199,388 research outputs found
miR-127 protects proximal tubule cells against ischemia/reperfusion : identification of Kinesin family member 3B as miR-127 target
No full textIschemia/reperfusion (I/R) is at the basis of renal transplantation and acute kidney injury. Molecular mechanisms underlying proximal tubule response to I/R will allow the identification of new therapeutic targets for both clinical settings. microRNAs have emerged as crucial and tight regulators of the cellular response to insults including hypoxia. Here, we have identified several miRNAs involved in the response of the proximal tubule cell to I/R. Microarrays and RT-PCR analysis of proximal tubule cells submitted to I/R mimicking conditions in vitro demonstrated that miR-127 is induced during ischemia and also during reperfusion. miR-127 is also modulated in a rat model of renal I/R. Interference approaches demonstrated that ischemic induction of miR-127 is mediated by Hypoxia Inducible Factor-1alpha (HIF-1α) stabilization. Moreover, miR-127 is involved in cell-matrix and cell-cell adhesion maintenance, since overexpression of miR-127 maintains focal adhesion complex assembly and the integrity of tight junctions. miR-127 also regulates intracellular trafficking since miR-127 interference promotes dextran-FITC uptake. In fact, we have identified the Kinesin Family Member 3B (KIF3B), involved in cell trafficking, as a target of miR-127 in rat proximal tubule cells. In summary, we have described a novel role of miR-127 in cell adhesion and its regulation by HIF-1α. We also identified for the first time KIF3B as a miR-127 target. Both, miR-127 and KIF3B appear as key mediators of proximal epithelial tubule cell response to I/R with potential al application in renal ischemic damage management
miR-200a silencing protects NSCs against OGD/R-induced injury.
No full textNSCs were transfected with shRNA against miR-200a or its negative control (scrambled), and then were exposed to OGD/R conditions. (A) Cell viability, (B) apoptotic cells population, (C) and (D) the expression of apoptosis-related factors, and (E) cell migration were respectively assessed by MTT, flow cytometry, Western blotting and Transwell assay. ** P P ## P < 0.01 versus OGD/R + sh-scramble group.</p
MiR-122 sensitized Huh7/R cells to doxorubicin inducing cell death via miR-122-PKM2 pathway.
No full text(A) Huh7/R cells were transfected with miR-122 mimics as well as PKM2 recombinant vector for 24 h, and then the cells were treated with doxorubicin (10 μg/ml) for another 48 h. Cell viability was measured by MTT assay. *p<0.05, t test. (B) Huh7/R cells were transfected with miR-122 mimics as well as PKM2 recombinant vector for 24 h, and then the cells were treated with doxorubicin (10 μg/ml) for another 24 h. Cell apoptosis was measured using Annexin V/PI staining. (C) Cleavage of caspase-3 and PARP was evaluated by western blot analysis.</p
Letter from R. R. Zellick, Assistant Trust Officer, Anglo California National Bank of San Francisco, to Joseph R. Goodman, October 2, 1942
No full textLetter from R. R. Zellick, Assistant Trust Officer at The Anglo California National Bank of San Francisco, to Joseph R. Goodman, regarding property owned by Dave Tatsuno. Zellick mentions a dispute between current tenants and Tatsuno, and that Tatsuno has asked Goodman to help locate trustworthy tenants.Personal correspondence, organizational records, government documents, publications, and other papers created or collected by Joseph R. Goodman documenting the forced removal and incarceration of Japanese Americans during World War II, as well as organized resistance to incarceration. Included in the collection are records of the Japanese Young Men's Christian Association and the Japanese American Citizens' League in San Francisco, including papers of the Japanese YMCA's executive secretary Lincoln Kanai; Sakai family papers; Goodman's correspondence to and from Japanese American incarcerees, organizations opposing forced removal and incarceration of Japanese Americans, the War Relocation Authority, and others; publications, photographs, and ephemera from the Topaz Relocation Center, where Goodman taught high school; War Relocation Authority records and publications; and newspaper clippings, pamphlets, and reports about forced removal and incarceration created by various government, religious, and civic organizations, in California and nationwide
"Closing the R&D Gap, Evaluating the Sources of R&D Spending"
No full textBoth spending and tax policies have been implemented in the United States with the goal of stimulating private sector research and development (R&D). Karier questions whether current R&D policy, especially the research and experimentation tax credit, can contribute to closing the gap between nondefense expenditures on R&D in the United States and such expenditures in other countries, such as Japan and Germany. He also explores possible changes to our current R&D policy to make it more effective.
NEW INSIGHTS OF MIR-145 FUNCTION AND REGULATION IN HUMAN BREAST CANCER.
No full textmiR-145 is down-regulated in the majority of human cancers, including breast cancer (BC).
However, its role remains largely unknown. Here, I provide evidence for miR-145 induced
anti-proliferative and pro-apoptotic effect in several BC cell lines, which was not detected in
BC cells lacking a functional TP53 gene and exhibiting an estrogen receptor alfa (ESR1)
negative status. I found that miR-145 anti-proliferative effects were dependent upon TP53
activation and that activation of TP53 could in turn stimulates miR-145 expression. I also
found that miR-145 could repress the expression of ESR1 protein by direct interaction with
two sites within its gene coding sequence. My findings support the existence of a positive
regulatory loop where miR-145 directly targets ESR1 and indirectly activates TP53, which in
turn sustains miR-145 expression and reinforces miR-145 overall effects on proliferation and
apoptosis
Serum microRNA-21 as marker for necroinflammation in hepatitis C patients with and without hepatocellular carcinoma
No full textBackground: MicroRNA-21 (miR-21) is up-regulated in tumor tissue of patients with malignant diseases, including hepatocellular carcinoma (HCC). Elevated concentrations of miR-21 have also been found in sera or plasma from patients with malignancies, rendering it an interesting candidate as serum/plasma marker for malignancies. Here we correlated serum miR-21 levels with clinical parameters in patients with different stages of chronic hepatitis C virus infection (CHC) and CHC-associated HCC.
Methodology/Principal Findings: 62 CHC patients, 29 patients with CHC and HCC and 19 healthy controls were prospectively enrolled. RNA was extracted from the sera and miR-21 as well as miR-16 levels were analyzed by quantitative real-time PCR; miR-21 levels (normalized by miR-16) were correlated with standard liver parameters, histological grading and staging of CHC. The data show that serum levels of miR-21 were elevated in patients with CHC compared to healthy controls (P<0.001); there was no difference between serum miR-21 in patients with CHC and CHC-associated HCC. Serum miR-21 levels correlated with histological activity index (HAI) in the liver (r = −0.494, P = 0.00002), alanine aminotransferase (ALT) (r = −0.309, P = 0.007), aspartate aminotransferase (r = −0.495, P = 0.000007), bilirubin (r = −0.362, P = 0.002), international normalized ratio (r = −0.338, P = 0.034) and γ-glutamyltransferase (r = −0.244, P = 0.034). Multivariate analysis revealed that ALT and miR-21 serum levels were independently associated with HAI. At a cut-off dCT of 1.96, miR-21 discriminated between minimal and mild-severe necroinflammation (AUC = 0.758) with a sensitivity of 53.3% and a specificity of 95.2%.
Conclusions/Significance: The serum miR-21 level is a marker for necroinflammatory activity, but does not differ between patients with HCV and HCV-induced HCC
Hansen, Lee (Lee R.). Union, non-union, and managerial pay plan state employees, 2008-2019
No full text1 online resource (2 pages)"July 1, 2021."Provides the number of union and non-union state employees in each of the last 14 years. Also provides the number of state employees paid under the state's managerial pay plan during each of those years. Updates OLR research report 2019-R-011
MicroRNAs in cardiac arrhythmia: DNA sequence variation of MiR-1 and MiR-133A in long QT syndrome.
No full textLong QT syndrome (LQTS) is a genetic cardiac condition associated with prolonged ventricular repolarization, primarily a result of perturbations in cardiac ion channels, which predisposes individuals to life-threatening arrhythmias. Using DNA screening and sequencing methods, over 700 different LQTS-causing mutations have been identified in 13 genes worldwide. Despite this, the genetic cause of 30-50% of LQTS is presently unknown. MicroRNAs (miRNAs) are small (∼ 22 nucleotides) noncoding RNAs which post-transcriptionally regulate gene expression by binding complementary sequences within messenger RNAs (mRNAs). The human genome encodes over 1800 miRNAs, which target about 60% of human genes. Consequently, miRNAs are likely to regulate many complex processes in the body, indeed aberrant expression of various miRNA species has been implicated in numerous disease states, including cardiovascular diseases. MiR-1 and MiR-133A are the most abundant miRNAs in the heart and have both been reported to regulate cardiac ion channels. We hypothesized that, as a consequence of their role in regulating cardiac ion channels, genetic variation in the genes which encode MiR-1 and MiR-133A might explain some cases of LQTS. Four miRNA genes (miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2), which encode MiR-1 and MiR-133A, were sequenced in 125 LQTS probands. No genetic variants were identified in miR-1-1 or miR-133a-1; but in miR-1-2 we identified a single substitution (n.100A> G) and in miR-133a-2 we identified two substitutions (n.-19G> A and n.98C> T). None of the variants affect the mature miRNA products. Our findings indicate that sequence variants of miR-1-1, miR-1-2, miR-133a-1 and miR-133a-2 are not a cause of LQTS in this cohort
R-4.2.0 with all libraries necessary for caMeL
No full textThis is a zipped file with R 4.2.0 and all libraries that are necessary for for caMeL interface operation. Simply follow the guidelines to prepare your environment.Disclaimer: this is a full environment for the software operations. I am not an author of it. You should cite the developers accordingly (https://ropensci.org/blog/2021/11/16/how-to-cite-r-and-r-packages/).</p
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