wide CRISPR screen identifies a restricted set of HIV host dependency factors". The authors of the paper are David M Sabatini, Eric S Lander, Nir Hacohen and Bruce D Walker.
Sabatini observed that "considering some of the previously published literature, we were surprised to find that there are so few host factors required for HIV infection." Moreover, Sabatini noted that "the beauty of this CRISPR-based screening method is that they produce Clear and reliable results."
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