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mTORC1 Coordinates Protein Synthesis and Immunoproteasome Formation via PRAS40 to Prevent Accumulation of Protein Stress. - Molecular cell
Reduction of translational fidelity often occurs in cells with high rates of protein synthesis, generating defective ribosomal products. If not removed, such aberrant proteins can be a major source of cellular stress causing human diseases. Here, we demonstrate that mTORC1 promotes the formation of immunoproteasomes for efficient turnover of defective proteins and cell survival. mTORC1 sequesters precursors of immunoproteasome Î² subunits via PRAS40. When activated, mTORC1 phosphorylates PRAS40 to enhance protein synthesis and simultaneously to facilitate the assembly of the Î² subunits for forming immunoproteasomes. Consequently, the PRAS40 phosphorylations play crucial roles inÂ clearing aberrant proteins that accumulate due toÂ mTORC1 activation. Mutations of RAS, PTEN, and TSC1, which cause mTORC1 hyperactivation, enhance immunoproteasome formation in cells and tissues. Those mutations increase cellular dependence on immunoproteasomes for stress response and survival. These results define a mechanism by which mTORC1 couples elevated protein synthesis with immunoproteasome biogenesis to protect cells against protein stress.Copyright Â© 2016 Elsevier Inc. All rights reserved.
Eukaryotic genome instability in light of asymmetric DNA replication. - Critical reviews in biochemistry and molecular biology
The eukaryotic nuclear genome is replicated asymmetrically, with the leading strand replicated continuously and the lagging strand replicated as discontinuous Okazaki fragments that are subsequently joined. Both strands are replicated with high fidelity, but the processes used to achieve high fidelity are likely to differ. Here we review recent studies of similarities and differences in the fidelity with which the three major eukaryotic replicases, DNA polymerases Î±, Î´, and É›, replicate the leading and lagging strands with high nucleotide selectivity and efficient proofreading. We then relate the asymmetric fidelity at the replication fork to the efficiency of DNA mismatch repair, ribonucleotide excision repair and topoisomerase 1 activity.
Mice with Hepatocyte-Specific FXR Deficiency are Resistant to Spontaneous but Susceptible to Cholic Acid Induced Hepatocarcinogenesis. - American journal of physiology. Gastrointestinal and liver physiology
Farnesoid X receptor (FXR) belongs to the nuclear receptor superfamily with its endogenous ligands bile acids. Mice with whole-body FXR deficiency develop liver tumors spontaneously, but the underlying mechanism is unclear. Moreover, it is unknown whether FXR deficiency in liver alone serves as a tumor initiator or promoter during liver carcinogenesis. this study aims to evaluate the effects of hepatocyte-specific FXR deficiency (FXR(hep-/-)) in liver tumor formation. The results showed that FXR(hep-/-) mice did not show spontaneous liver tumorigenesis with aging (up to 24 months of age). Therefore FXR(hep-/-) mice were fed a bile acid (cholic acid)-containing diet alone or along with a liver tumor initiator, diethylnitrosamine (DEN). Thirty weeks later, no tumors were found in WT or FXR(hep-/-) mice without any treatment or with DEN-only. However, with cholic acid, while only some wild-type mice developed tumors, all FXR(hep-/-)mice presented with severe liver injury and tumors. Interestingly, FXR(hep-/-) mouse livers increased basal expression of tumor suppressor p53 protein, apoptosis and decreased basal cyclin D1 expression, which may prevent tumor development in FXR(hep-/-) mice. However, cholic-acid feeding reversed these effects in FXR(hep-/-) mice, which is associated with an increased cyclin D1 and decreased cell cycle inhibitors. More in-depth analysis indicates that the increased in cell growth might be resulted from disturbance of the MAPK and JAK/STAT3 signaling pathways. In conclusion, this study shows that hepatic FXR deficiency may only serve as a tumor initiator and increased bile acids is required for tumor formation likely by promoting cell proliferation.Copyright Â© 2015, American Journal of Physiology- Gastrointestinal and Liver Physiology.
Design, development, and evaluation of printed educational materials for evidence-based practice dissemination. - International journal of evidence-based healthcare
Printed educational materials (PEMs) are one of the most common dissemination strategies for communicating information about evidence-based practices (EBPs) to healthcare professionals and organizations; however, evidence is conflicting regarding the conditions and circumstances in which PEMs are effective in achieving desired outcomes. The effectiveness of PEMs is largely dependent on the manner in which they are developed. This article reports on the findings from a comprehensive review of the literature regarding best practices for creating PEMs for health professionals and illustrates how these practices were used to design, develop, and evaluate an informational packet to disseminate information about motivational interviewing.The informational packet was disseminated to 92 community health organizations not currently implementing motivational interviewing. Evaluation surveys were completed by 212 healthcare directors and providers to examine quality and perceived helpfulness of the packets, intention to use information from the packet, and sharing of the packet with others. Associations between these and individual and organizational characteristics were also assessed.Overall, the packet was perceived as appropriate and helpful in making a decision to implement motivational interviewing. For example, 84.9% of participants stated that the content was 'about right'. Three-quarters (75.9%) of participants reported plans to use the information in the packet and almost half (46.7%) reported talking about the packet with others in the organizations. Higher levels of baseline interest in motivational interviewing adoption were significantly related to packet use and wanting to utilize additional resources presented in the packet. Positive attitudes toward EBPs were also significantly related to the desire to obtain resources in the packet. Perceptions of the packet did not differ by type of community health organization (i.e., community health center, community behavioral health organization) or whether the individual was a director or provider.Results indicated that PEMs can be a useful tool to disseminate EBP information to healthcare professionals particularly if they have a prior interest in the EBP and have general attitudes supportive of EBPs. Recommendations for the improvement of future PEMs are discussed.
Targeting Pink1-Parkin-mediated mitophagy for treating liver injury. - Pharmacological research
Alcoholic liver disease and acetaminophen overdose are common causes of severe liver disease and liver failure in the United States for which there is no cure. Therefore, development of new therapeutic strategies for treatment of liver injury caused by acetaminophen and alcohol is needed. We demonstrated that autophagy protects against alcohol and acetaminophen-induced liver injuries by removing damaged mitochondria via mitophagy, which is a selective form of autophagy specific for degradation of damaged mitochondria. Parkin is well-known to be required for mitophagy induction in in vitro models, and we previously showed that the Parkin-mediated mitophagy pathway likely plays a protective role against alcohol and acetaminophen-induced liver injuries. Therefore, pharmacological upregulation of the Parkin-mediated mitophagy pathway in the liver may provide a novel and effective therapeutic option for treatment of acetaminophen and alcohol-induced liver injuries. In this review, we discuss regulation of Parkin-mediated mitophagy and possible therapeutic targets of intervention in this pathway.Copyright Â© 2015 Elsevier Ltd. All rights reserved.
Sec13 Regulates Expression of Specific Immune Factors Involved in Inflammation In Vivo. - Scientific reports
The Sec13 protein functions in various intracellular compartments including the nuclear pore complex, COPII-coated vesicles, and inside the nucleus as a transcription regulator. Here we developed a mouse model that expresses low levels of Sec13 (Sec13(H/-)) to assess its functions in vivo, as Sec13 knockout is lethal. These Sec13 mutant mice did not present gross defects in anatomy and physiology. However, the reduced levels of Sec13 in vivo yielded specific immunological defects. In particular, these Sec13 mutant mice showed low levels of MHC I and II expressed by macrophages, low levels of INF-Î³ and IL-6 expressed by stimulated T cells, and low frequencies of splenic IFN-Î³+CD8+ T cells. In contrast, the levels of soluble and membrane-bound TGF-Î² as well as serum immunoglobulin production are high in these mice. Furthermore, frequencies of CD19+CD5-CD95+ and CD19+CD5-IL-4+ B cells were diminished in Sec13(H/-) mice. Upon stimulation or immunization, some of the defects observed in the naÃ¯ve mutant mice were compensated. However, TGF-Î² expression remained high suggesting that Sec13 is a negative modulator of TGF-Î² expression and of its immunosuppressive functions on certain immune cells. In sum, Sec13 regulates specific expression of immune factors with key functions in inflammation.
A Mechanistic Review of Mitophagy and Its Role in Protection against Alcoholic Liver Disease. - Biomolecules
Alcoholic liver disease (ALD) is a major health problem worldwide, and alcohol is well-known to cause mitochondrial damage, which exacerbates alcohol-induced liver injury and steatosis. No successful treatments are currently available for treating ALD. Therefore, a better understanding of mechanisms involved in regulation of mitochondrial homeostasis in the liver and how these mechanisms may protect against alcohol-induced liver disease is needed for future development of better therapeutic options for ALD. Mitophagy is a key mechanism for maintaining mitochondrial homeostasis by removing damaged mitochondria, and mitophagy protects against alcohol-induced liver injury. Parkin, an E3 ubiquitin ligase, is well-known to induce mitophagy in in vitro models although Parkin-independent mechanisms for mitophagy induction also exist. In this review, we discuss the roles of Parkin and mitophagy in protection against alcohol-induced liver injury and steatosis. We also discuss Parkin-independent mechanisms for mitophagy induction, which have not yet been evaluated in the liver but may also potentially have a protective role against ALD. In addition to mitophagy, mitochondrial spheroid formation may also provide a novel mechanism of protection against ALD, but the role of mitochondrial spheroids in protection against ALD progression needs to be further explored. Targeting removal of damaged mitochondria by mitophagy or inducing formation of mitochondrial spheroids may be promising therapeutic options for treatment of ALD.
Narratives to enhance smoking cessation interventions among African-American smokers, the ACCE project. - BMC research notes
Low-income, African-American smokers are less likely to have resources to aid in quitting smoking. Narrative communication may provide an enhancement to traditional smoking cessation interventions like NRT, medications, or behavioral treatments for this audience. After extensive pilot testing of stories and personal experiences with smoking cessation from African-Americans from a low-income community, we conducted a randomized control trial using stories to augment routine inpatient treatment among African-Americans at an urban Southern hospital (NÂ =Â 300).Differences in smoking cessation outcomes between the intervention (stories DVDÂ +Â routine clinical treatment) and control (routine clinical treatment) arms were compared using self-report and carbon monoxide measurement at 6-months. Compared to control, individuals who viewed the intervention stories DVD reported greater intentions to quit. Although continuous quitting marginally favored the intervention, our main result did not reach statistical significance (pÂ =Â 0.16).Narrative communication via storytelling to promote smoking cessation among African-Americans in the South is one method to communicate smoking cessation. Results suggest this may not be sufficient as a stand-alone augmentation of routine clinical treatment for continuous smoking cessation. Smoking cessation efforts need to continually assess different means of communicating to smokers about quitting.The ClinicalTrials.gov Identifier is NCT00101491. This trial was registered January 10, 2005.
Stimulation of Chromosomal Rearrangements by Ribonucleotides. - Genetics
We show by whole genome sequence analysis that loss of RNase H2 activity increases loss of heterozygosity (LOH) in Saccharomyces cerevisiae diploid strains harboring the pol2-M644G allele encoding a mutant version of DNA polymerase Îµ that increases ribonucleotide incorporation. This led us to analyze the effects of loss of RNase H2 on LOH and on nonallelic homologous recombination (NAHR) in mutant diploid strains with deletions of genes encoding RNase H2 subunits (rnh201Î”, rnh202Î”, and rnh203Î”), topoisomerase 1 (TOP1Î”), and/or carrying mutant alleles of DNA polymerases Îµ, Î±, and Î´. We observed an âˆ¼7-fold elevation of the LOH rate in RNase H2 mutants encoding wild-type DNA polymerases. Strains carrying the pol2-M644G allele displayed a 7-fold elevation in the LOH rate, and synergistic 23-fold elevation in combination with rnh201Î”. In comparison, strains carrying the pol2-M644L mutation that decreases ribonucleotide incorporation displayed lower LOH rates. The LOH rate was not elevated in strains carrying the pol1-L868M or pol3-L612M alleles that result in increased incorporation of ribonucleotides during DNA synthesis by polymerases Î± and Î´, respectively. A similar trend was observed in an NAHR assay, albeit with smaller phenotypic differentials. The ribonucleotide-mediated increases in the LOH and NAHR rates were strongly dependent on TOP1. These data add to recent reports on the asymmetric mutagenicity of ribonucleotides caused by topoisomerase 1 processing of ribonucleotides incorporated during DNA replication.Copyright Â© 2015 by the Genetics Society of America.
Validation of a New Metric for Assessing the Integration of Health Protection and Health Promotion in a Sample of Small- and Medium-Sized Employer Groups. - Journal of occupational and environmental medicine / American College of Occupational and Environmental Medicine
To conduct validation analyses for a new measure of the integration of worksite health protection and health promotion approaches developed in earlier research.A survey of small- to medium-sized employers located in the United States was conducted between October 2013 and March 2014 (nâ€Š=â€Š111). Cronbach Î± coefficient was used to assess reliability, and Pearson correlation coefficients were used to assess convergent validity.The integration score was positively associated with the measures of occupational safety and health and health promotion activities/policies-supporting its convergent validity (Pearson correlation coefficients of 0.32 to 0.47). Cronbach Î± coefficient was 0.94, indicating excellent reliability.The integration score seems to be a promising tool for assessing integration of health promotion and health protection. Further work is needed to test its dimensionality and validate its use in other samples.
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