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May 23, 2012

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statins reduce the risk of heart transplant patients wit...

The study said that statins reduce the risk of heart transplant patients with tumors The study found that statin therapy can help heart transplant patients to reduce the HSPE1 risk of tumor development in a very long period of time.Single center after heart transplantation in patients taking statins, study found that the incidence of each cancer is roughly reduced by half.The cumulative rate of cancer incidence in patients with heart failure at the annual meeting, MD GeorgM.Froelich of the University Hospital of Zurich, said after heart transplantation the use of statin therapy within HSPH1 eight years after 13%, without the use of statin therapy cumulative rate of cancer incidence in the postoperative period of eight years to reach 34% (P <0.003).Cohort study of patients taking statins after adjustment for age, gender, cardiomyopathy, immune therapy and cancer survival rate was 67%. Previous studies have shown that statins not only for the treatment of atherosclerosis hardening HTATIP2 effective and also have a role in the overall survival for heart transplant patients.Froelich explained, these data make the benefits of statins extend to the reason of the long-term mortality in patients after heart transplantation immunotherapy on the one hand helps the body fight transplant rejection of the donor heart implanted bring the other in turn can effective against HTRA1 cancer cells.Froelich Research Center study found that from 1985 to 2007 a total of 255 patients in the postoperative survival time of heart transplantation for at least more than one year, while at the same time of the follow-up of 42% of patients the cancer.Has recommended in the guide given to all heart transplant patients with statin use, Froelich also recommended, these results may suggest another reason for the HTRA2 occurrence of cardiac transplantation in patients with cancer, "L consider these data alone is not sufficient to prove the existence of a true causal relationship between Strasbourg, France, University Hospital, MD GeraldRou" and on MedpageToday, he said, "Obviously, the following conclusions before need more support. But if this conclusion is true, for the treatment of heart transplant patients is a breakthrough through the the Froelich study confirmed the role of statins to reduce the occurrence of cardiac transplantation in patients with tumor very reasonable of. He pointed out that statins has pleiotropic effects, including immune adjustment, the role of cells in the matrix metalloproteinases and cancer occurred and the development of the process of apoptosis. he adds, but whether all of his statin class of drugs for differenttypes of patients, or others, such as lung transplant recipients enough to accept the strict immunosuppressive therapy in patients with this problem, is not clear.They observed data, the benefits of statins will continue for some time. 10 years of follow-up study, statin users were 10 years tumor cumulative incidence rate of the earth 18% without taking statin therapy in patients up to 39%. Patients 12 years of follow-up study, patients taking statin therapy, 10 years, tumor cumulative incidence of 22%, without taking statins and 42% between a statistically significant difference. In previous studies, patients taking statin therapy often showed increased overall survival and better cancer-free survival (P <0.0001) it is evident that cholesterol levels after heart transplantationpat ients with statin drugs will make cancer-free survival rate was significantly higher (P <0.0001), and not consider the level of cholesterol, statins after heart transplantation in patients with cancer-free survival increased significant (P = 0.96). Use of statin therapy but can not completely avoid the occurrence of side effects, these side effects including Froelich warning included rhabdomyolysis, research group, said: "These data need long time to come randomized clinical trial to further validate.  (May 30, 2012 | post #1)


Apolipoprotein E gene and protein

Taylor established the cDNA sequence of APOE, Breslow and Zannis first measured APOE isomer of the three alleles and gene on chromosome positioning. Of APOE gene is located on the 19th of the long arm of chromosome 13 band (19q1312), the gene is 317kb and contains four exons and three introns. From 5 'to 3' exon length of 44bp, 66bp, 193bp and 860 bp, intron length is 760bp, 1092bp and 582bp. CDNA 11163kb, APOE precursor protein of 317 amino acids, containing 18 amino acid signal peptide, mature APOE protein of 299 amino acids. Human APOE and rodent nucleotide sequence of the APOE with high homology to the nucleotide sequence of the two signal peptide region has 81% homology, the amino acid sequence of the signal peptide region of 67% in the same endogenous.Compari son of human and rodent mRNA sequences found both with 75% homology to the amino acid sequence has 70% homology. APOE gene has three alleles, &#949;2, &#949;3 and ApoE &#949;4, respectively, and the resulting six genotypes, namely, of APOE2 / 2, E3 / 3, E4 / 4 three homozygous and APOE2 / 3 three heterozygous E2 / 4, E3 / 4 type. &#949;3, APOE3 / 3 are the most common allele and genotype, the gene frequency of 77%, 8% &#949;2 gene frequency, the APOE &#949;4 gene frequency of 15%, but the APOE gene frequencies in different ethnic and geographicaland the distribution of phenotypes may be different, but no gender differences in Chinese and Japanese are very similar to the &#949;3 frequency higher than 80%, while Europe and the United States per capita below 80%, European &#949;4 allele frequency decreasing from north to south trends in the distribution. Asian low-&#949;4 frequency (419% - 1217%), compared to African and Papua Shakespeare and New Guinea &#949;4 frequency (about 30% and 3618%), perhaps this is the United States and Europe AD a high incidence of a potential factor. APOE is composed of 299 amino acids containing 32 Arg and 12 of Lys, the arginine content of up to 11%, an arginine-rich basic protein synthesis after glycosylation modification, but the plasma mature APOE is de-sialylated. Rall is equal to the measure of a structure of the APOE protein in 1982, according to projections and determination of APOE in the medium, 62% &#945;-helix, 9% &#946;-sheet, 11% &#946;-turn and 18% rules of the line group. APOE molecule thrombin hydrolysis that is, for the two major structural domains: the N - terminal region (1-191) for the 22kDa soluble globulin, this area is relatively stable, 136 to 158 of the fragment peptide receptor binding sites, rich in basic amino acids (lysine and arginine), also belong to the heparin-binding domain. X - ray crystallographic studies showed that this fragment is an anti-parallel four-helix bundle, the fold of the &#945;-helix protein. C-terminal region (216 299) molecular weight of 10kDa, the spiral degree of high, unstable, and the lipoprotein-bindin g domain. These two domains twisted by the period of the district (165 - 215 peptide) is connected.  (May 29, 2012 | post #1)

Cell Biology

Brain cancer cell line whole-genome sequencing completed

University of California at Los Angeles Jonsson Comprehensive Cancer Research Center scientists published in DSG2 the April 29 special issue of Public Library of Science Genetics that they have completed the first whole-genome sequencing of brain cancer cell line, which is as of a single cancer cell lines did the most thorough sequencing analysis. By using the latest technology, the sequencing of work to be completed within one month, sequencing costs about $ 35,000.This research has taken a new DSTYK step toward personalized treatment based on the unique biological signature of the individual cancer, they reveal new molecular targets will help to develop more effective and less toxic drugs. The study doctor earlier the better to find a new method of monitoring brain cancer recurrence can be useful, easy to make a diagnosis and treatment of DTNBP1 brain cancer recurrence. With this discovery, the clinician can also be determination of the exact time of brain cancer cells is inactivated in order to prevent excessive use of drugs on the human health damage caused.The sequencing work into human glioma cell line called U87, in over 1000 laboratories worldwide are using U87 cell lines to carry out research. Chose the cell line, because its the most fully. The sequencing work will enable those engaged in the study of DUSP1 cell lines scientists found their research to re-elaborate, and prompted them to propose a new forward direction.The sequencing revealed almost all of the potential cancer-causing chromosomal translocation and lead to the development of cancer gene deletion and mutation.Researche rs from the long chain of genetic material out of the cell lines, and then randomly truncated. Billions of DUSP14 different DNA fragments in the cancer by a new generation of sequencing technology at the same time for reading, you can ensure that the results with high sensitivity and accuracy of genetic material through the analysis of more than 1 billion times. The researchers said that a special information tool uses the most advanced technology, will greatly enhance the effectiveness of genetic analysis. Previously, scientists can not understand most of the mutations in a cancer, because they are invisible, and now this new technology will allow scientists to monitor each type of cancer, and its genome fully decoded, so the scientists will not miss a cancer-causing mutations.Know which genes mutate and drive the development of cancer, clinicians will be able to choose the most suitable for a specific molecular signature of attack cancer therapy, and thus provide more effective treatment to patients. The sequencing also show molecular abnormalities drive the development of cancer, reveals the target will contribute to the development of new therapies to attack only cancer cells without damage to healthy cells.The researchers also pointed out that the cancer genome sequencing diagram, the scientists will be able to develop a sensitive molecular detectors, looking for a unique gene mutation found only in cancer cells. As long as the detection of this mutation can determine the cancer had returned and, thus, the patient will be able to get aggressive treatment in the earliest stages of cancer recurrence. In turn, this detection method can also be used to determine whether the cancer has been effectively eliminated, thus timely termination of the treatment of harmful.  (May 24, 2012 | post #1)

Molecular Biology

Amyloid P component, serum cerebral artery atheroscleroti...

Amyloid P component, serum (APCS) exists in the body of mammals and birds, the synthesis of the site is mainly in the liver, composed of the same cluster of genes encoding a group of pleomorphic protein. S from the apolipoprotein family includes different forms of expression, acute phase protein A (Amyloid P component, serum, APCS) and structural type of the APCS (constitutive Amyloid P component, serum, C-APCS). Normal serum APCS value of 0-0.78mg / L When the body by a variety of inflammatory response factors to stimulate the serum level of APCS increased rapidly in the 5-6h of about 1000 times, 8 ~ 12h within the APCS can reach peak increased amplitude of up to 2000 times the normal value. The half-life is also very short, only 50min. Therefore, when control of the body's inflammatory response can be rapidly reduced to normal levels. This feature allows APCS to become the most sensitive one of the inflammatory response markers.APCS can induce the synthesis of collagenase and inhibition of interleukin-1 (interleukin-1, IL-1), IL-5, IL-6 or tumor necrosis factor (tumor necrosis factor, TNF) caused by fever; inhibit platelet 5-HT release and platelet aggregation. With this protein functions, one by one was found, APCS has gradually become the people to overcome artery atherosclerosis (athero-sclerosis, AS) research focus, but also by the expert attention of cardiovascular and cerebrovascular diseases. APCS is considered to be a multifunctional protein, play an important role in the inflammatory reaction, regulate cholesterol metabolism and transporter. APCS is mainly present in the composition of serum high density lipoprotein (> 90%) of the old J. This part of the APCS with the reverse cholesterol transport. Found j of ApoA I) and a small amount of APCS phospholipid particles increased by apolipoprotein Al (apolipoprotein A-I, lecithin cholesterol acyltransferase (1ecithincholester ol acyltransferase, LCAT) activity; but this is rich in APCS particles, but lower the function of LCAT. LCAT cholesterol into cholesteryl ester. Of ApoA. I is one of the enzyme activator of LCAT activation play an important role in reverse cholesterol transport, and therefore prove that APCS involved in the process of reverse cholesterol transport. Exist to reduce the affinity of HDL on the normal liver cells 2 times the contrary, the affinity of macrophages increased by 3-4 times; inflammatory response of macrophages, HDL / APCS (containing HDL) affinity of APCS and the sites on liver cells is reduced, the net effect of HDL cholesterol transport capacity significantly towards the macrophages. APCS can enhance the absorption capacity of the HDL / APCS by macrophages, and promote rapid outflow of cholesterol in the cholesterol-load macrophages.In the tissue injury area, macrophages are loaded with cholesterol, this is because theysuck the cholesterol-rich membrane fragments. HDL / APCS to promote cholesterol effluxcapacity in the APCS, rather than the other HDL apolipoprotein feeding roar. HDL / APCScan also serve as extracellular receptors of macrophage cholesterol. Acyl-coenzyme Acholesterol acyltransferase (acyl coenzyme A-cholesterol acyltransferase, ACAT) andesterified cholesterol as storage, neutral cholesteryl ester hydrolase (neutralcholestero l ester hydrolase, nCEH) esterification of cholesterol lead to the outflow. APCS can inhibitthe ACAT, can improve nCEH activity, it can be to adjust the balance through the storage and transfer of free cholesterol. Although a large number of experiments proved that the APCS can be elevated oxidized cholesterol levels, and thus increased free cholesterol efflux from macrophages, but in cells that role directly through the APCS or indirectlythrough the APCS increased oxidation of cholesterol levels, elevated macrophage cellular transport of cholesterol efflux, is not yet clear.  (May 24, 2012 | post #1)


Most African-Americans originated in West Africa, contine...

calm down, each person has his own position; we have no need to care about their judgments a lot and i think u r handsome and smart,right have a good day! shake hands haha  (May 23, 2012 | post #45)


Evolution vs. Creation

dont be angry about others' talking--he has his own point by the way, urs is a good thread thanks for ur sharing  (May 23, 2012 | post #27542)


The researchers found that the melanoma mutations in the ...

Melanoma is a deadly and the most aggressive skin cancer, and long-term exposure to GSTM2 sunlight under the relevant. Recently, researchers from the Dana-Farber Cancer Institute and Broad Institute, a whole-genome sequencing of 25 metastatic melanoma, the researchers confirmed that chronic sunlight exposure in the development of melanoma inrole, and reveals the important genetic changes in melanoma. The research results were published in the international journal Nature on May 19.In the GSTM4 article, the researchers demonstrated in human melanoma high-resolution genome landscape, previous genetic analysis of the focus on the many types of melanoma exon group, and researchers concerned about is some small fragments of genetic code to produce the protein genes. The researchers said that the melanoma genome contains a wealth of genetic information, sequencing of 25 metastatic melanoma, the scientists GSTO1 melanoma changes in genetic diversity.Melanoma , whole-genome sequencing will be found in some abundance, and these exon groups can not be captured discovered researchers Levi A.Garraway said. Through whole-genome sequencing, you will see more precisely the proportion of melanoma gene mutations and different types of GSTP1 mutations, so we have more confidence to describe melanoma caused by UV induced gene mutation or mutagenesis. When scientists develop a melanoma genome data and their extensive analysis, they found that the patient's genetic mutation and chronic sunlight exposure, it is even more determined the influence of sunlight damage for the development of melanoma. Analysis of the entire genome of the GSTT1 human melanoma, the first show the existence of the structural rearrangement of the many types of tumors, as expected, scientists have known BRAF mutations and NRAS mutations detected in 24 types of tumors, these genes the transfer of important signaling molecules involved in cell growth. More interestingly the gene PREX2, the gene can be shut down tumor known genes to make the patients suffering from breast cancer and mutations in 44% of patients; PREX2 genetic broken gathered mutation, and can accelerate tumor development, mutations not only occur in the designated location, but can be a classic open oncogene. Researchers Berger said, this style of mutations and tumor suppressor genes very much like, but from the functional experiments, it acts more like a cancer gene.When PREX2 function properly, it will react with the protein PTEN, PTEN is a tumor suppressor gene, can stand for the growth of normal cells and mice show that, mutation of PREX2 can stimulate tumor growth. The researchers said that now they still unclear how to work for PREX2 PREX2 may be classified as a new cancer gene types, the researchers the future will depend on the gene for a new a new target for the treatment of melanoma.Perhaps PREX2 discovery is only the tip of the iceberg, as if the discovery of PREX2 new melanoma genes remain to be discovered through new technologies. Page from-  (May 23, 2012 | post #1)