Empathy as a Mediator of the Relation between Peer Influence and Prosocial Behavior in Adolescence: A Meta-Analysis.

During adolescence, empathy and prosocial behavior contribute to the establishment of positive interpersonal relationships and social connections, promoting holistic development in youth. A substantial amount of research has provided compelling evidence that there is a relationship between peer relationships and empathy and prosocial behavior. Empathy, as a key mediating factor, links the influence of peers with prosocial behavior in adolescents, yet there is currently a lack of robust meta-analytic evidence regarding this mediating role. This study employed a two-stage structural equation modeling approach to synthesize existing research on peer influence, empathy, and prosocial behavior during adolescence. Systematic searches were conducted across three databases (PubMed, Web of Science, and PsycINFO), identifying a total of 49 studies, with a systematic assessment of study quality. The results indicated that empathy plays a mediating role between peer influence and prosocial behavior. Positive peer influence is positively correlated with empathy and prosocial behavior, while negative peer influence is negatively correlated with empathy and prosocial behavior, and empathy is positively correlated with prosocial behavior. This meta-analysis demonstrates that during adolescence, empathy mediates the connection between peer influence and prosocial behavior, representing a potential process that can explain the relationship between peer influence and prosocial behavior.

Suicide in China: The Trends and Differentials From 2002 to 2021.

OBJECTIVE: The objective of this study was to provide an updated analysis of suicide characteristics in China from 2002 to 2021, with the aim of informing the development of evidence-based suicide prevention strategies. METHODS: The Ministry of Health-Vital Registration System (MOH-VR) provided the data on suicide mortality, which enabled us to examine the average annual percentage change (AAPC) in suicide rates using a Poisson regression model. RESULTS: Notably, there has been a significant decline in suicide rates observed in both urban and rural areas. In the early years of the study period, higher suicide rates were observed among females compared to males; however, a shift occurred after 2005, with male suicide rates surpassing those of females. Except for 2005, rural areas consistently exhibited higher suicide rates than urban areas. Furthermore, suicide rates exhibited an increasing trend with age, irrespective of gender or region. CONCLUSION: These findings highlight a decreasing trend in suicide rates in China over the past two decades, although gender and regional disparities persist. Going forward, sustained efforts in suicide prevention, with a specific focus on mental health, are warranted.

Body mass index and pressure injuries risk in hospitalized adult patients: A dose-response analysis.

BACKGROUND: The association between underweight and pressure injuries (PIs) has been established in several studies. However, there is a lack of well-designed research investigating the connection between overweight and obesity with these injuries. OBJECTIVE: This meta-analysis aims to investigate the dose-response relationship between body mass index (BMI) and the risk of PIs in adult hospitalized patients. METHODS: PubMed, Web of Science, and MEDLINE Databases were searched from inception to May 2024. Observational articles with at least three BMI categories were included in the study. BMI was defined as underweight, normal weight, overweight, and morbid obesity for the meta-analysis. The non-linear relationship between BMI and the risk of PIs in hospitalized adults was investigated using restricted cubic spline models. Fractional polynomial modeling was used. RESULTS: Eleven articles reporting at least 3 categories of BMI met the inclusion criteria, including 31,389 participants. Compared to patients with normal weight, those with underweight, obesity, and morbid obesity exhibited an increased risk of PIs, with odds ratios of 1.70 (95%CI:1.50-1.91), 1.12 (95%CI:1.02-1.24), 1.70 (95%CI:1.13-2.55), respectively. A J-shaped dose-response model was established for the relationship between PI risk and BMI (Pnon-linearity < 0.001, Plinearity = 0.745). CONCLUSION: The J-shaped dose-response pattern revealed that underweight, obesity and morbid obesity heightened the risk of PIs in hospitalized adults. Lower and higher BMI values may signify an increased risk for PIs, particularly among the elderly with lower BMI, providing valuable guidance for medical staff.

CERS6-derived ceramides aggravate kidney fibrosis by inhibiting PINK1-mediated mitophagy in diabetic kidney disease.

During diabetic kidney disease (DKD), ectopic ceramide (CER) accumulation in renal tubular epithelial cells (RTECs) is associated with interstitial fibrosis and albuminuria. As RTECs are primarily responsible for renal energy metabolism, their function is intimately linked to mitochondrial quality control. The role of CER synthesis in the progression of diabetic renal fibrosis has not been thoroughly investigated. In this study, we observed a significant upregulation of ceramide synthase 6 (Cers6) expression in the renal cortex of db/db mice, coinciding with increased production of CER (d18:1/14:0) and CER (d18:1/16:0) by Cer6. Concurrently, the number of damaged mitochondria in RTECs rose. Cers6 deficiency reduced the abnormal accumulation of CER (d18:1/14:0) and CER (d18:1/16:0) in the kidney cortex, restoring the PTEN-induced kinase 1 (PINK1)-mediated mitophagy in RTECs, and resulting in a decrease in damaged mitochondria and attenuation of interstitial fibrosis in DKD. Automated docking analysis suggested that both CER (d18:1/14:0) and CER (d18:1/16:0) could bind to the PINK1 protein. Furthermore, inhibiting PINK1 expression in CERS6 knockdown HK-2 cells diminished the therapeutic effect of CERS6 deficiency on DKD. In summary, CERS6-derived CER (d18:1/14:0) and CER (d18:1/16:0) inhibit PINK1-regulated mitophagy by possibly binding to the PINK1 protein, thereby exacerbating the progression of renal interstitial fibrosis in DKD.NEW & NOTEWORTHY This article addresses the roles of ceramide synthase 6 (CERS6) and CERS6-derived ceramides in renal tubular epithelial cells of diabetic kidney disease (DKD) associated interstitial fibrosis. Results from knockdown of CERS6 adjusted the ceramide pool in kidney cortex and markedly protected from diabetic-induced kidney fibrosis in vivo and in vitro. Mechanically, CERS6-derived ceramides might interact with PINK1 to inhibit PINK1/Parkin-mediated mitophagy and aggravate renal interstitial fibrosis in DKD.

Incidence, prevalence and risk factors of device-related pressure injuries in adult intensive care unit: A meta-analysis of 10,084 patients from 11 countries.

Device-related pressure injuries (DRPIs) prevail in the intensive care unit (ICU) and have much to do with medical devices and patients' conditions. This meta-analysis aims to systematically assess the incidence, prevalence and risk factors related to DRPIs among adults in ICU. Web of Science, Cochrane Library, MEDLINE, PubMed and CINAHL were searched from inception to March 2023. Observational studies were included, and the Newcastle-Ottawa scale (NOS) was used to assess literature quality. The primary outcomes were the incidence, prevalence and risk factors regarding DRPIs among adults in ICU. The 19 studies conformed to the criteria for inclusion in the review. The estimated pooled incidence of DRPIs was 14.7% (95% CI: 9.7%-19.6%) in 10 studies (4866 participants). The estimated pooled prevalence of DRPIs was 19.0% (95% CI: 13.6%-24.3%) in 9 studies (5218 participants). The most significant risk factor for DRPIs was using mechanical ventilation. The pooled analysis of the four studies showed that DRPIs were more likely to occur in patients who required mechanical ventilation compared with patients who did not use mechanical ventilation (OR: 9.67, 95% CI: 5.03-18.61, p < 0.001) and using vasopressors, age, length of ICU stays, APACHE II score, Braden score, fever, sex, oedema, diabetes and number of medical devices, SOFA score was also related to pressure injuries risk. The incidence and prevalence of DRPIs in adult ICU were high, and the most significant risk factor for DRPIs was using mechanical ventilation. It is imminent to identify patients of increased risk with DRPIs early.

Global prevalence of nursing burnout syndrome and temporal trends for the last 10 years: A meta-analysis of 94 studies covering over 30 countries.

AIMS AND OBJECTIVES: To determine the global prevalence of nursing burnout syndrome and time trends for the last 10 years. BACKGROUND: The prevalence of burnout syndrome varied greatly in different regions in the last 10 years, so the average prevalence and time trends of nursing burnout syndrome for the last 10 years were not completely clear. DESIGN: A meta-analysis conducted in the PRISMA guidelines. METHODS: CINAHL, Web of Science, and PubMed were searched for trials on the prevalence of nursing burnout syndrome from 2012 to 2022 systematically. Hoy's quality assessment tool was used to evaluate the risk of bias. The global prevalence of nursing burnout syndrome was estimated, and subgroup analysis was used to explore what caused heterogeneity. Time trends for the last 10 years were evaluated by meta-regression using Stata 11.0. RESULTS: Ninety-four studies reporting the prevalence of nursing burnout were included. The global prevalence of nursing burnout was 30.0% [95% CI: 26.0%-34.0%]. Subgroup analysis indicated that the specialty (p < .001) and the region (p < .001) and the year (p < .001) were sources of the high heterogeneity. Meta-regression indicated that it tended to increase gradually for the last 10 years (t = 3.71, p = .006). The trends increased in Europe (t = 4.23, p = .006), Africa (t = 3.75, p = .006) and obstetrics (t = 3.66, p = .015). However, no statistical significance was found in ICU (t = -.14, p = .893), oncology (t = -0.44, p = .691) and emergency department (t = -0.30, p = .783). CONCLUSIONS: A significant number of nurses were found to have moderate-high levels of burnout syndrome for the last 10 years. The meta-analysis also indicated an increased trend over time. Therefore, more attention to the prevalence of nursing burnout syndrome is urgently required. RELEVANCE TO CLINICAL PRACTICE: High prevalence of nursing burnout may attract more attention from the public. This analysis may serve as an impetus for relevant policy to change nurses' working conditions and reduce the occurrence of burnout.

Tubular epithelial cell-derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF-1α in diabetic kidney disease.

BACKGROUND: Albuminuria is a hallmark of diabetic kidney disease (DKD) that promotes its progression, leading to renal fibrosis. Renal macrophage function is complex and influenced by macrophage metabolic status. However, the metabolic state of diabetic renal macrophages and the impact of albuminuria on the macrophage metabolic state are poorly understood. METHODS: Extracellular vesicles (EVs) from tubular epithelial cells (HK-2) were evaluated using transmission electron microscopy, nanoparticle tracking analysis and western blotting. Glycolytic enzyme expression in macrophages co-cultured with HSA-treated HK-2 cell-derived EVs was detected using RT-qPCR and western blotting. The potential role of EV-associated HIF-1α in the mediation of glycolysis was explored in HIF-1α siRNA pre-transfected macrophages co-cultured with HSA-treated HK-2 cell-derived EVs, and the extent of HIF-1α hydroxylation was measured using western blotting. Additionally, we injected db/db mice with EVs via the caudal vein twice a week for 4 weeks. Renal macrophages were isolated using CD11b microbeads, and immunohistofluorescence was applied to confirm the levels of glycolytic enzymes and HIF-1α in these macrophages. RESULTS: Glycolysis was activated in diabetic renal macrophages after co-culture with HSA-treated HK-2 cells. Moreover, HSA-treated HK-2 cell-derived EVs promoted macrophage glycolysis both in vivo and in vitro. Inhibition of glycolysis activation in macrophages using the glycolysis inhibitor 2-DG decreased the expression of both inflammatory and fibrotic genes. Mechanistically, EVs from HSA-stimulated HK-2 cells were found to accelerate macrophage glycolysis by stabilizing HIF-1α. We also found that several miRNAs and lncRNAs, which have been reported to stabilize HIF-1α expression, were increased in HSA-treated HK-2 cell-derived EVs. CONCLUSION: Our study suggested that albuminuria induced renal macrophage glycolysis through tubular epithelial cell-derived EVs by stabilizing HIF-1α, indicating that regulation of macrophage glycolysis may offer a new treatment strategy for DKD patients, especially those with macroalbuminuria.

The HDAC2/SP1/miR-205 feedback loop contributes to tubular epithelial cell extracellular matrix production in diabetic kidney disease.

Extracellular matrix (ECM) accumulation is considered an important pathological feature of diabetic kidney disease (DKD). Histone deacetylase (HDAC) inhibitors protect against kidney injury. However, the potential mechanisms of HDACs in DKD are still largely unknown. Here, we describe a novel feedback loop composed of HDAC2 and miR-205 that regulates ECM production in tubular epithelial cells in individuals with DKD. We found that HDAC2 mRNA expression in peripheral blood was markedly higher in patients with DKD than in patients with diabetes. Nuclear HDAC2 protein expression was increased in TGFß1-stimulated tubular epithelial cells and db/db mice. We also found that miR-205 was regulated by HDAC2 and down-regulated in TGFß1-treated HK2 cells and db/db mice. In addition, HDAC2 reduced histone H3K9 acetylation in the miR-205 promoter region to inhibit its promoter activity and subsequently suppressed miR-205 expression through an SP1-mediated pathway. Furthermore, miR-205 directly targeted HDAC2 and inhibited HDAC2 expression. Intriguingly, miR-205 also regulated its own transcription by inhibiting HDAC2 and increasing histone H3K9 acetylation in its promoter, forming a feedback regulatory loop. Additionally, the miR-205 agonist attenuated ECM production in HK2 cells and renal interstitial fibrosis in db/db mice. In conclusion, the HDAC2/SP1/miR-205 feedback loop may be crucial for the pathogenesis of DKD.

Albumin-induced premature senescence in human renal proximal tubular cells and its relationship with intercellular fibrosis.

The presence of senescent cells is associated with renal fibrosis. This study aims to investigate the effect of albumin-induced premature senescence on tubulointerstitial fibrosis and its possible mechanism in vitro. Different concentrations of bovine serum albumim (BSA) with or without si-p21 are used to stimulate HK-2 cells for 72 h, and SA-ß-gal activity, senescence-associated secretory phenotypes (SASPs), LaminB1 are used as markers of senescence. Immunofluorescence staining is performed to characterize the G2/M phase arrest between the control and BSA groups. Alterations in the DNA damage marker γ-H2AX, fibrogenesis, and associated proteins at the G2/M phase, such as p21, p-CDC25C and p-CDK1, are evaluated. Compared with those in the control group, the SA-ß-gal activity, SASP, and γ-H2AX levels are increased in the BSA group, while the level of LaminB1 is decreased. Meanwhile, HK-2 cells blocked at the G2/M phase are significantly increased under the stimulation of BSA, and the levels of p21, p-CDC25C and p-CDK1, as well as fibrogenesis are also increased. When p21 expression is inhibited, the levels of p-CDC25C and p-CDK1 are decreased and the G2/M phase arrest is improved, which decreases the production of fibrogenesis. In conclusion, BSA induces renal tubular epithelial cell premature senescence, which regulates the G2/M phase through the CDC25C/CDK1 pathway, leading to tubulointerstitial fibrosis.

Extracellular Vesicles from Albumin-Induced Tubular Epithelial Cells Promote the M1 Macrophage Phenotype by Targeting Klotho.

Albumin absorbed by renal tubular epithelial cells induces inflammation and plays a key role in promoting diabetic kidney disease (DKD) progression. Macrophages are prominent inflammatory cells in the kidney, and their role there is dependent on their phenotypes. However, whether albuminuria influences macrophage phenotypes and underlying mechanisms during the development of DKD is still unclear. We found that M1 macrophage-related markers were increased in diabetes mellitus (DM) mouse renal tissues with the development of DKD, and coculture of extracellular vesicles (EVs) from human serum albumin (HSA)-induced HK-2 cells with macrophages induced macrophage M1 polarization in the presence of lipopolysaccharide (LPS). Through a bioinformatic analysis, miR-199a-5p was selected and found to be increased in EVs from HSA-induced HK-2 cells and in urinary EVs from DM patients with macroalbuminuria. Tail-vein injection of DM mice with EVs from HSA-induced HK-2 cells induced kidney macrophage M1 polarization and accelerated the progression of DKD through miR-199a-5p. miR-199a-5p exerted its effect by targeting Klotho, and Klotho induced macrophage M2 polarization through the Toll-like receptor 4 (TLR4) pathway both in vivo and in vitro. In summary, miR-199a-5p from HSA-stimulated HK-2 cell-derived EVs induces M1 polarization by targeting the Klotho/TLR4 pathway and further accelerates the progression of DKD.

Early growth response protein-1 upregulates long noncoding RNA Arid2-IR to promote extracellular matrix production in diabetic kidney disease.

Diabetic kidney disease (DKD) has surpassed chronic glomerulonephritis as the leading cause of end-stage renal disease. Previously, we showed that early growth response protein-1 (Egr1) plays a key role in DKD by enhancing mesangial cell proliferation and extracellular matrix (ECM) production. The long noncoding RNA (lncRNA) AT-rich interactive domain 2-IR (Arid2-IR) has been identified as a mothers against decapentaplegic homolog 3 (Smad3)-associated lncRNA in unilateral ureteral obstructive kidney disease. However, the effect of Egr1 on Arid2-IR in the development of DKD is still unknown. In this study, we found that Arid2-IR was increased in mice with high-fat diet and streptozotocin-induced type 2 diabetes and in mouse mesangial cells cultured with high glucose to mimic diabetes. Knockdown of Arid2-IR in mouse mesangial cells reduced the high expression levels of collagen-α1(I) (Col1a1) and α-smooth muscle actin (α-SMA) induced by high glucose. Furthermore, Arid2-IR expression changed the increased expression of Col1a1 and α-SMA caused by overexpression of Egr1. Overall, these data suggest that increased Arid2-IR likely contributes to ECM production in DKD and that Egr1 promotes ECM production in DKD partly by upregulating Arid2-IR. Thus, Arid2-IR may be a new target in the treatment of DKD.

MiR-4756 promotes albumin-induced renal tubular epithelial cell epithelial-to-mesenchymal transition and endoplasmic reticulum stress via targeting Sestrin2.

Accumulating evidence indicates that proteinuria promotes the progression of diabetic kidney disease (DKD) and induces renal epithelial tubular cell epithelial-to-mesenchymal transition (EMT) and endoplasmic reticulum (ER) stress, but the mechanism remains unclear. In our previous research, we found that miR-4756 levels were increased in the urinary extracellular vesicles of type 2 diabetes mellitus patients with macroalbuminuria. In a preliminary study, we found that miR-4756 may be derived from renal tubular epithelial cells, but its role has not been elucidated. Albumin stimulation significantly increased miR-4756 levels in HK-2 cells. In addition, an miR-4756 mimic accelerated albumin-stimulated HK-2 cell EMT and ER stress, and an miR-4756 inhibitor suppressed these events. We then found that miR-4756 targeted the 3'-untranslated region (UTR) of Sestrin2 and directly suppressed Sestrin2 expression. Furthermore, the induction of EMT and ER stress by the overexpression of miR-4756 was abolished by Sestrin2 overexpression. Moreover, the overexpression of miR-4756 increased ERK1/2 activation and decreased 5' monophosphate-activated protein kinase activation. Thus, our study provides evidence that miR-4756 accelerates the process of DKD through Sestrin2, suggesting that targeting miR-4756 may be a novel strategy for DKD treatment.

High glucose up-regulates microRNA-34a-5p to aggravate fibrosis by targeting SIRT1 in HK-2 cells.

Tubulointerstitial fibrosis (TIF) is crucial in the development of renal fibrosis in diabetic nephropathy(DN). Previous data shows that SIRT1 plays an important role on fibrosis, but the effect on TIF in DN and underlying mechanisms remains uncertain. In this study, we evaluated the vital role of SIRT1 and identified SIRT1 as a downstream target gene of microRNA-34a-5p (miR-34a-5p) in TIF of DN. The result revealed that expression of miR-34a-5p, fibronectin(FN),collagen type I (COL1) and transforming growth factor ß1 (TGF-ß1) were up-regulated accompanied by the corresponding down-regulation of SIRT1 in renal tissues of high fat diet and streptozotocin(HFD/STZ)induced diabetic mice with DN, and that the SIRT1 mRNA level was negatively correlated with miR-34a-5p expression in high glucose stimulated human proximal tubule cell line(HK-2) cells. We then demonstrated that overexpression of SIRT1 reduced, whereas small interfering RNA targeting SIRT1 enhanced the expressions of TGF-ß1 and fibrosis-related genes including FN and COL1 in HK-2 cells. Furthermore, we identified that miR-34a-5p directly suppressed SIRT1 to increase the profibrogenic effects of TGFß1 through targeting the 3'untranslated region of SIRT1. The functional correlation of miR-34a-5p induced SIRT1 decrease was supported by overexpression and inhibition of miR-34a-5p in HK-2 cells. All the results reveal that SIRT1 which is vital in the evolution of renal TIF in DN can be directly suppressed by miR-34a-5p, and suggest that miR-34a-5p is a new target for DN treatment.

Role of p53/miR-155-5p/sirt1 loop in renal tubular injury of diabetic kidney disease.

BACKGROUND: Diabetic kidney disease is a renal microvascular disease caused by diabetes, known as one of the most serious and lethal complications of diabetes. Early renal hypertrophy is the main pathological feature, which gradually leads to the deposition of glomerular extracellular matrix and tubulointerstitial fibrosis, eventually developing irreversible structural damage to the kidneys. Autophagy is a cell self-homeostatic mechanism that is activated under stress conditions and may serve as a protective response to the survival of renal fibrogenic cells. MicroRNA (miRNA) network may be involved in the regulation of fibrosis. The purpose of this study is to assess how miRNAs regulate diabetic kidney disease and autophagy and fibrosis in renal proximal tubular cells under high glucose conditions. METHODS: Human renal proximal tubular (HK-2) cells were exposed to high glucose in vitro. Bioinformatic analysis was used to select the candidate gene for potential target regulation of miR-155, Sirt1. ATG5, ATG7 is the key to autophagosome formation, regulated by Sirt1. p53 regulates miR-155 expression as a transcription factor. MiR-155 overexpression and inhibition were achieved by transfection of miR-155 mimic and inhibit to evaluate its effect on Sirt1 and autophagy and fibrosis markers. Dual luciferase reporter assays were used to confirm the direct interaction of Sirt1 with miR-155. Overexpression and inhibition of Sirt1 gene were achieved by transfection of Sirt1 plasmid and Sirt1 si to observe its effect on P53. Chip assay experiments confirmed the direct regulation of P53 on miR-155. RESULTS: Under high glucose conditions, miR-155 was detected in HK-2 cells in concentration gradient, increased expression of p53 and down-regulated expression of sirt1 and autophagy-associated proteins LC3II, ATG5 and ATG7. Dual luciferase reporter assays indicate that miR-155 can target its binding to the Sirt1 3'UTR region to reduce its expression. Under high glucose conditions, over expression of miR-155 decreased the expression of LC3-II and ATG5 in HK-2 cells, while inhibition of miR-155 reversed this effect. Using chip assay testing in HK-2 cells, we demonstrated that p53 binds directly to miR-155. CONCLUSIONS: The signaling axis of p53, miR-155-5p, and sirt1 in autophagic process might be a critical adapting mechanism for diabetic kidney injury.

Klotho down-regulates Egr-1 by inhibiting TGF-ß1/Smad3 signaling in high glucose treated human mesangial cells.

Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease worldwide and is associated with glomerular mesangial cell (MC) proliferation and excessive extracellular matrix (ECM) production. Klotho can attenuate renal fibrosis in part by inhibiting TGF-ß1/Smad3 signaling in DKD. Early growth response factor 1 (Egr-1) has been shown to play a key role in renal fibrosis in part by facilitating the formation of a positive feedback loop involving TGF-ß1. However, whether Klotho down-regulates Egr-1 by inhibiting TGF-ß1/Smad3 signaling in DKD is unclear. In the present study, we assessed human MCs that were incubated under high-glucose conditions to mimic diabetes. Then, we transfected the cells with Klotho plasmid or siRNA to overexpress or knock down Klotho gene and protein expression. Klotho, Egr-1, fibronectin (FN), collagen type I (Col I), Smad3 and phosphorylated Smad3 (p-Smad3) gene and protein expression levels were determined by RT-qPCR and western blotting respectively. High glucose time-dependently down-regulated Klotho mRNA and protein expression in cultured human MCs. pcDNA3.1-Klotho transfection-mediated Klotho overexpression down-regulated Egr-1, FN and Col I expression and the p-Smad3/Smad3 ratio in human MCs. Conversely, siRNA-mediated Klotho silencing up-regulated Egr-1, FN, and Col I expression and the p-Smad3/Smad3 ratio. Moreover, the effects of si-Klotho on Egr-1 expression were abolished by the TGF-ß1 inhibitor SB-431542. Klotho overexpression can prevent mesangial ECM production in high-glucose-treated human MCs, an effect that has been partially attributed to Egr-1 down-regulation facilitated by TGF-ß1/Smad3 signaling inhibition.

Efficacy of recombinant human epidermal growth factor in pressure injury healing: evidence from Chinese randomized controlled trials.

OBJECTIVE: To evaluate the efficacy of recombinant human epidermal growth factor (rhEGF) in healing pressure injuries (PIs). METHODS: A meta-analysis was conducted of randomized controlled trials (RCTs) involving rhEGF in the treatment of PIs that were identified in PubMed, Web of Science, the Cochrane Library, and China National Knowledge Infrastructure (CNKI). The population, intervention, comparison, outcomes, study design (PICOS) strategy was applied to determine analysis eligibility. The Cochrane risk of bias tool was used, and statistical analysis, including sensitivity analysis, was performed of 3 outcomes indicators: the primary outcome was total efficacy of rhEGF in treating PIs, and the secondary outcomes were the proportion of complete healing and the time to complete healing. Total efficacy refers to the proportion of cases that have been cured, obviously effective, or effective. Complete healing refers to cases where the wound has healed, scabbed, and the scab has sloughed off. RESULTS: Sixteen RCTs were included, comprising a total of 1,206 patients. Study and control group size varied by outcomes. The total effective healing rate in rhEGF group was 97.18%, which was significantly higher than 83.38% in control group (OR: 5.69, [95% CI: 3.61, 8.97], z=7.49, P < .001). The proportion of complete healing in the rhEGF group was 73.30%, which was higher than 39.52% in control group (OR: 3.88, [95% CI: 3.01, 5.01], z=10.39, P < .001). Furthermore, the healing time using rhEGF was shorter (SMD: -2.14 days, [95% CI: -2.60, -1.67], z=9.07, P < .001). Sensitivity analyses indicated that the results were robust. CONCLUSIONS: The meta-analysis indicated that rhEGF was effective in healing PIs with few negative effects. Further research beyond Chinese populations involving larger studies and studies that distinguish between results found in using rhEGF alone or in combination are recommended.

ncStem: a comprehensive resource of curated and predicted ncRNAs in cancer stemness.

Cancer stemness plays an important role in cancer initiation and progression, and is the major cause of tumor invasion, metastasis, recurrence, and poor prognosis. Non-coding RNAs (ncRNAs) are a class of RNA transcripts that generally cannot encode proteins and have been demonstrated to play a critical role in regulating cancer stemness. Here, we developed the ncStem database to record manually curated and predicted ncRNAs associated with cancer stemness. In total, ncStem contains 645 experimentally verified entries, including 159 long non-coding RNAs (lncRNAs), 254 microRNAs (miRNAs), 39 circular RNAs (circRNAs), and 5 other ncRNAs. The detailed information of each entry includes the ncRNA name, ncRNA identifier, disease, reference, expression direction, tissue, species, and so on. In addition, ncStem also provides computationally predicted cancer stemness-associated ncRNAs for 33 TCGA cancers, which were prioritized using the random walk with restart (RWR) algorithm based on regulatory and co-expression networks. The total predicted cancer stemness-associated ncRNAs included 11 132 lncRNAs and 972 miRNAs. Moreover, ncStem provides tools for functional enrichment analysis, survival analysis, and cell location interrogation for cancer stemness-associated ncRNAs. In summary, ncStem provides a platform to retrieve cancer stemness-associated ncRNAs, which may facilitate research on cancer stemness and offer potential targets for cancer treatment. Database URL: http://www.nidmarker-db.cn/ncStem/index.html.

COVID-19 impacted the suicidal ideation among health care workers and medical students: An interrupted time-series analysis of data from 30 countries.

AIM: To investigate the impact of public health emergencies on the prevalence of suicidal ideation among healthcare workers (HCWs) and medical students. METHODS: The prevalence of suicidal ideation among HCWs and medical students was searched for analysis. The platforms included PubMed, medRVix, bioRvix, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and Web of Science. Interrupted time-series analysis was employed to determine whether the COVID-19 pandemic influenced the prevalence and trends of suicidal ideation. To account for autocorrelation and heteroskedasticity, Newey-West standard errors were utilized with a lag of order one. RESULTS: Seventy studies with 145,641 HCWs and medical students from 30 countries were included in the final analysis, with 30 studies before COVID-19 and 40 studies during the pandemic. Before the pandemic outbreak (April 2020), the monthly increasing rate was 0.063 % (95 % CI: -0.009 %, 0.135 %, z = 1.73, P = 0.084). The tendency of suicidal ideation prevalence increased by 1.116 % (95%CI: 0.888 %, 1.344 %, z = 9.60, P < 0.001). In other words, the calculated monthly growth rate of suicidal ideation after the pandemic outbreak is 1.179 % (95%CI: 0.968 %, 1.391 %, z = 10.93, P < 0.001) per month. The overall growing trend of prevalence of suicidal ideation during the pandemic is 1.896 % per month in America; 1.590 % in Europe; 0.443 % (95%CI: 0.213 %, 0.673 %, z = 3.77, P < 0.001) in Asia; 1.055 % in HCWs; and 0.645 % in medical students. CONCLUSION: This study highlights that the COVID-19 pandemic can significantly impact the prevalence of suicidal ideation among HCWs and medical students, and the prevalence showed an upward trend.

Frailty and all-cause and cancer-related mortality in cancer patients: A prospective cohort study.

PURPOSE: To evaluate the associations between frailty and all-cause and cancer-related mortality. Additionally, the objective is to compare the magnitude of these associations between older adults and younger adults. METHODS: We gathered baseline data from NHANES (1999-2018) and developed a cumulative index consisting of 39 items to evaluate frailty. The National Death Index database was utilized to track the survival status of individuals. The Cox regression model was employed to estimate the associations between frailty status and all-cause and cancer-related mortality. RESULTS: Ultimately, 3398 cancer patients were included in the analysis, comprising 910 younger adults and 2488 older adults. Compared to non-frail patients, the elevated all-cause and cancer-related mortality among pre-frail patients was not statistically significant (HRs = 1.312, 95%CI: 0.956-1.800, P = 0.092; HRs = 1.462, 0.811-2.635, P = 0.207). However, a significant elevation of both all-cause and cancer-related mortality risk was observed among frail patients (HRs = 2.213, 1.617-3.030, P < 0.001; HRs = 2.463, 95%CI = 1.370-4.429, P = 0.003). Frailty individuals demonstrated a more pronounced association with the prediction of all-cause mortality in younger (HRs = 2.230, 1.073-4.634, P = 0.032) than in older adults (HRs = 2.090, 1.475-2.960, P < 0.001). Sensitivity analysis consistently revealed robust results. RCS plots suggested a progressively escalating dose-response correlation between frailty and both all-cause and cancer-related mortality risk. CONCLUSIONS: Pre-frailty did not result in an increase in mortality risks compared to non-frailty. However, frailty caused a higher all-cause and cancer-related mortality risk than non-frailty. Identifying those at risk and implementing targeted interventions may contribute to extending healthy life expectancy, regardless of age.