Advances in Label-Free Glucose Detection Using Self-Assembled Nanoparticles and Surface-Enhanced Raman Spectroscopy.

In the landscape of biomolecular detection, surface-enhanced Raman spectroscopy (SERS) confronts notable obstacles, particularly in the label-free detection of biomolecules, with glucose and other sugars presenting a quintessential challenge. This study heralds the development of a pioneering SERS substrate, ingeniously engineered through the self-assembly of nanoparticles of diverse sizes (Ag1@Ag2NPs). This configuration strategically induces 'hot spots' within the interstices of nanoparticles, markedly amplifying the detection signal. Rigorous experimental investigations affirm the platform's rapidity, precision, and reproducibility, and the detection limit of this detection method is calculated to be 6.62 pM. Crucially, this methodology facilitates nondestructive glucose detection in simulated samples, including phosphate-buffered saline and urine. Integrating machine learning algorithms with simulated serum samples, the approach adeptly discriminates between hypoglycemic, normoglycemic, and hyperglycemic states. Moreover, the platform's versatility extends to the detection and differentiation of monosaccharides, disaccharides, and methylated glycosides, underscoring its universality and specificity. Comparative Raman spectroscopic analysis of various carbohydrate structures elucidates the unique SERS characteristics pertinent to these molecules. This research signifies a major advance in nonchemical, label-free glucose determination with enhanced sensitivity via SERS, laying a new foundation for its application in precision medicine and advancing structural analysis in the sugar domain.

Autoimmune diseases: targets, biology, and drug discovery.

Autoimmune diseases (AIDs) arise from a breakdown in immunological self-tolerance, wherein the adaptive immune system mistakenly attacks healthy cells, tissues and organs. AIDs impose excessive treatment costs and currently rely on non-specific and universal immunosuppression, which only offer symptomatic relief without addressing the underlying causes. AIDs are driven by autoantigens, targeting the autoantigens holds great promise in transforming the treatment of these diseases. To achieve this goal, a comprehensive understanding of the pathogenic mechanisms underlying different AIDs and the identification of specific autoantigens are critical. In this review, we categorize AIDs based on their underlying causes and compile information on autoantigens implicated in each disease, providing a roadmap for the development of novel immunotherapy regimens. We will focus on type 1 diabetes (T1D), which is an autoimmune disease characterized by irreversible destruction of insulin-producing ß cells in the Langerhans islets of the pancreas. We will discuss insulin as possible autoantigen of T1D and its role in T1D pathogenesis. Finally, we will review current treatments of TID and propose a potentially effective immunotherapy targeting autoantigens.

A breakthrough in phytochemical profiling: ultra-sensitive surface-enhanced Raman spectroscopy platform for detecting bioactive components in medicinal and edible plants.

A perennial challenge in harnessing the rich biological activity of medicinal and edible plants is the accurate identification and sensitive detection of their active compounds. In this study, an innovative, ultra-sensitive detection platform for plant chemical profiling is created using surface-enhanced Raman spectroscopy (SERS) technology. The platform uses silver nanoparticles as the enhancing substrate, excess sodium borohydride prevents substrate oxidation, and methanol enables the tested molecules to be better adsorbed onto the silver nanoparticles. Subsequently, nanoparticle aggregation to form stable "hot spots" is induced by Ca2+, and the Raman signal of the target molecule is strongly enhanced. At the same time, deuterated methanol was used as the internal standard for quantitative determination. The method has excellent reproducibility, RSD ≤ 1.79%, and the enhancement factor of this method for the detection of active ingredients in the medicinal plant Coptis chinensis was 1.24 × 109, with detection limits as low as 3 fM. The platform successfully compared the alkaloid distribution in different parts of Coptis chinensis: root > leaf > stem, and the difference in content between different batches of Coptis chinensis decoction was successfully evaluated. The analytical technology adopted by the platform can speed up the determination of Coptis chinensis and reduce the cost of analysis, not only making better use of these valuable resources but also promoting development and innovation in the food and pharmaceutical industries. This study provides a new method for the development, evaluation, and comprehensive utilization of both medicinal and edible plants. It is expected that this method will be extended to the modern rapid detection of other medicinal and edible plants and will provide technical support for the vigorous development of the medicinal and edible plants industry.

Exploration of Polysaccharides from Phyllanthus emblica: Isolation, Identification, and Evaluation of Antioxidant and Anti-Glycolipid Metabolism Disorder Activities.

Phyllanthus emblica is a natural medicinal herb with diverse bioactivities. Certain extracts from this herb have been confirmed to possess anti-glycolipid metabolic disorder activity. To further develop its utility value and explore its potential in combating glycolipid metabolic disorders, we designed a series of experiments to investigate the structure, antioxidant activity, and anti-glycolipid metabolic disorder activity of Phyllanthus emblica polysaccharides. In this study, we extracted and purified polysaccharides from Phyllanthus emblica and thoroughly analyzed their structure using various techniques, including NMR, methylation analysis, and surface-enhanced Raman spectroscopy. We investigated the hypolipidemic and anti-glycolipid metabolism disorder activity of Phyllanthus emblica polysaccharides for the first time utilizing oleic acid (OA) and advanced glycation end products (AGEs) as inducers. Additionally, the antioxidant activity of Phyllanthus emblica polysaccharides was assessed in vitro. These findings lay the groundwork for future investigations into the potential application of Phyllanthus emblica polysaccharides as an intervention for preventing and treating diabetes.

Silencing long non-coding RNA SNHG3 repairs the dysfunction of pulmonary microvascular endothelial barrier by regulating miR-186-5p/Wnt axis.

Barrier permeability changes of human pulmonary microvascular endothelial cells (HPMVECs) are important in sepsis-related acute lung injury (ALI) pathogenesis. Long non-coding small nucleolar RNA host gene 3 (SNHG3) mediates the cell-biological phenotype of lung cancer cells and affects the progression of lung cancer, but its role in regulating functions of lung non-malignant cells is still rarely reported. Therefore, we evaluated the regulatory effect of SNHG3 on the function of PMVECs in sepsis-related ALI. Small interference RNA (siRNA)-mediated deletion of SNHG3 promoted the proliferation of PMVECs, reduced apoptosis and barrier permeability, and increased the expression of tight junction proteins claudin-5 and ZO-1. Knockdown of SNHG3 increased the miR-186-5p expression, while overexpression of SNHG3 upregulated the level of wnt5a. Through a dual luciferase reporter assay, we confirmed the binding between SNHG3 and miR-186-5p, miR-186-5p and wnt5a. We further found that knockout of miR-186-5p could inhibit cell proliferation, increase apoptosis and barrier permeability, and down-regulate claudin-5 and ZO-1. Importantly, silencing miR-186-5p and activating Wnt signal pathway could eliminate the barrier repair effect caused by down-regulation of SNHG3. To sum up, our results suggested that knockdown of long non-coding RNA SNHG3 repaired the dysfunction of pulmonary microvascular endothelial barrier through the miR-186-5p/Wnt axis.

The association between financial support of adult children to their parents and informal care provision in China and its differences in household registration, residence arrangement and community-based care services: 2008 ~ 2018.

BACKGROUND: The changes in demographic and family structures have weakened the traditional norms of filial piety and intergenerational relationships dramatically. This study aims to examine the dynamic association between financial support of adult children to their parents and informal care provision in China and its differences in household registration, residence arrangement and community-based care services. METHODS: Data was derived from the 2008-2018 Chinese Longitudinal Healthy Longevity Survey (CLHLS), which is a longitudinal survey of a nationally representative sample of individuals aged 60 and over. Random effects model was used to assess the association between financial support and informal care provision of adult children to their parents. RESULTS: It was found that financial support showed an upward trend while informal care provision showed a download trend from 2008 to 2018. The result indicated a significant and negative association between financial support and informal care provision of adult children to their parents (B = -0.500, 95% confidence interval (CI) = -0.761 to -0.239). And the association was significant among elderly people who were from urban areas (B = -0.628, 95% CI = -0.970 to -0.287), co-resided with adult children (B = -0.596, 95% CI = -0.939 to -0.253), and had community-based services (B = -0.659, 95% CI = -1.004 to -0.315). CONCLUSION: Financial support was negatively associated with informal care provision of adult children to their parents in China, and the association has differences in household registration, residence arrangement and community-based care services. It is suggested that policymakers should prioritize planning interventions for elderly care services and establish a family caregiver support system.

Development and validation of a Cancer Patient Suicidal Ideation Scale.

Aim: To develop a Cancer Patient Suicidal Ideation Scale (CAPASIS) and test its reliability and validity. Patients & methods: An initial CAPASIS was developed. Clinical assessment was conducted using an adjusted initial scale with 239 cancer patients for item reduction and 253 for scale validation. Results: Item selection analyses resulted in 22 items. The revised model fits were acceptable (normal chi-square [χ2/df] = 1.919; standardized root mean residual  = 0.057; root mean square error of approximation = 0.060; goodness fit index = 0.882; adjusted goodness fit index [AGFI] = 0.844; Tucker-Lewis index = 0.898; comparative fit index  = 0.915; incremental fit index  = 0.917). The Cronbach's alpha coefficient was 0.911. Conclusion: The CAPASIS has good validity and reliability, with a six-factor structure of 'entrapment', 'defeat', 'isolation', 'hopelessness', 'burdensomeness' and 'humiliation', which can help identify patients with suicidal ideation.

ESR1 mediated circ_0004018 suppresses angiogenesis in hepatocellular carcinoma via recruiting FUS and stabilizing TIMP2 expression.

Angiogenesis has been certified to account for tumor pathobiology. Circular RNAs (circRNAs) have been demonstrated to be involved in angiogenesis-related diseases, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory roles of most circRNAs remain obscure. This study aims to uncover the function of hsa_circ_0004018 on angiogenesis in HCC. Firstly, quantitative real-time RT-PCR (RT-qPCR) analyzed that circ_0004018 was definitely down-regulated in HCC. Western blot analysis was conducted to detect the protein level of fused protein in sarcoma (FUS) and TIMP metallopeptidase inhibitor 2 (TIMP2). Functional assays were carried out to assess the impacts of circ_0004018 on HCC. From the experimental results, we found that overexpression of circ_0004018 significantly inhibited angiogenesis in HCC. The regulatory mechanism of circ_0004018 in HCC was determined by chromatin immunoprecipitation (ChIP), luciferase reporter assays and RNA immunoprecipitation (RIP) assay. Therefore, we proved that estrogen receptor 1 (ESR1) mediated circ_0004018 regulated TIMP2 by recruiting FUS. A series of rescue assays verified that circ_0004018 participated in angiogenesis in HCC via modulating TIMP2. In summary, this paper disclosed that ESR1 activated circ_0004018 inhibited angiogenesis in HCC via binding to FUS and stabilizing TIMP2 expression.

Longitudinal associations between sleep duration and cognitive function in the elderly population in China: A 10-year follow-up study from 2005 to 2014.

OBJECTIVE: Sleep duration is increasingly recognized as an important determinant of cognitive function among elderly. However, longitudinal studies on the relationship between sleep duration and cognitive function in Chinese elderly are rare. We sought to investigate the longitudinal association between sleep duration and cognitive function in Chinese elderly during a 10-year follow-up. METHOD: This longitudinal study analyzed 2148 elderly (the baseline including 43.16% aged 70%-79%, 23.79% aged 80 and over) who had participated in four waves of the Chinese Longitudinal Healthy Longevity Survey during 2005-2014. Cognitive function (including global functioning and cognitive domains) was assessed using the Chinese version of the Mini-Mental State Examination. Sleep duration was assessed via self-reports. Mixed model analysis was used to evaluate the association between sleep duration and cognitive function, adjusting for sociodemographic variables and risk factors for cognitive function. RESULTS: There is an inverted U-shaped relationship between sleep duration and global cognition and cognitive domains, with the highest cognitive scores observed for sleep durations between 6 and 9 h and the curve shifting from smooth to steeper from 2005 to 2014. The regression model showed that long sleep duration (>9 h) is significantly associated with global cognition and four cognitive domains: orientation, attention and calculation, immediate recall and visual construction. Both long and short sleep durations are significantly associated with delayed recall and not significantly associated with category fluency, language or the ability to follow a three-stage command. The five cognitive domains related to sleep duration are the domains that exhibited a rapid rate of decline. CONCLUSIONS: Sleep duration can be identified as a modifiable risk factor for cognitive decline, as long or short sleep duration is associated with the five cognitive domains that exhibit cognitive decline. These findings suggest the need for intervention measures to maintain healthy sleep durations among Chinese elderly people.

Synthesis of New Lathyrane Diterpenoid Derivatives from Euphorbia lathyris and Evaluation of Their Anti-Inflammatory Activities.

Euphorbia factor L3 , a lathyrane diterpenoid extracted from Euphorbia lathyris, was found to display good anti-inflammatory activity with very low cytotoxicity. To find more potent anti-inflammatory drugs, two series of Euphorbia factor L3 derivatives with fatty and aromatic acids were designed and synthesized. Among them, lathyrane derivative 5n exhibited most potent inhibition on LPS-induced NO production in RAW264.7 cells with no obvious cytotoxicity. To determine the key characteristics of Euphorbia factor L3 derivatives that contribute to anti-inflammatory activity, we conducted a structure-activity relationship study of these compounds.

Anti-inflammatory Lathyrane Diterpenoids from Euphorbia lathyris.

Six new lathyrane diterpenoids (1-6) and 10 known analogues (7-16), were separated from the seeds of Euphorbia lathyris. The absolute configuration of 1 was determined by X-ray crystallography, and the C-2' configuration of 5 was elucidated by comparing experimental and calculated ECD data. These compounds were studied for their inhibition against nitric oxide (NO) generation induced by lipopolysaccharide in RAW264.7 macrophage cells. Compounds 1-3, 7, 9, 11, 13, 14, and 16 displayed inhibitory effects on NO production, with IC50 values of 2.6-26.0 µM. The new compound 1 (IC50 3.0 ± 1.1 µM), with no obvious cytotoxicity, was selected for further experiments. The production of cytokines such as IL-6 and IL-1ß, as well as the protein expression of iNOS, NF-κB, and phosphorylated IκBα, was reduced by 1 dose-dependently. These results suggested that lathyrane diterpenoids may be used as potential anti-inflammatory agents and are worth being further researched.

HBD Inhibits the Development of Colitis-Associated Cancer in Mice via the IL-6R/STAT3 Signaling Pathway.

Colitis-associated cancer (CAC) is a malignant disease of the colon that is caused by recurrent episodes of chronic intestinal inflammation. Huangqi Baizhu decoction (HBD) is a classic prescription comprised of Radix Astragali and Rhizoma Atractylodis, which are usually used to treat digestive conditions, such as peptic ulcers, colitis, or colorectal carcinoma in clinics. HBD is well known for "tonifying qi and spleen" based on the theories of traditional Chinese medicine, and has the preponderant effect of alleviating chronic intestinal mucosa damage associated with disease. However, the underlying mechanism behind this is still unknown. In the current study, we employed the AOM/DSS mouse model to analyze the effects of HBD on the development of inflammation in colonic carcinoma. The in vivo study showed that HBD could significantly reduce the mortality of mice and control the incidence and size of colonic tumors by inhibiting the IL-6/STAT3 signaling pathway. In vitro, Astragaloside and Atractylenolide (CAA), the main components of HBD, inhibited the proliferation of HCT-116 cells as determined by an MTT assay. Furthermore, CAA notably suppressed the protein expression of IL-6R, STAT3, Survivin, and Cyclin D1 induced by IL-6 in HCT-116 and RAW264.7 cells. These results suggested that HBD exhibits anti-inflammatory and anti-proliferative effects, inhibiting the development of CAC in mice.

Association of APOE Gene Polymorphisms with Cerebral Infarction in the Chinese Population.

BACKGROUND Apolipoprotein E (ApoE) is a multifunctional protein that plays an important role in lipoprotein metabolism. However, the relationship between APOE gene polymorphisms and cerebral infarction in the Chinese population remains unclear. Therefore, we studied the role of APOE gene polymorphisms in patients with cerebral infarction in a Chinese population. MATERIAL AND METHODS This study involved 906 patients with cerebral infarction and 1,141 individuals without cerebral infarction who served as controls. APOE genotypes were identified in all participants who participated in the study. Factors influencing cerebral infarction were also analyzed. RESULTS Statistically significant variances in the distribution and frequencies of the APOE genotypes in the patients were observed (ε2/ε3 versus ε2/ε4 versus ε3/ε3=22.85% versus 7.62% versus 56.95%) and controls (ε2/ε3 versus ε2/ε4 versus ε3/ε3=17.27% versus 2.72% versus 66.87%; p<0.001). Univariate analysis showed that the APOE ε3/ε3 genotype [OR, 0.393 (95% CI, 0.237-0.653); p<0.001] and ε3/ε4 genotype [OR, 0.376 (95% CI 0.221-0.637); p<0.001] played a protective role against cerebral infarction in Chinese men. CONCLUSIONS Statistically significant variances in the distribution and frequencies of the APOE genotypes of the patients and controls were observed. The study demonstrated that the APOE ε3/ε3 and ε3/ε4 genotypes played a protective role against cerebral infarction in Chinese men, but not women. Additionally, the ε2/ε4 genotype may be a potential risk factor in men, whereas ε3/ε4 genotype may play a potential protective role against this disease in women.

Sub-chronic 90-day toxicity of neamine in SD rats and its anti-liver cancer activity in vitro and in vivo.

Neamine, an inhibitor of angiogenin (ANG), is a new investigative anticancer drug currently in preclinical stage. Here we report the 90-day sub-chronic toxicity of neamine in SD rats and its anti-liver cancer activity in vitro and in vivo. Neamine has a No Observed Adverse Effect Level (NOAEL) of 12 and 16mg·kg-1·d-1 for female and male rats, respectively. No mortality was found. The adverse effects included increased organ coefficients of spleen and kidney, increased BUN in both female and male rats at high dose, increased CR and decreased organ coefficients of heart and liver in male rats at high dose. All of which, except the kidney coefficient and BUN in males, returned to normal levels after 28-day recovery. Histopathological examination revealed vacuolar degeneration of glomerulus, degeneration of renal tubules and cast in the kidneys, which were also recovered except in males of high-dosing group. These results indicate that kidney is the most susceptible organ for neamine toxicity. Tissue microarray analysis validated that ANG is up-regulated in hepatocellular carcinoma accompanied by increased nuclear translocation, suggesting that ANG is a possible target for drug development in liver cancer treatment. Neamine blocked nuclear translocation of ANG in HUVEC and HepG2 cells, and inhibited ANG-stimulated cell proliferation without affecting basal level cell proliferation. Neamine also inhibited progression of HepG2 xenografts in athymic mice accompanied by decreased angiogenesis and cancer cell proliferation. These results suggest that neamine is a specific ANG inhibitor with low toxicity and high anti-liver cancer efficacy.

pH-dependent binding engineering reveals an FcRn affinity threshold that governs IgG recycling.

The Fc domain of IgG has been the target of multiple mutational studies aimed at altering the pH-dependent IgG/FcRn interaction to modulate IgG pharmacokinetics. These studies have yielded antibody variants with disparate pharmacokinetic characteristics, ranging from extended in vivo half-life to those exhibiting extremely rapid clearance. To better understand pH-dependent binding parameters that govern these outcomes and limit FcRn-mediated half-life extension, we generated a panel of novel Fc variants with high affinity binding at acidic pH that vary in pH 7.4 affinities and assessed pharmacokinetic outcomes. Pharmacokinetic studies in human FcRn transgenic mice and cynomolgus monkeys showed that multiple variants with increased FcRn affinities at acidic pH exhibited extended serum half-lives relative to the parental IgG. Importantly, the results reveal an underappreciated affinity threshold of neutral pH binding that determines IgG recycling efficiency. Variants with pH 7.4 FcRn affinities below this threshold recycle efficiently and can exhibit increased serum persistence. Increasing neutral pH FcRn affinity beyond this threshold reduced serum persistence by offsetting the benefits of increased pH 6.0 binding. Ultra-high affinity binding to FcRn at both acidic and neutral pH leads to rapid serum clearance.

Analysis of Association between MAP2K4 Gene Polymorphism rs3826392 and IL-1b Serum Level in Southern Chinese Han Ischemic Stroke Patients.

BACKGROUND: Mitogen-activated protein kinase kinase 4 (MAP2K4) gene acts as the direct upstream activator of c-Jun NH2-terminal kinase pathway, which plays an important role in regulating neuron survival and apoptosis in response to cerebral ischemia. However, the association between MAP2K4 gene polymorphisms and ischemic stroke (IS) has not yet been published. Therefore, this study investigates the association between MAP2K4 gene polymorphism rs3826392 and IS susceptibility, as well as its quantitative traits in Southern Chinese Han population. METHODS: A total of 816 Chinese patients with IS and 816 age- and sex-matched controls were recruited. Rs3826392 was genotyped using Sequenom MassARRAY iPLEX platform (Sequenom, San Diego, CA, USA). The mRNA expression of MAP2K4 gene in peripheral blood mononuclear cells was detected using reverse transcription-polymerase chain reaction. The levels of serum cytokines, including IL-1b, IL-6, IL-8, IL-12, and tumor necrosis factor-α (TNF-α), were measured by enzyme-linked immunosorbent assay. RESULTS: Significant association was not observed between MAP2K4 gene polymorphism rs3826392 and IS susceptibility in all genetic models (P > .05). A significant difference was found in IL-1b, IL-6, IL-8, and TNF-α serum levels between patients with IS and control groups. MAP2K4 gene polymorphism rs3826392 C/A genotype carriers showed significantly higher IL-1b serum levels compared with AA genotype carriers (P = .029) in patients with IS. CONCLUSION: MAP2K4 gene polymorphism rs3826392 did not contribute to IS susceptibility, but rs3826392 C/A genotype carriers showed significantly higher IL-1b serum levels. This result suggests that rs3826392 may play a potential role in the IS inflammatory process.

iTRAQ-Based Proteomics Analysis of Serum Proteins in Wistar Rats Treated with Sodium Fluoride: Insight into the Potential Mechanism and Candidate Biomarkers of Fluorosis.

Fluorosis induced by exposure to high level fluoride is quite widespread in the world. The manifestations of fluorosis include dental mottling, bone damage, and impaired malfunction of soft tissues. However, the molecular mechanism of fluorosis has not been clarified until now. To explore the underlying mechanisms of fluorosis and screen out serum biomarkers, we carried out a quantitative proteomics study to identify differentially expressed serum proteins in Wistar rats treated with sodium fluoride (NaF) by using a proteomics approach of isobaric tagging for relative and absolute quantitation (iTRAQ). We fed Wistar rats drinking water that had 50, 150, and 250 mg/L of dissolved NaF for 24 weeks. For the experimental duration, each rat was given an examination of the lower incisors to check for the condition of dental fluorosis (DF). By the end of the treatment, fluoride ion concentration in serum and lower incisors were detected. The results showed that NaF treatment can induce rat fluorosis. By iTRAQ analysis, a total of 37 differentially expressed serum proteins were identified between NaF-treated and control rats. These proteins were further analyzed by bioinformatics, out of which two proteins were validated by enzyme-linked immunoadsorbent assays (ELISA). The major proteins were involved in complement and coagulation cascade, inflammatory response, complement activation, defense response, and wound response, suggesting that inflammation and immune reactions may play a key role in fluorosis pathogenesis. These proteins may contribute to the understanding of the mechanism of fluoride toxicity, and may serve as potential biomarkers for fluorosis.

miR-186-5p improves alveolar epithelial barrier function by targeting the wnt5a/ß-catenin signaling pathway in sepsis-acute lung injury.

BACKGROUND: Alveolar epithelial barrier dysfunction is one of the pathological features of sepsis-acute lung injury(ALI). However, the molecular mechanisms that regulate the function of alveolar epithelial barrier remain unclear. This study aimed to determine the regulatory role of miR-186-5p in alveolar epithelial barrier function in sepsis-ALI and its underlying molecular mechanism. METHODS: We established sepsis-ALI models in vivo and in vitro, detected the miR-186-5p and wnt5a/ß-catenin expressions, and observed the functional changes of the alveolar epithelial barrier by miR-186-5p overexpression. We used rescue experiments to clarify whether miR-186-5p works through wnt5a/ß-catenin. RESULTS: miR-186-5p expression was decreased, wnt5a expression was increased, and the wnt5a/ß-catenin signaling pathway was activated in mouse lung tissues and A549 cells after inflammatory stimulation. miR-186-5p overexpression resulted in wnt5a/ß-catenin signaling pathway inhibition, decreased apoptosis in A549 cells, improved alveolar epithelial barrier function, reduced lung tissue injury in ALI mice, decreased IL-6 and TNF-α levels, and increased claudin4 and ZO-1 expression. Using miRNA-related database prediction and dual-luciferase reporter gene analysis, the targeting relationship between miR-186-5p and wnt5a was determined. The protective effect produced by miR-186-5p overexpression on the alveolar barrier was reversed after the application of the wnt5a/ß-catenin activator Licl. CONCLUSION: Our experimental data suggest miR-186-5p targets the wnt5a/ß-catenin pathway, thereby regulating alveolar epithelial barrier function. Furthermore, both miR-186-5p and wnt5a/ß-catenin are potential therapeutic targets that could impact sepsis-ALI.

A meta-analysis on the lifetime and period prevalence of self-injury among adolescents with depression.

Background: Adolescents are vulnerable to mental disorders due to physiological, psychosocial, and cognitive changes during this critical developmental stage. Depression, in particular, can lead to high-risk behaviors such as self-injury (SI) and suicide. This study aims to estimate the pooled prevalence of SI behaviors among adolescents with depression. Materials and methods: We systematically searched databases including EMBASE, Scopus, PubMed, and Web of Sciences for relevant articles published on adolescents with depression from January 1, 2000, to January 1, 2024. The quality assessment of the studies was conducted using the Joanna Briggs Institute (JBI) criteria. The global prevalence of SI was calculated based on a random effects model using Stata software version 17. Results: Our analysis included 29 studies involving 12,934 adolescents. The lifetime prevalence of SI was 52% (95% Confidence Interval [CI]: 41-64), while the period prevalence was 57% (95% CI: 49-64). Notably, a significant relationship was observed between the prevalence of SI and the year of publication of articles (p = 0.002). Furthermore, publication bias was not significant for both lifetime prevalence (p = 0.281) and period prevalence (0.358). Conclusion: The prevalence of self-injurious behaviors in adolescents with depression is alarmingly high, with more than half of adolescents having engaged in these high-risk behaviors during their lifetime or within the last year. Given the associated risk of suicide, it is crucial to identify individuals at risk and provide timely interventions.