Adipose tissue accumulation represents a significant challenge to both human metabolic health and agricultural productivity. While Ras and Rab Interactor 2 (RIN2) has been characterized as a Rab5 effector protein, its precise role in adipogenesis remains poorly defined. Here, we identified RIN2 as a novel critical regulator of adipogenesis in chicken. We found that RIN2 was widely expressed across various tissues and dynamic expression patterns during adipocyte differentiation. Through comprehensive functional analyses in both ICP-1 cells and primary preadipocytes, we identified that RIN2 overexpression enhances cellular proliferation, cell cycle progression, and adipogenic differentiation, whereas RIN2 knockdown produced contrasting inhibitory effects. Transcriptomic profiling uncovered that RIN2 functions through modulation of the cholesterol metabolic pathway and promotes fatty acid metabolism. Most notably, in vivo knockdown of RIN2 specifically reduced abdominal fat deposition without compromising other carcass characteristics. In summary, our findings identify RIN2 as a key regulator of fat accumulation and highlight its potential as a genetic target for improving poultry carcass composition.

To create and verify a machine learning model that integrates social determinants of health (SDoH) for assessing post-stroke depression (PSD) and examining the association between SDoH and disease outcomes. Data were acquired from the National Health and Nutrition Examination Survey. Logistic regression was employed to analyse the association between SDoH and PSD, whereas Cox regression was utilized to assess the correlation between SDoH and all-cause mortality in PSD. The Boruta algorithm was employed for feature selection, and four machine learning models were constructed (CatBoost, Logistic, Multilayer Perceptron, and Random Forest) to evaluate the predictive effectiveness, calibration, and clinical applicability of these ML models. SHAP values were computed to ascertain the predictive significance of each feature in the model that exhibited the highest predictive performance. Logistic regression analysis revealed a significant positive correlation between SDoH and PSD prevalence(p for trend < 0.0001). Compared to the other three models, CatBoost (AUC = 0.966) demonstrated the best overall predictive performance. Moreover, the decision curve analysis (DCA) and calibration curve findings demonstrated that the CatBoost model possessed considerable clinical utility and consistent predictive efficacy. The ten-fold cross-validation method further confirmed the model’s robustness and generalization ability. A linear relationship exists between SDoH and PSD, with CatBoost demonstrating the best performance in predicting PSD. SHAP values emphasize the importance of SDoH.

Purpose:Increasing evidence indicates that various types of immune cells are associated with different forms of neuropathic pain (NP). However, the causal relationships among these associations remain unclear. To elucidate the causal relationships between immune cells and NP, we conducted a two-sample Mendelian randomization (MR) analysis. Patients and Methods:The exposure and outcome Genome-wide association analysis (GWAS) data used in this study were obtained from open-access databases. This study employed a two-sample MR analysis to evaluate the causal relationships between 731 immune cell traits and four types of NP, including postherpetic neuralgia (PHN), trigeminal neuralgia (TN), diabetic peripheral neuropathy (DPN), and drug-induced peripheral neuropathy (DIPN). Results:The relative count of CD39+ CD4+ %T cells was positively associated with TN, while the mean fluorescence intensity (MFI) of CD20 on IgD+ CD38br (B cell) and forward scatter area (FSC-A) on myeloid dendritic cells (DCs) were negatively associated with TN. Additionally, the relative count of CD8br NKT %lymphocytes was positively associated with PHN, and the MFI of HLA DR on CD33br HLA DR+ CD14 (myeloid cells) was negatively associated with PHN. The MFI of CD4 on activated and secreting T regulatory (Treg) cells was positively associated with DPN. Furthermore, the relative count of B cell % CD3- lymphocytes was negatively associated with DIPN. Conclusion:This MR study, using genetic data from individuals of European descent, provides evidence supporting the causal relationships between several specific immune cell phenotypes and various NP subtypes.

BackgroundSepsis associated encephalopathy (SAE) is prevalent among elderly patients in the ICU and significantly affects patient prognosis. Due to the symptom similarity with other neurological disorders and the absence of specific biomarkers, early clinical diagnosis remains challenging. This study aimed to develop a predictive model for SAE in elderly ICU patients.MethodsThe data of elderly sepsis patients were extracted from the MIMIC IV database (version 3.1) and divided into training and test sets in a 7:3 ratio. Feature variables were selected using the LASSO-Boruta combined algorithm, and five machine learning (ML) models, including Extreme Gradient Boosting (XGBoost), Categorical Boosting (CatBoost),Light Gradient Boosting Machine(LGBM), Multilayer Perceptron (MLP), and Support Vector Machines (SVM), were subsequently developed using these variables. A comprehensive set of performance metrics was used to assess the predictive accuracy, calibration, and clinical applicability of these models. For the machine learning model with the best performance, we employed the SHapley Additive Explanations(SHAP) method to visualize the model.ResultsBased on strict inclusion and exclusion criteria, a total of 3,156 elderly sepsis patients were enrolled in the study, with an SAE incidence rate of 48.7%. The mortality rate of elderly sepsis patients who developed SAE was significantly higher than that of patients in the non-SAE group (28.78% vs. 12.59%, P < 0.001). A total of 18 feature variables were selected for the construction of the ML model using the LASSO-Boruta combined algorithm. Compared to the other four models and traditional scoring systems, the XGBoost model demonstrated the best overall predictive performance, with Area Under the Curve(AUC)=0.898, accuracy=0.830, recall=0.819, F1-Score=0.820, specificity=0.840, and Precision=0.821. Furthermore, the results from the Decision Curve Analysis (DCA) and calibration curves demonstrated that the XGBoost model has significant clinical value and stable predictive performance. The ten-fold cross-validation method further confirmed the robustness and generalizability of the model. In addition, we simplified the model based on the SHAP feature importance ranking, and the results indicated that the simplified XGBoost model retains excellent predictive ability (AUC=0.858).ConclusionsThe XGBoost model effectively predicts SAE in elderly ICU patients and may serve as a reliable tool for clinicians to identify high-risk patients.

Total hip arthroplasty can cause moderate and severe pain that can have a profound impact during postoperative rehabilitation. Regional nerve block is recommended for anesthesia and analgesia during hip surgery. In particular, the iliac fascia space block of the inguinal ligament is a widely used technique in clinical practice that can block the femoral nerve trunk, obturator nerve trunk, and lateral femoral cutaneous nerve simultaneously. This study aimed to compare the effect of supra-inguinal fascia iliaca compartment block (S-FICB) to a combination of pericapsular nerve group block (PNGB) and lateral femoral cutaneous nerve block (LFCNB) on block range and analgesia as well as motor function of patients with total hip arthroplasty. Sixty patients undergoing total hip arthroplasty through posterolateral approach were randomly divided into two groups with 30 patients each. After complete awakening from general anesthesia, patients received ultrasound-guided S-FICB with 40 mL 0.4% ropivacaine (group S) or 20 mL 0.4% ropivacaine PNGB combined with 3 mL 0.4% ropivacaine LFCNB (PH group). We used the Numerical Rating Scale and cumulative dosage of sufentanil to grade pain during the first 48 h. Quadriceps femoris muscle and adductor muscle strength, range of sensory block, length of stay, and complications were also recorded. No significant differences were found in analgesic indicators of both groups (P>0.05). The Numerical Rating Scale scores of resting pain at each time point after the blockage were significantly lower than those before the blockage (P<0.05). However, the PH group had significantly less incidence of analgesia sensation in the anterior and medial side of the thigh (P < 0.05), and less incidence of quadriceps and adductor weakness (P<0.05) at 1 h and 6 h after the blockage compared to that in group S. Compared to S-FICB, the combination of PNGB and LFCNB provided equivalent analgesic effect and significantly lowered the risk of numbness and muscle weakness of the thigh, which is more conducive to early postoperative exercise and rehabilitation .This combination can be used as a new option in multimodal analgesia after total hip arthroplasty.Trial registration: Chinese Clinical Trial Registry (no. ChiCTR2200055963, date of registration 29/01/2022).

Background Ischemic stroke (IS) is an important disease causing death and disability worldwide, and further investigation of IS-related genes through genome-wide association study (GWAS) data is valuable. Methods The study included GWAS data from 62,100 IS patients of European origin and 1,234,808 controls in a cross-tissue transcriptome association study (TWAS). A joint analysis was first performed by the Unified Test for Molecular Markers (UTMOST) and FUSION methods. The results of the joint analysis were also validated by fine-mapping through FOCUS. Mendelian randomisation analysis was performed to determine whether the obtained genes were causally related to IS. Genome Annotated Multiple Marker Analysis (MAGMA) explored which biological functions the genes associated with IS. We used Coloc to co-localise GWAS and eQTL of the genes. We also biologically validated the results by Western blotting and immunofluorescence staining in the middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model. Results Four TWAS methods identified only one new susceptibility gene (USP38) associated with IS risk. Mendelian randomization and colocalization analysis found that USP38 may be protective against IS development. Functional enrichment analysis indicated IS-related genes were mainly associated with the intrinsic fibrinogen activation, acute myocardial infarction, exogenous fibrinogen activation, coagulation cascade response, TNF signalling pathway and GRB2 signalling pathway. Western blotting and immunofluorescence staining demonstrated a reduction in USP38 expression in MCAO/R mice. Conclusion Our research indicates that USP38 is an essential gene related to IS, with its expression strongly connected with IS risk, thus providing new perspectives on the genetic framework of IS.

Purpose:Pyroptosis, a programmed inflammatory cell death mechanism, plays a significant role in neuropathic pain (NP) pathogenesis. However, the specific pyroptosis-related genes (PRGs) driving NP development remain poorly understood. This study employs systematic approaches to identify and validate PRGs, aiming to delineate their mechanistic contributions to NP progression. Methods:To elucidate pyroptosis-related genes (PRGs) in neuropathic pain pathogenesis, we first performed integrated bioinformatics analysis of the GSE236754 dataset, revealing differentially expressed PRGs in the spinal cord dorsal horn of spared nerve injury (SNI) rats. Subsequent functional enrichment analyses coupled with protein-protein interaction network construction delineated pathway convergences among identified PRGs. Experimental validation utilizing SNI rat model, Western blot and immunofluorescence quantification confirmed protein expression patterns, and immunofluorescence mapping determined cellular localization collectively. Statistical analyses via ANOVA method. Results:Bioinformatics screening identified 11 candidate PRGs in the SNI model, particularly highlighting Nlrc4 and Nlrp3 as the most upregulated targets. Gene Ontology (GO) analysis demonstrated significant enrichment in three domains, pyroptosis regulation, inflammasome complex assembly, and cysteine-type endopeptidase activity associated. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis specifically identified the "NOD-like receptor signaling pathway" as significantly enriched. Gene Set Enrichment Analysis (GSEA) further corroborated these findings. Behavioral quantification showed progressive mechanical hypersensitivity, with mechanical pain and cold pain reaching maximal sensitivity at day 7 post-injury (p<0.001). Western blot detected synchronized elevation of NLRP3 and NLRC4 inflammasome components and downstream effectors across the observation window (all p<0.05). Immunofluorescence analysis demonstrated a time-dependent increase in the expression of GSDMD-N, the pyroptotic-executing protein, a trend consistent with the findings from behavioral tests and Western blot analysis (p<0.05). And cellular localization analysis revealed neuron-predominant accumulation of GSDMD-N. Conclusion:We identified 11 potential biomarkers for NP. Our data conclusively show that SNI induced NLRP3/NLRC4 inflammasome activation and neuronal pyroptosis in the rat spinal cord.

BACKGROUND:Sepsis is a critical and life-threatening clinical syndrome. Abnormal plasma lipid levels are associated with disease progression. However, causal links remain uncertain due to limitations of observational studies. METHODS:This study conducted a comprehensive two-sample Mendelian randomization (MR) analysis utilizing publicly available pooled genome-wide association study data on 179 plasma phospholipid subtypes, 731 immune cell phenotypes, and genetic data related to sepsis-related mortality outcomes. The causal associations between plasma lipids, immune cell phenotypes, and the risk of sepsis-related death were investigated. RESULTS:MR results demonstrated significant causal associations between five subtypes of phosphatidylcholine (PC) and one sphingomyelin (SM) and the clinical outcome of 28-day mortality in sepsis patients. Notably, PC (16:0_18:2), PC (18:0_18:1), PC (18:0_20:4), PC (O-16:1_16:0), and SM (d34:0) demonstrated a protective effect in reducing the risk of 28-day mortality ( P  < 0.05). Conversely, PC (16:1_20:4) was associated with an increased risk of 28-day mortality in sepsis patients( P  < 0.05). Comprehensive sensitivity analyses confirmed the robustness of these results. The inverse Mendelian randomization analysis did not reveal a significant causal effect of sepsis on the aforementioned lipid profile. Mediation analysis identified two key immune cell-mediated factors, including circulating CD39 on CD39+ CD8br cells and CX3CR1 on CD14+ CD16+ monocytes, as mediators of the reduced risk of sepsis-associated mortality due to PC (O-16:1_16:0), with mediation proportions of 17.4% and 13.6%, respectively. CONCLUSIONS:Our study supports a causal relationship between plasma lipid metabolism disorders and sepsis-associated mortality and provides new insights into the critical role of immune cell alterations induced by lipid metabolism disorders in sepsis progression.

BackgroundAs population aging and unhealthy living habits may exacerbate the prevalence and burden of low back pain (LBP), effective treatment and improvement of patient quality of life are particularly critical. Silver needle therapy (SNT), having evolved from traditional acupuncture, involves placing silver needles into muscles, tendons, and fascia for treatment. However, it still lacks robust clinical evidence to substantiate its effectiveness. Therefore, it is necessary to conduct more emphasis on meta-analysis to evaluate the clinical efficacy of SNT for treating LBP.MethodsWe will search PubMed, Medline, Cochrane Library, Embase, China National Knowledge Infrastructure (CNKI), and Wanfang Databases up until December 2023 to identify randomized controlled trials of SNT treatment in adult patients with LBP. The primary outcome will be the intensity of pain after pain management. Secondary outcomes will include the Oswestry Disability Index, Japanese Orthopedic Association Back Pain Evaluation Questionnaire, requirement for analgesic drugs, and treatment-related adverse reactions. Two investigators conducted the literature search, selected studies that might meet the inclusion criteria based on the title and abstract, and extracted data from the eligible literature independently and will independently assess the risk of bias using the Revised Cochrane Risk-of-Bias (RoB2) tool. Multivariate analyses (including subgroup analysis, trial sequential analysis (TSA), sensitivity analysis, etc.) will be conducted to improve the quality of evidence.Clinical trial registrationRegistration: PROSPERO Registration Number: CRD42023466207, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023466207.

BackgroundImmunity and neuroinflammation play crucial roles in the pathogenesis of Parkinson’s disease (PD). Nonetheless, prior investigations into the correlation between immune inflammation and PD have produced varying results. Identifying specific immune cell phenotypes that are truly associated with PD is challenging, and the causal relationship between immune cells and PD remains elusive.MethodsThis study conducted a comprehensive two-sample Mendelian randomization (MR) analysis, employing five distinct analytical approaches, to clarify the causal connection between immune cell characteristics and the risk of PD. Utilizing GWAS data, we investigated the causal relationship between 731 immune cell traits and PD. These immune cell phenotypes encompass absolute cell (AC) counts, median fluorescence intensity (MFI), and relative cell (RC) counts for B cells, cDCs, mature stage T cells, monocytes, myeloid cells, TBNK (T cells, B cells, and natural killer cells), and Tregs, as well as the logistic parameter (MP) for cDCs and TBNK.ResultsThe inverse variance weighted (IVW) analysis indicated that Myeloid DCs (p = 0.004), HVEM expression on CD45RA− CD4+ T cells (p = 0.007), CD62L− CD86+ Myeloid DCs (p = 0.015), and HLA DR expression on monocytes (p = 0.019) were associated with a reduced risk of PD. CD14+ CD16+ monocytes (p = 0.005), HLA DR+ NK cells within CD3− lymphocytes (p = 0.023), and CD28 expression on activated & secreting Tregs (p = 0.032) were associated with an increased risk of PD.ConclusionThis study establishes a causal link between immune cell phenotype and the pathogenesis of PD, identifying several specific immune cell characteristics associated with PD. This could inspire researchers to delve into the pathogenesis of PD at the cellular subtype level, and aid in the identification of potential pharmacological protein targets for PD.

Abstract Blood group is a potential genetic element in coronary artery disease. Nevertheless, the relationship between different ABO blood groups and myocardial injury after non-cardiac surgery (MINS) is poorly understood. This study verified whether ABO blood group is a potential MINS influencing factor. This retrospective cohort study included 1201 patients who underwent elective non-cardiac surgery and a mandatory troponin test on postoperative days 1 and 2 from 2019 to 2020 at a university-affiliated tertiary hospital. The primary outcome was associations between ABO blood groups and MINS, assessed using univariate and multivariate logistic-regression analyses. Path analysis was used to investigate direct and indirect effects between blood group and MINS. MINS incidence (102/1201, 8.5%) was higher in blood-type B patients than in non-B patients [blood-type B: 44/400 (11.0%) vs. non-B: 58/801 (7.2%); adjusted odds ratio = 1.57 (1.03–2.38); p = 0.036]. In the confounding factor model, preoperative hypertension and coronary artery disease medical history were associated with MINS risk [adjusted odds ratio: 2.00 (1.30–3.06), p = 0.002; 2.81 (1.71–4.61), p < 0.001, respectively]. Path analysis did not uncover any mediating role for hypertension, diabetes, or coronary artery disease between blood type and MINS. Therefore, blood-type B is associated with higher MINS risk; potential mediators of this association need to be investigated.

Molecular breeding accelerates animal breeding and improves efficiency by utilizing genetic mutations. Structural variations (SVs), a significant source of genetic mutations, have a greater impact on phenotypic variation than SNPs. Understanding SV functional mechanisms and obtaining precise information are crucial for molecular breeding. In this study, association analysis revealed significant correlations between 198-bp SVs in the GSTA2 promoter region and abdominal fat weight, intramuscular fat content, and subcutaneous fat thickness in chickens. High expression of GSTA2 in adipose tissue was positively correlated with the abdominal fat percentage, and different genotypes of GSTA2 exhibited varied expression patterns in the liver. The 198-bp SVs regulate GSTA2 expression by binding to different transcription factors. Overexpression of GSTA2 promoted preadipocyte proliferation and differentiation, while interference had the opposite effect. Mechanistically, the 198-bp fragment contains binding sites for transcription factors such as C/EBPα that regulate GSTA2 expression and fat synthesis. These SVs are significantly associated with chicken fat traits, positively influencing preadipocyte development by regulating cell proliferation and differentiation. Our work provides compelling evidence for the use of 198-bp SVs in the GSTA2 promoter region as molecular markers for poultry breeding and offers new insights into the pivotal role of the GSTA2 gene in fat generation.

Background: Although genome-wide association studies (GWAS) have identified 14 loci associated with frailty index (FI) susceptibility, the underlying causative genes and biological mechanisms remain elusive.Methods: A cross-tissue transcriptome-wide association study (TWAS) was conducted utilizing the Unified Test for Molecular Markers (UTMOST), which integrates GWAS summary statistics from 164,610 individuals of European ancestry and 10,616 Swedish participants, alongside gene expression matrices from the Genotype-Tissue Expression (GTEx) Project. Validation of the significant genes was performed through three distinct methods: FUSION, FOCUS, and Multiple Marker Analysis of Genome-wide Annotation (MAGMA). Exploration of tissue and functional enrichment for FI-associated SNPs was conducted using MAGMA. Conditional and joint analyses, along with fine mapping, were employed to enhance our understanding of FI’s genetic architecture. Mendelian randomization was employed to ascertain causal relationships between significant genes and FI, and co-localization analysis was utilized to investigate shared SNPs between significant genes and FI.Results: In this study, two novel susceptibility genes associated with the risk of FI were identified through the application of four TWAS methods. Mendelian randomization demonstrated that HTT may elevate the risk of developing frailty, whereas LRPPRC could offer protection against the onset of frailty. Additionally, co-localization analysis identified a shared SNP between LRPPRC and FI. Tissue enrichment analyses revealed that genomic regions linked to SNPs associated with frailty were predominantly enriched in various brain regions, including the frontal cortex, cerebral cortex, and cerebellar hemispheres. Conditional, combined analyses, and fine mapping collectively identified two genetic regions associated with frailty: 2p21 and 4q16.3. Functional enrichment analyses revealed that the pathways associated with frailty were primarily related to the MHC complex, PD-1 signaling, cognition, inflammatory response to antigenic stimuli, and the production of second messenger molecules.Conclusion: This investigation uncovers two newly identified genes with forecasted expression levels associated with the risk of FI, offering new perspectives on the genetic architecture underlying FI.

Insomnia, recognized as a prevalent sleep disorder, has garnered extensive attention within the realm of public health. Recent studies indicate a close interaction between the immune system and sleep; however, the specific mechanism remains not yet fully understood. Based on the publicly available Genome-Wide Association Study (GWAS) data, we used two-sample Mendelian randomization (MR) analyses to investigate the associations between 731 immune cell traits and insomnia risk. Five MR analysis methods and a comprehensive sensitivity analysis were used to evaluate the reliability of the results. In this study, we identified that 14 immune characteristics among four immune profiles [median fluorescence intensity (MFI), relative cell count (RC), absolute cell count (AC), and morphological parameters (MP)] demonstrated a significant causal association with insomnia. Specifically, eight immune cell characteristics were associated with an increased risk of insomnia, including CD11c+ monocyte% (P < 0.001), CD11c+ HLA DR++ monocyte% (P = 0.004), CD86+ plasmoid dendritic cell (DC) AC (P < 0.001), CD33br HLA DR+ CD14dim AC (P < 0.001), CD8dim AC (P = 0.002), CCR2 on CD14+ CD16- monocyte (P < 0.001), CD39 on monocyte (P < 0.001), and SSC-A on myeloid DC (P < 0.001). Six immune cell characteristics demonstrated protective effects against insomnia, including PB/PC %B cell (P < 0.001), CM CD4+% CD4+ (P < 0.001), T-cell AC (P < 0.001), BAFF-R on IgD- CD38br (P < 0.001), CD16-CD56 on HLA DR+ NK cells (P < 0.001), and CD14 on CD33br HLA DR+ CD14dim (P < 0.001). Our study established the correlation between immune cell characteristics and insomnia, offering a novel theoretical foundation for the concept of sleep-immune cross talk. NEW & NOTEWORTHY This study investigated the association between 731 immune cell characteristics and insomnia using Mendelian randomization, revealing that 14 immune cell characteristics across four groups of immune traits (MFI, RC, AC, and MP) have a significant and causal association with insomnia risk. Our results contribute to the understanding of the sleep-immune cross talk doctrine and offer a new theoretical basis for immune modulation in treating insomnia.

BackgroundThe epidemiological association between frailty and insomnia is well established, yet the presence of a common genetic etiology is still uncertain. Further exploration is needed to ascertain the causal relationship between frailty and insomnia.MethodsUtilizing data obtained from genome-wide association studies (GWAS) summaries, we utilized the linkage disequilibrium score regression (LDSC) to determine the genetic correlation existing between frailty and insomnia. The determination of causality was achieved through the application of two-sample Mendelian randomization. We investigated the enrichment of single nucleotide polymorphism (SNP) at various tissue types utilizing stratified LD score regression (S-LDSC) and multimarker analysis of genome annotation (MAGMA). Common risk SNPs were identified using Multi-Trait Analysis of GWAS (MTAG) and Cross-Phenotype Association (CPASSOC). We further investigated the expression profiles of risk genes in tissues using Summary-data-based Mendelian randomization(SMR) based on pooled data, to explore potential functional genes.ResultsOur findings indicated a significant genetic correlation between frailty and insomnia, highlighting SNPs sharing risk (rs34290943, rs10865954), with a pronounced correlation in the localized genomic region 3p21.31. Partitioned genetic analysis revealed 24 functional elements significantly associated with both frailty and insomnia. Furthermore, mendelian randomization revealed a causal connection between frailty and insomnia. The genetic correlation between frailty and insomnia showed enrichment in 11 brain regions (S-LDSC) and 9 brain regions (MAGMA), where four functional genes (RMB6, MST1R, RF123, and FAM212A) were identified.ConclusionThis study suggests the existence of a genetic correlation and common risk genes between frailty and insomnia, contributing to a deeper comprehension of their pathogenesis and assists in identifying potential therapeutic targets.

Abstract Background: Total hip arthroplasty can cause moderate and severe pain that can have a profound impact during postoperative rehabilitation. Regional nerve block is recommended for anesthesia and analgesia during hip surgery. In particular, the iliac fascia space block of the inguinal ligament is a widely used technique in clinical practice that can block the femoral nerve trunk, obturator nerve trunk, and lateral femoral cutaneous nerve simultaneously. This study aimed to compare the effect of supra-inguinal fascia iliaca compartment block (S-FICB) to a combination of pericapsular nerve group block (PNGB) and lateral femoral cutaneous nerve block (LFCNB) on block range and analgesia as well as motor function of patients with total hip arthroplasty. Methods: Sixty patients undergoing total hip arthroplasty through posterolateral approach were randomly divided into two groups with 30 patients each. After complete awakening from general anesthesia, patients received ultrasound-guided S-FICB with 40 mL 0.4% ropivacaine (group S) or 20 mL 0.4% ropivacaine PNGB combined with 3 mL 0.4% ropivacaine LFCNB (PL group). We used the Numerical Rating Scale and cumulative dosage of sufentanil to grade pain during the first 48 h. Quadriceps femoris muscle and adductor muscle strength, range of sensory block, length of stay, and complications were also recorded. Results: No significant differences were found in analgesic indicators of both groups (P＞0.05). The Numerical Rating Scale scores of resting pain at each time point after the blockage were significantly lower than those before the blockage (P＜0.05). However, the PL group had significantly less incidence of analgesia sensation in the anterior and medial side of the thigh (P<0.05), and less incidence of quadriceps and adductor weakness (P＜0.05) at 1 h and 6 h after the blockage compared to that in group S. Conclusions: Compared to S-FICB, the combination of PNGB and LFCNB provided equivalent analgesic effect and significantly lowered the risk of numbness and muscle weakness of the thigh. This combination can be used as a new option in multimodal analgesia after total hip arthroplasty. Trial registration: Chinese Clinical Trial Registry (no. ChiCTR2200055963, date of registration: 29/01/2022)

Introduction Stellate ganglion block (SGB) is usually used in the department of algiatry. But preoperative SGB may reduce adverse cardiovascular events in high-risk patients, although evidence remains sparse. Therefore, we aim to determine whether a single-shot postoperative SGB can reduce the incidence of myocardial injury after non-cardiac surgery (MINS) and improve recovery in patients undergoing laparoscopic radical resection for colorectal cancer.Methods and analysis This is an investigator-initiated, single-centre, randomised, two-arm clinical trial enrolling patients aged over 45 years and scheduled for elective laparoscopic radical colorectal surgery with at least one risk factor for MINS. A total of 950 eligible patients will be randomised into a routine or block groups. The primary outcome is the incidence of MINS. The secondary outcomes include the Visual Analogue Scale of pain during rest and movement, the incidence of delirium, quality of recovery (QOR) assessed by QOR-15, and sleep quality assessed by Richards Campbell Sleep Questionnaire. Tertiary outcomes include time to first flatus, gastrointestinal complications such as anastomotic leak or ileus, length of hospital stay, collapse incidence of severe cardiovascular and cerebrovascular complications of myocardial infarction, cardiac arrest, ischaemic or haemorrhagic stroke, and all-cause mortality within 30 days after the operation.Ethics and dissemination The protocol was approved by Medical Ethics Committee of the China-Japan Union Hospital, Jilin University (Approval number: 2021081018) prior to recruitment. The study will be performed according to the guidelines of the Declaration of Helsinki. The findings of this study will be published and presented through various scientific forums.Trial registration number ChiCTR2200055319.

Objective Evaluate the feasibility of a trial of perioperative hypotension and serious complications.Design A patient and assessor-blinded randomised feasibility trial.Setting We included patients in a tertiary university hospital.Participants We enrolled 80 adults scheduled for major non-cardiac surgery.Interventions In patients randomised to tight blood pressure control, intraoperative mean arterial pressure (MAP) was targeted to ≥85 mm Hg maintained with norepinephrine infusion, and restarting chronic antihypertensive medications was delayed until the third postoperative day. In the reference group, intraoperative blood pressure was managed per routine and antihypertensive medications were restarted immediately after surgery.Primary and secondary outcome measures Our first co-primary outcome was the fraction of time when intraoperative MAP was >85 mm Hg, intraoperative area (time integral) of MAP >85 mm Hg and MAP <65 mm Hg. The second co-primary outcome was time until antihypertensive medications were restarted after surgery. Secondary outcomes were time-weighted average intraoperative MAP, cumulative minimum MAP for 10 min, average postoperative systolic blood pressure (SBP) and mean of the lowest three postoperative SBPs.Results Forty patients in each group were analysed. The median for intraoperative area of MAP >85 mm Hg was 1303 (772–2419) mm Hg*min in routine blood pressure (BP) cases and 2425 (1926–3545) mm Hg*min in tight BP control. The area for intraoperative MAP <65 mm Hg was 7 (0–40) mm Hg*min with routine BP management, and 0 (0–0) mm Hg*min with tight BP control. The fraction of time with MAP >85 mm Hg was 0.52 (0.25) and 0.87 (0.15). Antihypertensive medications were restarted 2 (1–3) days later in tight BP control cases. However, postoperative SBPs were similar.Conclusions Tight BP management markedly increased intraoperative MAP and reduced the amount of hypotension. In contrast, delaying chronic antihypertensive medications had little effect on postoperative SBP. The full trial appears feasible and remains necessary but should not include postoperative antihypertensive management.Trial registration NCT04789733.

This study explored the risk factors and established a prediction model for intraoperative hypothermia (IOH) in patients undergoing robotic surgery. We conducted a retrospective survey of patients undergoing elective robotic surgery at the China-Japan Union Hospital of Jilin University during June 2020-October 2021 using institutional medical records. Intraoperative core temperatures and potential influencing factors were collected, and regression analyses were used to assess the risk factors for IOH and establish a prediction model for the incidence of IOH. Overall, 833 patients who underwent robotic surgery were included in the final analysis; IOH was observed in 344 patients (incidence, 0.41; 95% confidence interval [CI] 0.38-0.45). A higher body mass index (BMI) and baseline core temperature were protective factors for IOH. A final prediction model for IOH was developed based on the determining factors with an area under the receiver operating characteristic curve of 0.85 under fivefold cross validation (95% CI 0.83-0.88). Accordingly, a lower BMI and baseline core temperature, thoracic surgeries, morning surgeries, and surgeries with longer durations were risk factors for IOH during robotic surgeries. Our prediction model has an excellent discrimination ability for predicting IOH in robotic surgeries.

Molecular breeding can accelerate the process of animal breeding and improve the breeding efficiency. To date, many Indel molecular markers have been identified in livestock and poultry, but how Indels affect economic traits is not well understood. For molecular breeding, it is crucial to reveal the mechanism of action of Indels and to provide more accurate information. The purpose of this study was to investigate how the 52/224-bp multiallelic Indels of the chicken QPCTL promoter area affect the daily weight gain of chickens and the potential regulatory mechanism of the QPCTL gene. The analysis was conducted by association analysis, qPCR, dual-fluorescence assay and Western blotting. The results showed that Indels in the QPCTL promoter region were significantly associated with the daily weight gain in chickens and that QPCTL expression showed a decreasing trend in embryonic breast muscle tissues. Furthermore, QPCTL expression was significantly higher in breast muscle tissues of the AC genotype than in those of the AB and BB genotypes. Based on the transcriptional activity results, the pGL3-C vector produced more luciferase activity than pGL3-A and pGL3-B. In addition, overexpression of QPCTL promoted chicken primary myoblast (CPM) proliferation and inhibited differentiation. The results of this study suggest that Indels in the promoter region of the QPCTL gene may regulate the proliferation and differentiation of CPMs by affecting the expression of QPCTL, which ultimately affects the growth rate of chickens. These Indels have important value for the molecular breeding of chickens, and QPCTL can be used as a candidate gene to regulate and improve chicken growth and development.