{"title":"Are Shwachman-diamond syndrome patients radiosensitive?","authors":"Nimrat Chatterjee","doi":"10.14304/SURYA.JPR.V5N3.3","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.3","url":null,"abstract":"","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44941246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sodium tungstate mimics insulin effect on nuclear translocation of FBPase in rat liver","authors":"R. Bertinat, F. Nualart, J. C. Slebe, A. Yáñez","doi":"10.14304/SURYA.JPR.V5N3.1","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.1","url":null,"abstract":"Sodium tungstate (NaW) is an inorganic salt that has proven to be a potent insulin-mimetic agent, although the molecular events seems to differ. Inhibition of hepatic gluconeogenesis is one significant physiological action of insulin, therefore studying the effect of NaW on gluconeogenic enzymes will contribute to understand its elusive mechanism of action. Here, we show that NaW has no inhibitory effect over the gluconeogenic enzyme fructose 1,6-bisphosphatase (FBPase) in vitro, but mimics insulin in the induction of the nuclear translocation of FBPase in rat liver, which may have a negative impact on its activity. Then, at least in part, NaW may inhibit hepatic gluconeogenesis by inducing the proper subcellular distribution of FBPase, without directly interfering with its phosphatase activity.","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48461502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mfd and UvrD proteins: essential mediators to the maintenance of life","authors":"Nerea Sanvisens-Delgado","doi":"10.14304/SURYA.JPR.V5N3.4","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.4","url":null,"abstract":"","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47068487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Toward therapeutic genome editing in post-mitotic retinal cells","authors":"Benjamin Bakondi","doi":"10.14304/SURYA.JPR.V5N3.6","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.6","url":null,"abstract":"The repertoire of nuclease-guided genome modifications was recently expanded to include homology-independent targeted integration (HITI) of exogenous DNA by a report published in the December 2016 issue of Nature (Suzuki et al. 2016). The key feature distinguishing HITI from homology-based DNA Knock-in is its applicability in post-mitotic cells of nonregenerative tissues, such as the brain and retina. Suzuki et al. demonstrated the therapeutic utility of HITI through genomic knock-in of an exon previously deleted by a naturally occurring mutation that causes blindness in rats. The potential therapeutic impacts are farther-reaching than the replacement of deleted genomic segments. Targeted integration of therapeutic genes in post-mitotic cells in vivo may improve treatments that rely on continued gene augmentation or silencing.","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48645328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Can The Entrepreneurial University Solve The Postdoc Problem","authors":"Thomas J. Simmons","doi":"10.14304/SURYA.JPR.V5N3.7","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.7","url":null,"abstract":"Recently numerous commentators have raised serious concerns over the inability of the academic system to appropriately deal with the rapid growth in the number of postdocs it is training – particularly in light of the far more moderate growth in the number of permanent academic positions. Concomitantly, in the context of an increased emphasis for universities to contribute to economic activity, many commentators have criticised the poor entrepreneurial performance of universities. Here I explore various proposed remedies to the postdoc problem and to the poor entrepreneurial performance of universities. I highlight shared interests in each other’s missions and suggest that a solution to the postdoc problem could be found in the vision of the ‘entrepreneurial university’.","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42992603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Morphological Characterization of Bacteriogenic Manganese Oxides From Three Model Manganese (II/III) Oxidizing Bacterial Species","authors":"Wendy F. Smythe","doi":"10.14304/SURYA.JPR.V5N3.2","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N3.2","url":null,"abstract":"Currently there is limited knowledge as to the morphology of bacteriogenic manganese (Mn)oxide minerals, making it difficult to identify Mn minerals from geologic deposits as being biotic or abiotically formed. When investigating mineral deposits it is critical to understand what environmental processes lead to mineral formation in order to accurately interpret the information locked inside each mineral. This study aims to characterize the morphology, structural variability, and microbe-mineral association of bacteriogenic Mn(III/IV) oxides produced by Mn(II/III)-oxidizing bacteria, using pure cultures of three known Mn-oxidizing bacteria. Morphology and localization of bacteriogenic Mn-oxides was characterized using high resolution scanning electron (HR-SEM) and transmission electron microscopy (TEM). We found that the morphology of bacteriogenic Mn-oxides varies between bacterial species, and that the localization of Mn oxidizing enzymes determines if Mn-oxides are closely associated with the cellular surface or form in exopolysaccharides (EPS). Knowledge acquired from this study illustrates the complexity of identifying bacteriogenic Mn-oxides and oxidation products from more complex natural environmental settings like ancient geologic deposits.","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67014779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cell Competition: Advances & mechanisms","authors":"A. Kale","doi":"10.14304/SURYA.JPR.V5N1.5","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N1.5","url":null,"abstract":"","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49543277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Editorial: The Transformative Age of Leptin in Diabetes Treatment","authors":"A. Fenn","doi":"10.14304/SURYA.JPR.V5N1.1","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N1.1","url":null,"abstract":"","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47914561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Editorial: Glycolysis as a target for cancer therapy","authors":"T. Chakraborty","doi":"10.14304/SURYA.JPR.V5N1.3","DOIUrl":"https://doi.org/10.14304/SURYA.JPR.V5N1.3","url":null,"abstract":"Cancer is a highly heterogeneous disease and each cancer has its individual metabolic fingerprint. Even within a single cancer, its constituent cells are heterogeneous and the metabolic fingerprint varies from one cell to another (Jie Zheng 2012). Unlike normal cells, glycolysis is enhanced in cancer cells (Warburg 1927, 1956; Robert A. Gatenby et.al. 2004; Jie Zheng 2012). This was first described by German scientist Otto Warburg in the 1920s. Following Warburg’s observations that cancer cells have a higher rate of glycolysis than normal cells, interest in the metabolic property of cancers has steadily increased. In recent years, understanding the features and complexity of the metabolism and energetics of cancer cells has been rekindled, mainly because therapy targeting metabolism hits the “core” of the cancer and has the potential to cripple a cancer cell’s ability to self-renew.","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42949794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pleotropic Acute and Chronic Effects of Leptin to Reverse Type 1 Diabetes.","authors":"Rachel J Perry","doi":"10.14304/surya.jpr.v5n1.2","DOIUrl":"https://doi.org/10.14304/surya.jpr.v5n1.2","url":null,"abstract":"<p><p>Recent studies have demonstrated that leptin can prolong life chronically in rats with poorly-controlled type 1 diabetes (T1D). Multiple explanations have been proposed to explain leptin's chronic antihyperglycemic effect, including suppression of glucagon release and/or signaling, reductions in hyperphagia and ectopic lipid content, and improvements in insulin sensitivity; it is leptin's ability to reduce plasma glucose relies on all of these effects. In addition, leptin reverses hyperglycemia and diabetic ketoacidosis (DKA) acutely, within 6 hours of leptin infusion, by suppressing hypothalamic-pituitary-adrenal (HPA) axis activity in insulinopenic rats. Thus current evidence suggests that leptin's acute, insulin-independent effect to reverse DKA by suppressing HPA axis activity occurs through a different mechanism from its chronic, pleotropic, insulin-dependent effect to reverse hyperglycemia and prolong survival in rodents with T1D. Leptin may therefore represent an attractive therapeutic target to improve glycemic control in humans with poorly-controlled T1D.</p>","PeriodicalId":90946,"journal":{"name":"Postdoc journal : a journal of postdoctoral research and postdoctoral affairs","volume":"5 1","pages":"3-11"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5321081/pdf/nihms-847401.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34766399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}