Job insecurity, employability, and mental health in the new era: A test of plausible influence mechanisms and temporal effects.

Although job insecurity and employability have drawn much research attention, the plausible relationships between them and how they jointly influence mental health remain unclear in the literature. We draw upon JD-R and COR theories to test and contrast three plausible relationships between job insecurity and employability, using a longitudinal sample of 1216 employees over 18 years. We further expand tests of these theoretical positions by considering temporal dynamics, using dynamic structural equation models (DSEMs) for stronger mediation evidence and latent growth models (LGMs) to compare the effects of job insecurity and employability trends in predicting the trend of mental health. In general, findings showed that job insecurity mediated the relationship between employability and mental health, supporting the mediation hypothesis. We also found that employability moderated the relationship between job insecurity and mental health, supporting the moderation hypothesis, although the effect was weak. Results further suggested that the effect magnitudes of job insecurity and employability predicting mental health were significantly different. Specifically, job insecurity was a stronger predictor of mental health than employability across all 18 years; the trend of job insecurity also predicted the trend of mental health more strongly than the trend of employability. Taken together, this study not only advances theory precision but also methodological soundness of research on job insecurity, employability, and mental health, supporting the value of considering temporal factors in examining mental health effects of job insecurity and employability.

Exosomal Circsafb2 Reshaping Tumor Environment to Promote Renal Cell Carcinoma Progression by Mediating M2 Macrophage Polarization.

Background: Macrophages are the most abundant infiltrating immune-related stromal cells present in and around tumors, showing different phenotypes and functions. M2 macrophages mainly exert immunosuppressive functions and promote tumor growth. Exosomes are emerging as important mediators of cross-talk between tumor cells and the microenvironment. CircRNAs are novel members of non-coding RNAs that regulate cancer proliferation and progression. However, the mechanism by which exosomal circRNA regulates macrophage polarization in renal cell carcinoma (RCC) is still largely unknown. Methods: RCC-derived exosomes were characterized using transmission electron microscopy and nanoparticle tracking analysis (NTA). CCK-8, wound healing, and Transwell assays were performed to assess whether exosomes would affect the proliferation, migration, and invasion of RCC. Furthermore, we performed a bioinformatics analysis to identify circRNAs in RCC serum-derived exosomes from the GEO database. The fluorescence in situ hybridization (FISH) assay was used to detect the cellular distribution of circSAFB2. Bioinformatics analyses (StarBase 2.0) were used to pool the miRNA targets of circSAFB2. Luciferase assays were performed to verify the direct interactions. Western blotting was used to detect markers of macrophage M2 polarization. Lastly, mouse xenograft and bioluminescence imaging were used to examine the clinical relevance of exosomal circSAFB2 in vivo. Results: We report the circRNA derived from SAFB2 and evaluate its biological function in promoting the immune escape of RCC. We found that circSAFB2 was highly expressed in RCC tissues and RCC-derived exosomes. Furthermore, we demonstrated that exosomal circSAFB2 mediates the polarization of M2 macrophages through the miR-620/JAK1/STAT3 axis to promote RCC metastasis. Conclusions: Our data first demonstrated that circSAFB2 leads to immune escape from RCC by mediating M2 macrophage polarization via the miR-620/JAK1/STAT3 axis. These findings indicate a novel molecular mechanism of exosomal circSAFB2 in the progression of RCC and implicate circSAFB2 as a target for exosome-mediated tumor immune evasion.

When Does Safety Climate Help? A Multilevel Study of COVID-19 Risky Decision Making and Safety Performance in the Context of Business Reopening.

Businesses are gradually reopening as lockdown measures for the coronavirus disease 2019 (COVID-19) pandemic are being relieved in many places across the globe. It is challenging but imperative for businesses to manage the risk of infection in the workplace and reopen safely. Drawing on risky decision-making theory and the job demands-resource model of workplace safety, we examined the influences of employees' COVID-19 risk perception on their safety performance at work. On the one hand, COVID-19 risk perception motivates employees to perform safely; on the other hand, COVID-19 risk perception could also undermine safety performance through triggering anxiety. In an effort to find ways that alleviate the negative implications of risk perception, we also tested a cross-level interaction model where the risk perception-anxiety relation is weakened with a favorable team safety climate as well as low abusive supervision. Our data were collected from car dealership employees located in China in March 2020, when businesses just started to reopen in locations where these data were collected. Results showed that COVID-19 risk perception was positively related to anxiety, which in turn undermined safety performance. This negative effect canceled out the direct positive effects of COVID-19 risk perception on safety performance. In addition, cross-level interaction results showed that the buffering effect of team safety climate on the risk perception-anxiety relation was diminished with an abusive supervisor. Our findings provide valuable and timely implications on risk management and workplace safety during a public health crisis such as the COVID-19 pandemic.

Effect of Magnesium Supplementation on Chronic Kidney Disease-Mineral and Bone Disorder in Hemodialysis Patients: A Meta-Analysis of Randomized Controlled Trials.

OBJECTIVES: Research about the effects of magnesium (Mg) supplementation on chronic kidney disease-mineral bone disorder (CKD-MBD) among hemodialysis (HD) patients is controversial. Thus, we conducted a meta-analysis to examine Mg supplementation's effects on CKD-MBD in patients requiring dialysis. METHODS: The PubMed and EMBASE databases were searched for English language studies up to September 2020. The main indicators of our study were changes in serum Mg, calcium (Ca), phosphate, parathyroid hormone (PTH), and C-reactive protein levels, and carotid intima-media thickness (CIMT) after Mg supplementation. Mg efficacy was evaluated by weighted mean difference (WMD) and confidence intervals (CIs), and subgroup analyses of intervention type and intervention duration were also performed. RESULTS: Eight eligible studies comprising 309 HD patients were included in our meta-analysis. Mg supplementation alone produced a negative effect on serum PTH levels (WMD = -236.56; 95% CI -349.71 to -123.41) and CIMT (WMD = -0.18; 95% CI -0.34 to -0.01). A subgroup analysis based on intervention type showed a significant improvement in serum Mg (WMD = 1.08; 95% CI 0.51-1.64) and Ca (WMD = -0.50; 95% CI -0.77 to -0.23) levels when Mg was administered via dialysate and oral medication, respectively. Different intervention durations had no effect on serum Mg levels. Mg supplementation had no significant effect on serum phosphate (WMD = -0.25; 95% CI -0.64 to 0.14) and C-reactive protein levels (WMD = -0.02; 95% CI -2.80 to 2,76). CONCLUSIONS: Our results showed that Mg supplementation alone could improve CKD-MBD by regulating serum Ca and PTH metabolism and decreasing CIMT among HD patients.

Metformin alleviates ß-glycerophosphate-induced calcification of vascular smooth muscle cells via AMPK/mTOR-activated autophagy.

The aim of the present study was to investigate the effect of metformin on ß-glycerophosphate-induced calcification of vascular smooth muscle cells (VSMCs) and the possible mechanisms underlying this. Using an established VSMC calcification model, VSMCs were first treated with ß-glycerophosphate, before metformin, 3-methyladenine and compound C were added to the cell cultures in different combinations. Calcium deposition in the cells was examined by Alizarin Red S staining and using the O-cresolphthalein complexone method. To assess the occurrence of autophagy, autophagosomes inside the cells were studied using a transmission electron microscope and green fluorescent microtubule-associated protein 1 light chain 3 (LC3) puncta were examined using a fluorescent microscope. Additionally, protein expression levels of α-smooth muscle actin (α-SMA), runt-related transcription factor 2 (RUNX2), LC3II/I, beclin 1 and 5' adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway-associated proteins were determined by western blot analysis. Metformin increased the number of autophagosomes, green fluorescent LC3 puncta and the levels of LC3II/I, beclin 1, α-SMA and phosphorylated (p)-AMPK in the VSMCs that were treated with ß-glycerophosphate when compared to controls; whereas, calcium deposition and the expression levels of RUNX2 and p-mTOR were found to be decreased. Treating the VSMCs with 3-methyladenine or compound C reversed the effects of metformin. The results of the present study suggested that metformin may alleviate ß-glycerophosphate-induced calcification of VSMCs, which may be attributed to the activation of AMPK/mTOR signaling pathway-dependent autophagy.

Effect of local anti-vascular endothelial growth factor therapy to prevent the formation of stenosis in outflow vein in arteriovenous fistula.

BACKGROUND AND OBJECTIVES: Vascular stenosis and angiogenesis are the major causes of short expectancy of arteriovenous fistula (AVF). Increased expression of vascular endothelial growth factor-A (VEGF-A) has been suggested to play an important role in the pathophysiologic process. Anti-VEGF has been proved to be effective on anti-angiogenesis and applied in clinical practice, but its effect on anti-stenosis remains to be verified before it could be applied to prevent stenosis of AVF. This study was aimed to evaluate the effect of local anti-VEGF therapy to prevent the formation of stenosis in the outflow vein in AVF and its mechanism. METHODS: Bioinformatics of VEGF-A and its downstream-regulated molecules from the STRING PPI database were analyzed in this study. The biopsy samples from outflow veins of AVF in patients and C57BL/6 mouse models were analyzed to examine the mechanisms of pathologic vascular stenosis associated with VEGF pathways and their potential therapeutic targets. RESULTS: We found that the reduction of VEGF-A could downregulate downstream molecules and subsequently reduce the intimal hyperplasia and abnormal vascular remodeling by analyzing the STRING PPI database. Venous wall thickening, intimal neointima formation, and apoptosis of vascular endothelial cells in the proliferative outflow vein of the AVF were significantly more obvious, and upregulation of expression of VEGF was observed in dysfunctional AVF in patients. In mouse models, the expression of VEGF, Ephrin receptor B4 (EphB4), matrix metalloproteinase (MMP)2, MMP9, tissue inhibitor of metalloproteinase (TIMP)1, TIMP2, and caspase 3 in the control-shRNA surgical group was significantly higher than in the sham group (P < 0.05), and all of these indicators were significantly lower in lentiviral transfection group and Avastin group than in control-shRNA surgical group (P < 0.05) on the 14th day after AVF operation. CONCLUSION: VEGF expression is significantly increased in vascular endothelial cells in stenosed or occluded outflow veins of dysfunctional AVF. Local injection of Avastin into the adventitia of the proximal outflow vein in autologous AVF procedure has an excellent potential to prevent the subsequent local stenosis of the proximal outflow vein.

Where you came from and where you are going: The role of performance trajectory in promotion decisions.

Despite the clear theoretical link between promotions and job performance, the few studies that have tested this relationship have instead found that the role of job performance level in determining promotions is much less than might be expected. In 4 studies, we propose and test a different way of thinking about the performance-promotion relationship. Prospect theory, spiraling theory, and sponsored and contest mobility were used to support the notion that change in performance is at least as important to the prediction of promotion decisions as is absolute level of performance. In Study 1, performance and promotion data were collected for 563 white-collar employees at each of 4 time points spread over 6 years. As hypothesized, change in job performance significantly predicted change in workers' hierarchical level (i.e., promotion) beyond previous performance level. In Study 2, we found that upward trends are associated with ratings of future performance expectation and promotability through their effects on attributions of conscientiousness, proactive personality, and job dedication. In Study 3, we replicated the findings of Study 2 and found no evidence of a performance trend by performance level interaction. In Study 4, we showed that those with upward trends are preferred even to those with performance that is consistent and strong. Taken together, our results suggest that the reason for the modest performance-promotion relationships found in previous research may be that performance trends are seen by decision makers as containing at least as much promotion-relevant information as do performance averages or recent performance levels. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

OGT-Mediated KEAP1 Glycosylation Accelerates NRF2 Degradation Leading to High Phosphate-Induced Vascular Calcification in Chronic Kidney Disease.

Unraveling the complex regulatory pathways that mediate the effects of phosphate on vascular smooth muscle cells (VSMCs) may provide novel targets and therapies to limit the destructive effects of vascular calcification (VC) in patients with chronic kidney disease (CKD). Our previous studies have highlighted several signaling networks associated with VSMC autophagy, but the underlying mechanisms remain poorly understood. Thereafter, the current study was performed to characterize the functional relevance of O-linked N-acetylglucosamine (GlcNAc) transferase (OGT) in high phosphate-induced VC in CKD settings. We generated VC models in 5/6 nephrectomized rats in vivo and VSMC calcification models in vitro. Artificial modulation of OGT (knockdown and overexpression) was performed to explore the role of OGT in VSMC autophagy and VC in thoracic aorta, and in vivo experiments were used to substantiate in vitro findings. Mechanistically, co-immunoprecipitation (Co-IP) assay was performed to examine interaction between OGT and kelch like ECH associated protein 1 (KEAP1), and in vivo ubiquitination assay was performed to examine ubiquitination extent of nuclear factor erythroid 2-related factor 2 (NRF2). OGT was highly expressed in high phosphate-induced 5/6 nephrectomized rats and VSMCs. OGT silencing was shown to suppress high phosphate-induced calcification of VSMCs. OGT enhances KEAP1 glycosylation and thereby results in degradation and ubiquitination of NRF2, concurrently inhibiting VSMC autophagy to promote VSMC calcification in 5/6 nephrectomized rats. OGT inhibits VSMC autophagy through the KEAP1/NRF2 axis and thus accelerates high phosphate-induced VC in CKD.

Efficacy and safety of cinacalcet compared with other treatments for secondary hyperparathyroidism in patients with chronic kidney disease or end-stage renal disease: a meta-analysis.

BACKGROUND: It is controversial for the effect and safety between cinacalcet and other treatments in treating secondary hyperparathyroidism for patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD). METHODS: Embase, PubMed, and Cochrane Library were searched through Feb 2017. 21 randomized controlled trials were included. We calculated the pooled mean difference (MD), relative risk (RR) and corresponding 95% confidence interval (CI). RESULT: Patients received calcimimetic agents had significantly decreased serum parathyroid hormone (MD = - 259.24 pg/mL, 95% CI: - 336.23 to - 182.25), calcium (MD = - 0.92 mg/dL, 95% CI: - 0.98 to - 0.85) and calcium phosphorus product (MD = - 5.97 mg2/dL2, 95% CI: - 9.77 to - 2.16) concentration compared with control treatment. However, the differences in cardiovascular mortality and all-cause mortality between calcimimetics agents and control group were not statistically significant. The incidence of nausea (RR = 2.13, 95% CI: 1.62 to 2.79), vomiting (RR = 1.99, 95% CI: 1.78 to 2.23) and hypocalcemia (RR = 10.10, 95% CI: 7.60 to 13.43) in CKD patients with calcimimetics agents was significantly higher than that with control treatment. CONCLUSION: Cinacalcet improved the biochemical parameters in CKD patients, but did not improve all-cause mortality and cardiovascular mortality. Moreover, cinacalcet can cause some adverse events.

From alpha to omega and beyond! A look at the past, present, and (possible) future of psychometric soundness in the Journal of Applied Psychology.

The psychometric soundness of measures has been a central concern of articles published in the Journal of Applied Psychology (JAP) since the inception of the journal. At the same time, it isn't clear that investigators and reviewers prioritize psychometric soundness to a degree that would allow one to have sufficient confidence in conclusions regarding constructs. The purposes of the present article are to (a) examine current scale development and evaluation practices in JAP; (b) compare these practices to recommended practices, previous practices, and practices in other journals; and (c) use these comparisons to make recommendations for reviewers, editors, and investigators regarding the creation and evaluation of measures including Excel-based calculators for various indices. Finally, given that model complexity appears to have increased the need for short scales, we offer a user-friendly R Shiny app (https://orgscience.uncc.edu/about-us/resources) that identifies the subset of items that maximize a variety of psychometric criteria rather than merely maximizing alpha. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

OGT knockdown counteracts high phosphate-induced vascular calcification in chronic kidney disease through autophagy activation by downregulating YAP.

AIMS: Pathological vascular calcification (VC), a major risk factor for cardiovascular mortality, is a highly prevalent finding in patients with chronic kidney disease (CKD). We previously analyzed several pathways protecting against high phosphate-induced VC through induction of autophagy. Here, we explored how O-GlcNAc transferase (OGT) affected high phosphate-induced VC of CKD though mediation of autophagy. MAIN METHODS: In the rats with CKD induced by 5/6 nephrectomy, the VC process was accelerated by a high phosphate diet. The calcification of vascular smooth muscle cells (VSMCs) was induced by high phosphate treatment. We then experimentally tested the effect of OGT on high phosphate-induced VC by conducting loss-of-function experiments. Co-immunoprecipitation and GST pull-down assays were performed to evaluate interaction between OGT and Yes-associated protein (YAP). In mechanistic studies of this pathway, we measured autophagy protein expression and autophagosome formation, as well as calcium deposition and calcium content in VSMCs and in vivo in response to altered expression of OGT and/or YAP. KEY FINDINGS: OGT was up-regulated in high phosphate-induced VC models in vitro and in vivo. High phosphate-induced calcification in the rat aorta and VSMCs were suppressed by OGT silencing. OGT promoted the glycosylation of YAP to enhance its stability. Importantly, over-expressing YAP reduced autophagy and OGT expedited high phosphate-induced VC by inhibiting autophagy through upregulation of YAP. SIGNIFICANCE: OGT silencing downregulated YAP to induce autophagy activation, thus suppressing high phosphate-induced VC, which highlighted a promising preventive target against high phosphate-induced VC in CKD.

Restoration of microRNA-30b expression alleviates vascular calcification through the mTOR signaling pathway and autophagy.

Pathological calcification represents an event that consequently leads to a distinct elevation in the morbidity and mortality of patients with chronic kidney disease (CKD) in addition to strengthening its correlation with hyperphosphatemia. Epigenomic regulation by specific microRNAs (miRNAs) is reported to be involved in ectopic calcification. However, the finer molecular mechanisms governing this event remain unclear. Hence, this study aimed to identify the potential miRNAs involved in vascular calcification (VC) development and progression. Initially, mitochondrial membrane potential (MMP), autophagy-specific markers (LC3II/LC3I and Beclin1) and phenotype-specific markers of osteoblasts (runt-related transcription factor 2 and Msx2) were measured to evaluate autophagy and VC in ß-glycerophosphate-induced vascular smooth muscle cells (VSMCs) with either miR-30b restoration or miR-30b knockdown performed in vitro. The VC in vivo was represented by calcified nodule formation in the aorta of the rats undergoing 5/6 nephrectomy followed by a 1.2% phosphorus diet using Alizarin Red staining. SOX9 was verified as the target of miR-30b according to luciferase activity determination. Restoration of miR-30b was revealed to markedly diminish the expression of SOX9 while acting to inhibit activation of the mTOR signaling pathway. Knockdown of miR-30b reduced MMP and autophagy, elevated VC, and suppressed the presence of rapamycin (an inhibitor of the mTOR signaling pathway). In addition, upregulated expression of miR-30b attenuated VC in vivo. Taken together, the key findings of this study identified the inhibitory role of miR-30b in VC, presenting an enhanced understanding of miRNA as a therapeutic target to curtail progressive VC in hyperphosphatemia of CKD.

Sclerostin/Receptor Related Protein 4 and Ginkgo Biloba Extract Alleviates ß-Glycerophosphate-Induced Vascular Smooth Muscle Cell Calcification By Inhibiting Wnt/ß-Catenin Pathway.

BACKGROUND: Abnormal mineral metabolism in patients with chronic kidney disease (CKD) may lead to vascular calcification, which is markedly associated with adverse events, including ischemic cardiac diseases and all-cause cardiovascular mortality. Thus, preventing and treating vascular calcification play an important role in improving the prognosis of CKD patients. OBJECTIVES: To investigate the potential functions of sclerostin and low-density lipoprotein receptor-related protein 4 (Lrp4) in alleviating the ß-glycerophosphate (ß-GP)-induced vascular smooth muscle cell (VSMC) calcification, and the protective effect of Ginkgo biloba extract (GBE). METHODS: VSMC were extracted from Sprague-Dawley rat aorta and cultured in medium. The VSMCs were divided into 3 groups: (1) Negative control group, (2) ß-GP group, in which the VSMCs were treated with ß-GP, and (3) GBE and ß-GP group, where the VSMCs were treated with both ß-GP and GBE. The calcium nodules within the cells were examined by using Alizarin red S staining. The mRNA expression levels of ß-catenin and bone gamma-carboxyglutamic-acid-containing proteins (BGP) were detected by real-time PCR. The protein levels of sclerostin and Lrp4 were determined by Western blot. RESULTS: Alizarin red S staining showed that the VSMCs in ß-GP group had a distinct orange-red precipitate when compared with VSMCs in the negative control group, while the orange-red precipitate of the GBE and ß-GP group was significantly reduced compared to the ß-GP group. Real-time PCR showed that the mRNA levels of ß-catenin and BGP in VSMCs of ß-GP group were significantly higher than those of the negative control group (p < 0.05); while they were significantly reduced in VSMCs of the GBE and ß-GP group (p < 0.05). Western blot results showed that the expression of sclerostin in the ß-GP group was significantly higher than that in the control group (p < 0.05), whereas Lrp4 was significantly lower than in control group (p < 0.05). Sclerostin in GBE and ß-GP group was significantly reduced (p < 0.05), but Lrp4 was significantly elevated when compared with that of the ß-GP group (p < 0.05). CONCLUSION: ß-GP induced VSMC calcification by activating the Wnt/ß-catenin signaling pathway. Sclerostin and Lrp4 were involved in ß-GP-induced VSMC calcification and play an important role. GBE could alleviate VSMC calcification induced by ß-GP through inhibiting the Wnt/ß-catenin signaling pathway.

Specific knockdown of WNT8b expression protects against phosphate-induced calcification in vascular smooth muscle cells by inhibiting the Wnt-ß-catenin signaling pathway.

In the last 10 years, the prevalence, significance, and regulatory mechanisms of vascular calcification (VC) have gained increasing recognition. The aim of this study is to explore the action of WNT8b in the development of phosphate-induced VC through its effect on vascular smooth muscle cells (VSMCs) in vitro by inactivating the Wnt-ß-catenin signaling pathway. To explore the effect of WNT8b on the Wnt-ß-catenin signaling pathway and VC in vitro, ß-glycerophosphate (GP)-induced T/G HA-VSMCs were treated with small interfering RNA against WNT8b (Si-WNT8b), Wnt-ß-catenin signaling pathway activator (LiCl) and both, respectively. Reverse transcription quantitative polymerase chain reaction and western blot analysis were used to determine the messenger RNA and protein levels of WNT8b, α-smooth muscle actin (α-SMA), calcification-associated molecules, and molecules related to the Wnt signaling pathway. The TOP/FOP-Flash reporter assay was performed to detect the transcription activity mediated by ß-catenin. Si-WNT8b reduced calcium deposition and the activity of alkaline phosphatase (ALP), increased the α-SMA level, and decreased bone morphogenetic protein 2, Pit1, MSX2, and Runt-related transcription factor 2 levels, whereas stimulation of LiCl worsened ß-GP-induced calcium deposition, increased the activity of ALP, and reduced the α-SMA expression level. Si-WNT8b reduced the levels of WNT8b, frizzled-4, ß-catenin, phospho-GSK-3ß (p-GSK-3ß), and cyclin-D, whereas it increased the levels of p-ß-catenin and GSK-3ß, indicating that si-WNT8b could alter the Wnt-ß-catenin signaling pathway and thus hamper the VC in T/G HA-VSMC, which was further demonstrated by the TOP/FOP-Flash assay and detection of the ß-catenin expression level in the nucleus. Altogether, we conclude that WNT8b knockdown terminates phosphate-induced VC in VSMCs by inhibiting the Wnt-ß-catenin signaling pathway.

Situational Strength Cues from Social Sources at Work: Relative Importance and Mediated Effects.

Situational strength is considered one of the most important situational forces at work because it can attenuate the personality-performance relationship. Although organizational scholars have studied the consequences of situational strength, they have paid little attention to its antecedents. To address this gap, the current study focused on situational strength cues from different social sources as antecedents of overall situational strength at work. Specifically, we examined how employees combine situational strength cues emanating from three social sources (i.e., coworkers, the immediate supervisor, and top management). Based on field theory, we hypothesized that the effect of situational strength from coworkers and immediate supervisors (i.e., proximal sources of situational strength) on employees' perceptions of overall situational strength on the job would be greater than the effect of situational strength from the top management (i.e., the distal source of situational strength). We also hypothesized that the effect of situational strength from the distal source would be mediated by the effects of situational strength from the proximal sources. Data from 363 full-time employees were collected at two time points with a cross-lagged panel design. The former hypothesis was supported for one of the two situational strength facets studied. The latter hypothesis was fully supported.

Obesity-related glomerulopathy: pathogenesis, pathologic, clinical characteristics and treatment.

In light of the rapid increase in the number of obesity incidences worldwide, obesity has become an independent risk factor for chronic kidney disease. Obesity-related glomerulopathy (ORG) is characterized by glomerulomegaly in the presence or absence of focal and segmental glomerulosclerosis lesions. IgM and complement 3 (C3) nonspecifically deposit in lesions without immune-complex-type deposits during ORG immunofluorescence. ORG-associated glomerulomegaly and focal and segmental glomerulosclerosis can superimpose on other renal pathologies. The mechanisms under ORG are complex, especially hemodynamic changes, inflammation, oxidative stress, apoptosis, and reduced functioning nephrons. These mechanisms synergize with obesity to induce end-stage renal disease. A slow increase of subnephrotic proteinuria ( < 3.5 g/d) is the most common clinical manifestation of ORG. Several treatment methods for ORG have been developed. Of these methods, renin-angiotensin-aldosterone system blockade and weight loss are proven effective. Targeting mitochondria may offer a novel strategy for ORG therapy. Nevertheless, more research is needed to further understand ORG.

MicroRNA-30b Regulates High Phosphorus Level-Induced Autophagy in Vascular Smooth Muscle Cells by Targeting BECN1.

BACKGROUND/AIMS: Autophagy is an evolutionarily conserved mechanism that affects the survival and functions of vascular smooth muscle cells (VSMCs). We explored the role of microRNAs (miRNAs) in regulating autophagy in VSMCs exposed to high phosphorus (Pi) levels. METHODS: VSMCs were isolated from the thoracic aorta of rats and were cultured primarily. Real-time PCR was used to measure the mRNA expression of indicated genes. Western blotting was performed to detect the protein expression of autophagy-related markers. RESULTS: We found that treatment with high Pi levels (1 and 3 mM) activated LC3II expression and promoted autophagic flux in VSMCs. Conversely, treatment with an autophagy inhibitor decreased LC3II expression. Pi stimulation dysregulated the expression of several miRNAs such as miR-18a, miR-21, miR-23a, miR-30b, and miR-31a. However, miR-30b overexpression decreased Pi-induced expression of autophagy-related marker genes such as BECN1, ATG5, and LC3b, whereas miR-30b downregulation increased Pi-induced expression of these genes. In addition, we found that miR-30b directly targeted BECN1. CONCLUSIONS: These data suggest that miR-30b plays an important role in the regulation of high Pi level-induced autophagy in VSMCs by targeting BECN1.

Activation of the Nrf2-ARE Signaling Pathway Prevents Hyperphosphatemia-Induced Vascular Calcification by Inducing Autophagy in Renal Vascular Smooth Muscle Cells.

This study investigates the effect of nuclear factor erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) signaling pathway in vascular calcification (VC) via inducing Autophagy in renal vascular smooth muscle cells (VSMCs). VSMCs were assigned into six experimental groups: the normal control, high phosphorus, si-negative control (si-NC), Nrf2-siRNA, over-expressed Nrf2, and negative control (NC) groups. RT-PCR was applied to detect the mRNA expressions of the desired Nrf2-ARE signaling pathway-related genes (Nrf2, NQO-1, HO-1, γ-GCS). The protein products of these genes: apoptosis-related genes (LC3I and LC3II), osteogenic marker proetins (Runt-related transcription factor 2) Runx2 and BMP2 were all detected by Western blotting. Autophagosomes in VSMCs were observed under a transmission electron microscope. We discovered an increased calcium ion concentration and upregulated Runx2, BMP2, Nrf2, HO-1, γ-GCS, NQO-1, and LC3II/LC3I expressions in the high phosphorous, si-NC and Nrf2-siRNA, and NC groups, compared with the normal control group. Compared to the high phosphorus and si-NC groups, higher levels of Runx2 and BMP2 but decreased Nrf2, HO-1, γ-GCS, NQO-1, and LC3II/LC3I expressions were detected in the Nrf2-siRNA group. The high phosphorus, si-NC and over-expressed Nrf2 experimental groups all had increased Nrf2, NQO-1, HO-1, γ-GCS, and LC3II/LC3I expressions as well as high numbers of autophagosomes compared with the normal control group. Finally, we detected a lower amount of autophagosomes presence and Nrf2, NQO-1, HO-1 γ-GCS, and LC3II/LC3 protein expression of Nrf2-siRNA group than that of the high phosphorus and si-NC groups. Activation of Nrf2-ARE signaling pathway may prevent hyperphosphatemia-induced VC by inducing autophagy in VSMCs. J. Cell. Biochem. 118: 4708-4715, 2017. © 2017 Wiley Periodicals, Inc.

Analyzing matrices of meta-analytic correlations: current practices and recommendations.

Researchers have become increasingly interested in conducting analyses on meta-analytic correlation matrices. Methodologists have provided guidance and recommended practices for the application of this technique. The purpose of this article is to review current practices regarding analyzing meta-analytic correlation matrices, to identify the gaps between current and best practices, and to offer a comprehensive set of recommendations regarding the planning, collection, analysis, and interpretation of studies that utilize meta-analytic correlation matrices. Copyright © 2016 John Wiley & Sons, Ltd.

The moderating role of attachment anxiety on social network site use intensity and social capital.

This study examined the moderating role of attachment anxiety on the relationship between intensity of social network site use and bridging, bonding, and maintained social capital. Data from 322 undergraduate Chinese students were collected. Hierarchical regression analyses showed positive relationships between online intensity of social network site use and the three types of social capital. Moreover, attachment anxiety moderated the effect of intensity of social network site use on social capital. Specifically, for students with lower attachment anxiety, the relationships between intensity of social network site use and bonding and bridging social capital were stronger than those with higher attachment anxiety. The result suggested that social network sites cannot improve highly anxiously attached individuals' social capital effectively; they may need more face-to-face communications.