The Kuroshio Extension : a leading mechanism for the seasonal sea-level variability along the west coast of Japan

Author Posting. © The Author(s), 2009. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Ocean Dynamics 60 (2010): 667-672, doi:10.1007/s10236-009-0239-9.Sea level changes coherently along the two coasts of Japan on the seasonal time scale. AVISO satellite altimetry data and OFES (OGCM for the Earth Simulator) results indicate that the variation propagates clockwise from Japan's east coast through the Tsushima Strait into the Japan/East Sea (JES) and then northward along the west coast. In this study, we hypothesize and test numerically that the sea level variability along the west coast of Japan is remotely forced by the Kuroshio Extension (KE) off the east coast. Topographic Rossby waves and boundary Kelvin waves facilitate the connection. Our 3-d POM model when forced by observed wind stress reproduces well the seasonal changes in the vicinity of JES. Two additional experiments were conducted to examine the relative roles of remote forcing and local forcing. The sea level variability inside the JES was dramatically reduced when the Tsushima Strait is blocked in one experiment. The removal of the local forcing, in another experiment, has little effect on the JES variability. Both experiments support our hypothesis that the open-ocean forcing, possibly through the KE variability, is the leading forcing mechanism for sea level change along the west coast of Japan.This work was conducted when Chao Ma was a visiting graduate student at WHOI. His visit has been supported by China Scholarship Council and WHOI Academics Office. This study has been supported by WHOI’s Coastal Ocean Institute, the National Basic Research Program of China 2005CB422303 and 2007CB481804), the International Science and Technology Cooperation Program of China (2006DFB21250), the Natural Science Foundation of China (40706006) , and the Ministry of Education’s 111 Project (B07036). Lin was supported by the Program for New Century Excellent Talents in University (NECT-07-0781)

Molecular Dynamics Simulation of the Complex PBP-2x with Drug Cefuroxime to Explore the Drug Resistance Mechanism of Streptococcus suis R61

Drug resistance of Streptococcus suis strains is a worldwide problem for both humans and pigs. Previous studies have noted that penicillin-binding protein (PBPs) mutation is one important cause of β-lactam antibiotic resistance. In this study, we used the molecular dynamics (MD) method to study the interaction differences between cefuroxime (CES) and PBP2x within two newly sequenced Streptococcus suis: drug-sensitive strain A7, and drug-resistant strain R61. The MM-PBSA results proved that the drug bound much more tightly to PBP2x in A7 (PBP2x-A7) than to PBP2x in R61 (PBP2x-R61). This is consistent with the evidently different resistances of the two strains to cefuroxime. Hydrogen bond analysis indicated that PBP2x-A7 preferred to bind to cefuroxime rather than to PBP2x-R61. Three stable hydrogen bonds were formed by the drug and PBP2x-A7, while only one unstable bond existed between the drug and PBP2x-R61. Further, we found that the Gln569, Tyr594, and Gly596 residues were the key mutant residues contributing directly to the different binding by pair wise energy decomposition comparison. By investigating the binding mode of the drug, we found that mutant residues Ala320, Gln553, and Thr595 indirectly affected the final phenomenon by topological conformation alteration. Above all, our results revealed some details about the specific interaction between the two PBP2x proteins and the drug cefuroxime. To some degree, this explained the drug resistance mechanism of Streptococcus suis and as a result could be helpful for further drug design or improvement

Gut-Microbial Metabolites, Probiotics and Their Roles in Type 2 Diabetes

Type 2 diabetes (T2D) is a worldwide prevalent metabolic disorder defined by high blood glucose levels due to insulin resistance (IR) and impaired insulin secretion. Understanding the mechanism of insulin action is of great importance to the continuing development of novel therapeutic strategies for the treatment of T2D. Disturbances of gut microbiota have been widely found in T2D patients and contribute to the development of IR. In the present article, we reviewed the pathological role of gut microbial metabolites including gaseous products, branched-chain amino acids (BCAAs) products, aromatic amino acids (AAAs) products, bile acids (BA) products, choline products and bacterial toxins in regulating insulin sensitivity in T2D. Following that, we summarized probiotics-based therapeutic strategy for the treatment of T2D with a focus on modulating gut microbiota in both animal and human studies. These results indicate that gut-microbial metabolites are involved in the pathogenesis of T2D and supplementation of probiotics could be beneficial to alleviate IR in T2D via modulation of gut microbiota

Cardiovascular, cerebrovascular, and renal co-morbidities in COVID-19 patients: A systematic-review and meta-analysis.

BackgroundCOVID-19 has infected over 35 million people worldwide and led to over 1 million deaths. Several risk factors that increase COVID-19 severity have emerged, including age and a history of cardiovascular disease, hypertension, or kidney disease. However, a number of outstanding questions persist, including whether the above comorbidities correlate with increased mortality from COVID-19 or whether age is a significant confounding variable that accounts for the observed relationship between COVID-19 severity and other comorbidities.Methods and findingsWe conducted a systematic review and meta-analysis of studies documenting COVID-19 patients with hypertension, cardiovascular disease, cerebrovascular disease, or chronic kidney disease. We classified COVID-19 cases into severe/non-severe or deceased/surviving and calculated the odds ratio (OR) for each of the four comorbidities in these cohorts. 36 studies, comprising 22,573 patients, are included in our meta-analysis. We found that hypertension is the most prevalent comorbidity in deceased COVID-19 patients (55.4%; CI: 49.4-61.3%), followed by cardiovascular disease (30.7%; CI: 22.6-38.8%), cerebrovascular disease (13.4%; CI: 9.12-19.2%), then chronic kidney disease (9.05%; CI: 5.57-15.0%). The risk of death is also significantly higher for patients with these comorbidities, with the greatest risk factor being chronic kidney disease (OR: 8.86; CI: 5.27-14.89), followed by cardiovascular disease (OR: 6.87; CI: 5.56-8.50), hypertension (OR: 4.87; CI: 4.19-5.66), and cerebrovascular disease (OR: 4.28; CI: 2.86-6.41). These risks are significantly higher than previously reported, while correlations between comorbidities and COVID-19 severity are similar to previously reported figures. Using meta-regression analysis with age as a moderating variable, we observed that age contributes to the observed risks but does not explain them fully.ConclusionsIn this meta-analysis, we observed that cardiovascular, cerebrovascular, and kidney-related comorbidities in COVID-19 significantly contributes to greater risk of mortality and increased disease severity. We also demonstrated that age may not be a confounder to these associations

Influence of Intratumor Microbiome on Clinical Outcome and Immune Processes in Prostate Cancer

Although 1 in 9 American men will receive a diagnosis of prostate cancer (PC), most men with this diagnosis will not die from it, as most PCs are indolent. However, there is a subset of patients in which the once-indolent PC becomes metastatic and eventually, fatal. In this study, we analyzed microbial compositions of intratumor bacteria in PC to determine the influence of the microbiome on metastatic growth. Using large-scale RNA-sequencing data and corresponding clinical data, we correlated the abundance of microbes to immune pathways and PC risk factors, identifying specific microbes that either significantly deter or contribute to cancer aggressiveness. Interestingly, most of the microbes we found appeared to play anti-tumor roles in PC. Since these anti-tumor microbes were overrepresented in tumor samples, we believe that microbes thrive in the tumor microenvironment, outcompete cancer cells, and directly mitigate tumor growth by recruiting immune cells. These include Listeria monocytogenes, Methylobacterium radiotolerans JCM 2831, Xanthomonas albilineans GPE PC73, and Bradyrhizobium japonicum, which are negatively correlated with Gleason score, Tumor-Node-Metastasis (TNM) stage, prostate-specific antigen (PSA) level, and Androgen Receptor (AR) expression, respectively. We also identified microbes that contribute to tumor growth and are positively correlated with genomic alterations, dysregulated immune-associated (IA) genes, and prostate cancer stem cells (PCSC) genes