Enhanced Noise-Resilient Pressure Mat System Based on Hyperdimensional Computing.

Traditional systems for indoor pressure sensing and human activity recognition (HAR) rely on costly, high-resolution mats and computationally intensive neural network-based (NN-based) models that are prone to noise. In contrast, we design a cost-effective and noise-resilient pressure mat system for HAR, leveraging Velostat for intelligent pressure sensing and a novel hyperdimensional computing (HDC) classifier that is lightweight and highly noise resilient. To measure the performance of our system, we collected two datasets, capturing the static and continuous nature of human movements. Our HDC-based classification algorithm shows an accuracy of 93.19%, improving the accuracy by 9.47% over state-of-the-art CNNs, along with an 85% reduction in energy consumption. We propose a new HDC noise-resilient algorithm and analyze the performance of our proposed method in the presence of three different kinds of noise, including memory and communication, input, and sensor noise. Our system is more resilient across all three noise types. Specifically, in the presence of Gaussian noise, we achieve an accuracy of 92.15% (97.51% for static data), representing a 13.19% (8.77%) improvement compared to state-of-the-art CNNs.

Efficacy analysis of neuroendoscopy-assisted burr-hole evacuation for chronic subdural hematoma: a systematic review and meta-analysis.

The purpose of this study was to compare neuroendoscopy-assisted burr-hole evacuation with conventional burr-hole evacuation in the treatment of chronic subdural hematoma (CSDH), and to evaluate the curative effect of neuroendoscopy. This study follows PRISMA guidelines and uses the keywords "chronic subdural hematoma," "neuroendoscopies," "neuroendoscopy," "endoscopy," "endoscopic neurosurgery," and "neuroendoscopic surgery" to conduct an electronic search of online databases, including PubMed, Embase, Web of Science, and Cochrane Library. There were no restrictions on language or publication year. This meta-analysis involved 948 patients in six studies. The results showed that the recurrence rate in the neuroendoscopy group was significantly lower than that in the conventional burr-hole group (3.1% vs. 13.8%, P<0.001). Compared with the control group, the neuroendoscopy group had a longer operation time (P<0.001) and a shorter postoperative drainage time (P<0.001). In addition, there was no significant difference in hospital stay (P=0.14), mortality (P=0.39), postoperative morbidity (P=0.12), or 6-month neurological outcomes (P=0.32) between the two groups. It should be noted that the comparison of neurological outcomes was based on 269 patients (6/106 vs. 14/163). Compared with conventional burr-hole evacuation, neuroendoscopy-assisted burr-hole evacuation reduces the recurrence rate of CSDH and shortens the postoperative drainage time. However, the neuroendoscopy group did not have lower mortality or morbidity or better functional outcomes. In the future, randomized controlled trials are needed to further evaluate the efficacy and safety of neuroendoscopic surgery.

The prognostic nutrition index is a predictor for long-term outcomes after revascularization in adult moyamoya disease.

BACKGROUND AND PURPOSE: The prognostic nutrition index (PNI) has been associated with the prognosis of various medical disorders. This study aimed to explore the correlation between PNI and the long-term outcomes of adult patients afflicted with moyamoya disease (MMD). METHODS: This prospective study initially employed 138 adult patients diagnosed with MMD. After excluding 15 patients who did not meet the criteria, a total of 123 patients were included. Participants were divided into three groups based on the tertile of change in the PNI score. Statistical analysis compared clinical information and lab tests among the groups. The study was conducted between July 1 and December 31, 2019. RESULTS: After adjusting for multiple variables, patients in the upper two tertiles (tertiles 2-3) exhibited a significantly lower risk of adverse long-term outcomes compared to those in the lowest tertile (tertile 1) (OR, 0.089; 95% CI, 0.009-0.895; P = 0.040). Furthermore, adding PNI tertile to traditional risk factors substantially improved predicting adverse long-term outcomes (net reclassification improvement: 98.03%, P = 0.000; integrated discrimination improvement: 4.65%, P = 0.030). However, there was no statistically significant difference between the first PNI tertile (tertile 1) and the upper two tertiles (tertiles 2-3) in the Kaplan-Meier curve of stroke incidence (log-rank test, P = 0.244). CONCLUSIONS: A higher PNI level was significantly associated with a reduced risk of unfavorable long-term outcomes. Nevertheless, the PNI score did not predict stroke recurrence during extended follow-up. This study provides insights into a potential predictor of adverse long-term outcomes after revascularization in MMD patients. REGISTRATION NUMBER: ChiCTR2000031412.

Postoperative pneumocephalus and recurrence and outcome of chronic subdural hematoma: a systematic review and meta-analysis.

We conducted a meta-analysis to analyze the effects of pneumocephalus after chronic subdural hematoma (CSDH) surgery on hematoma recurrence, mortality, and functional outcomes. In this meta-analysis, following PRISMA guidelines, PubMed, Embase, Cochrane Library, and Web of Science online databases were queried using the keywords "pneumocephalus," "pneumoencephalos," "intracranial pneumatocele," "pneumo encephalon," "subdural air," and "chronic subdural hematoma." The results were limited to English-language articles. Through the online database, we identified a total of 276 articles and finally included 14 articles for meta-analysis. The results showed that the recurrence rate in the pneumocephalus group was higher than that in the control group, with a pooled OR of 3.35 (CI: 2.51-4.46, P < 0.001). There was no difference in recurrence rate between the no/few and moderate pneumocephalus groups (OR: 1.27, CI: 0.68-2.37, P = 0.46), but the recurrence rate of the large pneumocephalus group was significantly higher than that of the moderate group, with a pooled OR of 3.29 (CI: 1.71-6.32, P < 0.001). This study failed to show higher mortality and worse outcomes in the pneumocephalus group than in the control. Pneumocephalus after surgical evacuation of CSDH was associated with the recurrence rate of hematoma. Pneumocephalus affecting recurrence was correlated with gas volume, and moderate pneumocephalus may have less impact, while patients with large pneumocephalus are more likely to recur than those with moderate pneumocephalus. More prospective cohort studies are needed for further investigation and verification. This meta-analysis was registered (PROSPERO CRD42022321800).

Long noncoding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy modulation.

Induction of autophagy promotes cardiomyocyte survival and confers a cardioprotective effect on acute myocardial infarction (AMI). Our previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse AMI. Herein, this study further investigated whether the mechanisms by which MALAT1 enhanced cardiomyocyte apoptosis involved the autophagy regulation. To address this, cardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The cell apoptosis was evaluated using TUNEL staining and Western blot analysis of apoptosis-related proteins. The autophagy level was assessed using GFP-LC3 immunofluorescence and Western blot analysis of autophagy-related proteins. The results showed that H/R injury increased MALAT1 expression. Furthermore, MALAT1 overexpression significantly enhanced apoptosis and regulated autophagy of cardiomyocytes, whereas MALAT1 knockdown exerted the opposite effect. Moreover, rapamycin (an autophagy activator) effectively attenuated the MALAT1-mediated enhancement of cardiomyocyte apoptosis. Overall, our findings demonstrated that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis, at least in part, through autophagy modulation.

Identification and validation of smoking-related genes in lung adenocarcinoma using an in vitro carcinogenesis model and bioinformatics analysis.

BACKGROUND: Lung cancer is one of the most common carcinomas in the world, and lung adenocarcinoma (LUAD) is the most lethal and most common subtype of lung cancer. Cigarette smoking is the most leading risk factor of lung cancer, but it is still unclear how normal lung cells become cancerous in cigarette smokers. This study aims to identify potential smoking-related biomarkers associated with the progression and prognosis of LUAD, as well as their regulation mechanism using an in vitro carcinogenesis model and bioinformatics analysis. RESULTS: Based on the integration analysis of four Gene Expression Omnibus (GEO) datasets and our mRNA sequencing analysis, 2 up-regulated and 11 down-regulated genes were identified in both S30 cells and LUAD. By analyzing the LUAD dataset in The Cancer Gene Analysis (TCGA) database, 3 of the 13 genes, viz., glycophorin C (GYPC), NME/NM23 nucleoside diphosphate kinase 1 (NME1) and slit guidance ligand 2 (SLIT2), were found to be significantly correlated with LUAD patients' smoking history. The expression levels of GYPC, NME1 and SLIT2 in S30 cells and lung cancer cell lines were validated by quantitative PCR, immunofluorescence, and western blot assays. Besides, these three genes are associated with tumor invasion depth, and elevated expression of NME1 was correlated with lymph node metastasis. The enrichment analysis suggested that these genes were highly correlated to tumorigenesis and metastasis-related biological processes and pathways. Moreover, the increased expression levels of GYPC and SLIT2, as well as decreased expression of NME1 were associated with a favorable prognosis in LUAD patients. Furthermore, based on the multi-omics data in the TCGA database, these genes were found to be regulated by DNA methylation. CONCLUSION: In conclusion, our observations indicated that the differential expression of GYPC, NME1 and SLIT2 may be regulated by DNA methylation, and they are associated with cigarette smoke-induced LUAD, as well as serve as prognostic factors in LUAD patients.

The Sertoli cell marker FOXD1 regulates testis development and function in the chicken.

FOXD1, one of the transcription factors of the FOX family, has been shown to be important for mammalian reproduction but little is known about its function in avian species. In the present study, we identified the expression pattern and location of FOXD1 in chicken tissues and testis by performing quantitative polymerase chain reaction, immunohistochemistry and immunofluorescence, and further investigated the regulatory relationship of FOXD1 with genes involved in testis development by RNA interference. Our results showed that FOXD1 is confirmed to be significantly male-biased expressed in the brain, kidney and testis of adults as well as in embryonic gonads, and it is localised in the testicular Sertoli cell in chicken, consistent with its localisation in mammals. After knock-down of FOXD1 in chicken Sertoli cells, the expression of anti-Müllerian hormone (AMH), sex-determining region Y-box 9 (SOX9) and PKA regulatory subunits type I α (RIα) was significantly downregulated, expression of androgen receptor (AR) was notably increased whereas double-sex and MAB-3-related transcription factor 1 (DMRT1) showed no obvious change in expression. These results suggest that FOXD1 is an essential marker for Sertoli cells upstream of SOX9 expression and a potential regulator of embryonic testis differentiation and development and of normal testis function in the chicken.

Role of DNA methylation regulation of miR-130b expression in human lung cancer using bioinformatics analysis.

MicroRNAs (miRNAs) are involved in various crucial biological processes including regulation of cell differentiation, proliferation, and migration, and are closely associated with tumor development. This study aimed to investigate miR-130b expression levels in lung cancer patient tissues. Two Gene Expression Omnibus (GEO) databases, including GSE48414 and GSE74190, and two The Cancer Genome Atlas (TCGA) databases including TCGA LUAD and TCGA LUSC, were accessed to obtain information for differential expression analysis and clinical-pathological correlation analysis. The results showed that miR-130b expression levels were significantly increased in lung cancer compared to normal tissues. Data also demonstrated that confounding factors such as tumor clinical stages and tumor invasion depth markedly affected miR-130b expression levels in cancer patients. A total of 169 target genes modified by miR-130b expression were identified by using 4 online websites for target gene prediction. Further enrichment analysis indicated that these 169 target genes were significantly enriched in several cancer-related biological processes and signaling pathways, including wound healing, cell proliferation, Wnt signaling, Ras signaling, and mTOR signaling. It was also of interest to examine the seven sites on the promoter region of miR-130b encoding gene in lung cancer patients and then compare methylation at these loci with miR-130b expression. The correlation analysis between encoding gene methylation and miR-130b expression in TCGA datasets revealed that decreased methylation in the promoter region was significantly associated with elevated miR-130b expression. This phenomenon was markedly dependent upon smoking history and clinical-pathological features. In conclusion, data indicated alterations in the methylation of DNA promoter region of miR-130b encoding gene were associated with disturbances in miR-130b expression in lung cancer patients suggesting that the DNA methylation process and miR-130b expression may serve as biomarkers for detection of lung cancer.

The role of miR-130a-3p and SPOCK1 in tobacco exposed bronchial epithelial BEAS-2B transformed cells: Comparison to A549 and H1299 lung cancer cell lines.

In the pathogenesis of human lung cancer induced by tobacco smoke decreased expression levels of microRNAs (miRNAs) are known to occur. At present, the specific miRNAs expression levels reduced by tobacco smoke and subsequent lung cellular transformation remain to be determined. The aim of this study was thus to identify the miRNAs affected following cigarette-smoke exposure in bronchial epithelial BEAS-2B cells that were malignantly transformed into S30 cells. In addition, the miRNAs in S30 transformed cells were compared to human lung cancer cell lines A549 and H1299. Our results identified miR-130a-3p which was down-regulated in S30 cells as well as A549 and H1299 lung cancer cell lines. Using miRNA mimic, a correlation between elevated miR-130a-3p expression levels and reduced migration in A549 and H1299 cell lines and S30 cells was noted as evidenced by transwell and wound healing assays accompanied by enhanced apoptosis. Further, two online target genes prediction programs TargetScan and miRDB were employed to identify the miRNA target gene SPOCK1 in all three cell types. SPOCK1 expression was higher in unexposed bronchial epithelial BEAS-2B cells. It is of interest that however silencing SPOCK1 in transformed S30 cells exposed to cigarette-smoke a marked depression in cell migration was noted. Our findings demonstrate that upregulated miR-130a-3p was associated with reduced SPOCK1 expression in transformed S30 as well as lung cancer A549 and H1299 cell lines indicating that cigarette transformed cells behave similar to lung cancer cells and this process involves diminished lung cancer cells migration.

Multi-platform analysis of methylation-regulated genes in human lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is the most frequent pathological type of lung cancer that has a poor prognosis and high mortality rate. DNA methylation plays a critical role in various biological processes during development, while dysregulation results in pathological consequences. Thus, this study aimed to identify DNA methylation-regulated genes involved in LUAD occurrence. Initially, 300 downregulated and 168 upregulated mRNA expression levels were identified in two databases: Gene Expression Omnibus (GEO) and The Cancer Genome Atlas. In addition, GEO was utilized to detect 243 DNA hyper-methylated sites. Based on our observations, it was possible to correlate downregulation of mRNA expression and DNA hyper-methylation of six genes (ABCA3, COX7A1, HOXA5, SLIT3, SOX17, and SPARCL1). Functional analysis of the six genes indicated that these genes are predominantly enriched in cancer-related pathways and may promote carcinogenesis by regulating epithelialmesenchymal transition processes. In conclusion, our study identified a panel of DNA methylation-regulated genes involved in LUAD and may serve as potential epigenetic markers for this type of carcinoma.

Long non-coding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy inhibition by regulating TSC2-mTOR signaling.

BACKGROUND: Our previous study showed that knockdown of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) attenuated myocardial apoptosis in mouse acute myocardial infarction (AMI). This study aims to explore whether MALAT1 enhanced cardiomyocyte apoptosis via autophagy regulation and the underlying mechanisms of MALAT1 regulating autophagy. METHODS: Cardiomyocytes were isolated from neonatal mice and then stimulated with hypoxia/reoxygenation (H/R) injury to mimic AMI. The autophagy level was assessed using GFP-LC3 immunofluorescence and western blot analysis of autophagy-related proteins. RNA pull-down and RNA immunoprecipitation (RIP) was performed to analyze the binding of MALAT1 and EZH2. Chromatin immunoprecipitation (ChIP) assay was performed to analyze the binding of TSC2 promoter and EZH2. The cell apoptosis was evaluated using TUNEL staining and western blot analysis of apoptosis-related proteins. RESULTS: H/R injury increased MALAT1 expression in cardiomyocytes. Furthermore, MALAT1 overexpression inhibited, whereas MALAT1 knockdown enhanced the autophagy of cardiomyocytes. Moreover, MALAT1 overexpression recruited EZH2 to TSC2 promoter regions to elevate H3K27me3 and epigenetically inhibited TSC2 transcription. Importantly, TSC2 overexpression suppressed mTOR signaling and then activated the autophagy. Further results showed that MALAT1 inhibited proliferation and enhanced apoptosis of cardiomyocytes through inhibiting TSC2 and autophagy. CONCLUSION: These findings demonstrate that the increased MALAT1 expression induced by H/R injury enhances cardiomyocyte apoptosis through autophagy inhibition by regulating TSC2-mTOR signaling.

Event-specific detection of transgenic potato AV43-6-G7 using real-time and digital PCR methods.

BACKGROUND: The isolation of unknown DNA sequences flanked by known sequences is an important task in the event-specific detection of GMOs. None of event-specific detection method was developed based on the junction sequence of an exogenous integrant in the transgenic potato AV43-6-G7. RESULTS: The flanking sequence between the exogenous fragment and recombinant chromosome of this potato was successfully acquired through exogenous gene 5'-RACE. The event-specific primers and Taqman probe were designed to amplify fragments spanning the exogenous DNA and potato genomic DNA. The specific real-time PCR and digital PCR detection methods for AV43-6-G7 potato were established based on primers designed according to the flanking sequences. The detection limit of the qualitative PCR assay was 0.01 % for AV43-6-G7 potato in 100 ng of potato genomic DNA, corresponding to approximately 11.6 copies of the potato haploid genome. The ddPCR assays for Potato AV43-6-G7 achieved a limit of quantification of approximately 58 target copies, with RSD ≤ 25 %. The aLOQ of this system was approximately 1.2 copies. CONCLUSIONS: These results indicated that these event-specific methods would be useful for the identification of potato AV43-6-G7.

Dexmedetomidine ameliorates acute lung injury following orthotopic autologous liver transplantation in rats probably by inhibiting Toll-like receptor 4-nuclear factor kappa B signaling.

BACKGROUND: To investigate whether pretreatment with dexmedetomidine (Dex) has a protective effect against acute lung injury (ALI) in an orthotopic autologous liver transplantation (OALT) rat model and to explore the mechanisms responsible for the protective effect of Dex against lung injury. METHODS: Forty-eight rats underwent OALT and were randomly divided into six groups (n = 8 in each group) that received 10 µg/kg Dex, 50 µg/kg Dex, 50 µg/kg Dex + nonspecific α2-adrenergic receptor (AR) antagonist atipamezole, 50 µg/kg Dex + specific α2B/C-AR antagonist ARC-239, 50 µg/kg Dex + specific α2A-AR antagonist BRL-44408, or the same amount of normal saline. The sham rats (n = 8) underwent anesthesia induction, laparotomy, and separation of the portal vein without liver ischemia and reperfusion. Lung tissue sections were stained with hematoxylin and eosin (HE) to visualize the damage. The expression of Toll-like receptor 4 (TLR4) and the phospho-nuclear factor (NF)-κB p65 subunit as well as inflammatory cytokines was measured. RESULTS: Rats exhibited increased histological lung injury scores and pulmonary edema following OALT. Pretreatment with 50 µg/kg Dex attenuated OALT-induced lung injury in rats, probably by inhibiting the activation of the TLR4-NF-κB signaling pathway. The protective effect of Dex could be blocked by atipamezole or BRL-44408, but not by ARC-239, suggesting these effects of Dex were mediated, at least in part, by the α2A-AR. CONCLUSIONS: Dex exerts protective effects against ALI following OALT, and this protection is associated with the suppression of TLR4-NF-κB signaling. Thus, pretreatment with Dex may be a useful method for reducing lung damage caused by liver transplantation.

Users' continuance intention towards an AI painting application: An extended expectation confirmation model.

With the rapid advancement of technology, Artificial Intelligence (AI) painting has emerged as a leading intelligence service. This study aims to empirically investigate users' continuance intention toward AI painting applications by utilizing and expanding the Expectation Confirmation Model (ECM), Technology Acceptance Model (TAM), Unified Theory of Acceptance and Use of Technology (UTAUT), and the Flow Theory. A comprehensive research model is proposed. A total of 443 questionnaires were distributed to users with AI painting experiences for data collection. The hypotheses were tested through structural equation modeling. The primary conclusions drawn from this research include: 1) Confirmation plays a crucial role, significantly and positively predicting satisfaction and social impact. 2) Personal innovativeness has a significant effect on confirmation. 3) Satisfaction, flow experience, and social influence directly and positively predict intention, with social influence showing the most significant impact, while perceived usefulness, perceived enjoyment, and performance expectancy show no significant impact on intention. 4) Habit plays a negative moderating role in the association between social influence and continued intention to use. These findings offer valuable insights and inspiration for users seeking to understand the appropriate utilization of AI painting and provide actionable directions for the development of AI painting.

Triglyceride-glucose body mass index predicts prognosis in patients with ST-elevation myocardial infarction.

Triglyceride glycemic-body mass index (TyG-BMI) is a simple and reliable surrogate for insulin resistance (IR). However, it is still unclear if TyG-BMI has any predictive value in patients having percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). The purpose of this study was to examine the TyG-BMI index's prognostic significance and predictive power in patients with STEMI. The study comprised a total of 2648 consecutive STEMI patients who underwent PCI. The primary endpoint was the occurrence of major adverse cardiovascular events (MACE), defined as the combination of all-cause death, nonfatal myocardial infarction, nonfatal stroke, and coronary revascularization. The TyG-BMI index was formulated as ln [fasting triglycerides (mg/dL) × fasting plasma glucose (mg/dL)/2] × BMI. 193 patients in all experienced MACE over a median follow-up of 14.7 months. There was a statistically significant difference between the Kaplan-Meier survival curves for the TyG-BMI index tertiles (log-rank test, p = 0.019) for the cumulative incidence of MACE. The adjusted HRs for the incidence of MACE in the middle and highest quartiles of the TyG-BMI index compared with the lowest quartile were 1.37 (95% CI 0.92, 2.03) and 1.53 (95% CI 1.02, 2.29), respectively, in the fully adjusted Cox regression model. At six months, one year, and three years, the TyG-BMI area under the curve (AUC) for predicting MACE was 0.691, 0.666, and 0.637, respectively. Additionally, adding the TyG-BMI index to the risk prediction model enhanced outcome prediction. In STEMI patients undergoing PCI, TyG-BMI was independently linked to MACE. TyG-BMI could be a simple and solid way to assess MACE risk and prognosis.

[Predictive value of von Willebrand factor for venous thromboembolism in critically ill patients based on propensity score matching].

OBJECTIVE: To analyze the predictive value of von Willebrand factor (vWF) for venous thromboembolism (VTE) of patients in intensive care unit (ICU) by using propensity score matching (PSM). METHODS: Patients admitted to ICU of the Second Affiliated Hospital of Kunming Medical University from December 2020 to June 2022 who stayed in ICU for ≥72 hours and underwent daily bedside vascular ultrasound screening were included. Baseline data such as age, gender, primary disease, and chronic comorbidities were collected. Coagulation indexes before admission to ICU and 24 hours and 48 hours after ICU admission were collected, including prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), international normalized ratio (INR), fibrinogen (Fib), fibrin monomer (FM), vWF, D-dimer, antithrombin III (ATIII), etc. Patients were divided into VTE group and non-VTE group according to whether they had VTE or not [diagnosis of VTE: patients underwent daily ultrasound screening of bedside blood vessels (both upper and lower limbs, visceral veins), and those suspected of having thrombosis were confirmed by ultrasonographer or pulmonary angiography]. Using PSM analysis method, the VTE group was used as the benchmark to conduct 1 : 1 matching of age, whether there was malignant tumor, whether there was infection, whether there was diabetes, and coagulation indicators before admission to ICU. Finally, the cases with balanced covariates between the two groups were obtained. The risk factors of VTE were analyzed by multivariate Logistic regression analysis. Receiver operator characteristic curve (ROC curve) was drawn to evaluate the predictive value of vWF in the occurrence of VTE in critically ill patients. RESULTS: A total of 120 patients were enrolled, of which 18 (15.0%) were diagnosed with VTE within 72 hours after admission to ICU, and 102 (85.0%) were not found to have thrombus in ICU. Before PSM, there were significant differences in age, gender, proportion of malignant tumor and infection, and coagulation indexes between VTE group and non-VTE group. After PSM, 14 pairs were successfully matched, and the unbalanced covariables between the two groups reached equilibrium. Multivariate Logistic regression analysis showed that vWF was an independent risk factor for VTE at 48 hours after ICU admission in critically ill patients [odds ratio (OR) = 1.165, 95% confidence interval (95%CI) was 1.000-1.025, P = 0.004]. ROC curve analysis showed that the area under the ROC curve (AUC) of vWF at 48 hours after ICU admission for predicting VTE was 0.782, 95%CI was 0.618-0.945, P = 0.007. When the optimal cut-off value was 312.12%, the sensitivity was 67.7% and the specificity was 93.0. CONCLUSIONS: Dynamic monitoring of vWF is helpful to predict the occurrence of VTE in ICU patients, and vWF at 48 hours after ICU admission has certain value in predicting the occurrence of VTE.

Genetic Foundation of Male Spur Length and Its Correlation with Female Egg Production in Chickens.

Spurs, which mainly appear in roosters, are protrusions near the tarsometatarsus on both sides of the calves of chickens, and are connected to the tarsometatarsus by a bony core. As a male-biased morphological characteristic, the diameter and length of spurs vary significantly between different individuals, mainly related to genetics and age. As a specific behavior of hens, egg-laying also varies greatly between individuals in terms of traits such as age at first egg (AFE), egg weight (EW), and so on. At present, there are few studies on chicken spurs. In this study, we investigated the inheritance pattern of the spur trait in roosters with different phenotypes and the correlations between spur length, body weight at 18 weeks of age (BW18), shank length at 18 weeks of age (SL18), and the egg-laying trait in hens (both hens and roosters were from the same population and were grouped according to their family). These traits related to egg production included AFE, body weight at first egg (BWA), and first egg weight (FEW). We estimated genetic parameters based on pedigree and phenotype data, and used variance analysis to calculate broad-sense heritability for correcting the parameter estimation results. The results showed that the heritability of male left and right spurs ranged from 0.6 to 0.7. There were significant positive correlations between left and right spur length, BW18, SL18, and BWA, as well as between left and right spur length and AFE. We selected 35 males with the longest spurs and 35 males with the shortest spurs in the population, and pooled them into two sets to obtain the pooled genome sequencing data. After genome-wide association and genome divergency analysis by FST, allele frequency differences (AFDs), and XPEHH methods, we identified 7 overlapping genes (CENPE, FAT1, FAM149A, MANBA, NFKB1, SORBS2, UBE2D3) and 14 peak genes (SAMD12, TSPAN5, ENSGALG00000050071, ENSGALG00000053133, ENSGALG00000050348, CNTN5, TRPC6, ENSGALG00000047655,TMSB4X, LIX1, CKB, NEBL, PRTFDC1, MLLT10) related to left and right spur length through genome-wide selection signature analysis and a genome-wide association approach. Our results identified candidate genes associated with chicken spurs, which helps to understand the genetic mechanism of this trait and carry out subsequent research around it.

High glutamine increases stroke risk by inducing the endothelial-to-mesenchymal transition in moyamoya disease.

At present, there is limited research on the mechanisms underlying moyamoya disease (MMD). Herein, we aimed to determine the role of glutamine in MMD pathogenesis, and 360 adult patients were prospectively enrolled. Human brain microvascular endothelial cells (HBMECs) were subjected to Integrin Subunit Beta 4 (ITGB4) overexpression or knockdown and atorvastatin. We assessed factors associated with various signaling pathways in the context of the endothelial-to-mesenchymal transition (EndMT), and the expression level of related proteins was validated in the superficial temporal arteries of patients. We found glutamine levels were positively associated with a greater risk of stroke (OR = 1.599, p = 0.022). After treatment with glutamine, HBMECs exhibited enhanced proliferation, migration, and EndMT, all reversed by ITGB4 knockdown. In ITGB4-transfected HBMECs, the MAPK-ERK-TGF-ß/BMP pathway was activated, with Smad4 knockdown reversing the EndMT. Furthermore, atorvastatin suppressed the EndMT by inhibiting Smad1/5 phosphorylation and promoting Smad4 ubiquitination in ITGB4-transfected HBMECs. We also found the protein level of ITGB4 was upregulated in the superficial temporal arteries of patients with MMD. In conclusion, our study suggests that glutamine may be an independent risk factor for hemorrhage or infarction in patients with MMD and targeting ITGB4 could potentially be therapeutic approaches for MMD.

Involution of brown adipose tissue through a Syntaxin 4 dependent pyroptosis pathway.

Aging, chronic high-fat diet feeding, or housing at thermoneutrality induces brown adipose tissue (BAT) involution, a process characterized by reduction of BAT mass and function with increased lipid droplet size. Single nuclei RNA sequencing of aged mice identifies a specific brown adipocyte population of Ucp1-low cells that are pyroptotic and display a reduction in the longevity gene syntaxin 4 (Stx4a). Similar to aged brown adipocytes, Ucp1-STX4KO mice display loss of brown adipose tissue mass and thermogenic dysfunction concomitant with increased pyroptosis. Restoration of STX4 expression or suppression of pyroptosis activation protects against the decline in both mass and thermogenic activity in the aged and Ucp1-STX4KO mice. Mechanistically, STX4 deficiency reduces oxidative phosphorylation, glucose uptake, and glycolysis leading to reduced ATP levels, a known triggering signal for pyroptosis. Together, these data demonstrate an understanding of rapid brown adipocyte involution and that physiologic aging and thermogenic dysfunction result from pyroptotic signaling activation.

Molecular genetic foundation of a sex-linked tailless trait in Hongshan chicken by whole genome data analysis.

As a Chinese local chicken breed, Hongshan chickens have 2 kinds of tail feather phenotypes, normal and taillessness. Our previous studies showed that taillessness was a sex-linked dominant trait. Abnormal development of the tail vertebrae could be explained this phenomenon in some chicken breeds. However, the number of caudal vertebrae in rumpless Hongshan chickens was normal, so rumplessness in Hongshan chicken was not related to the development of the caudal vertebrae. Afterwards, we found that rumplessness in Hongshan was due to abnormal development of tail feather rather than abnormal development of caudal vertebrae. In order to understand the genetic foundation of the rumplessness of Hongshan chickens, we compared and reanalyzed 2 sets of data in normal and rumpless Hongshan chickens from our previous studies. By joint analysis of genome-wide selection signature analysis and genome-wide association approach, we found that 1 overlapping gene (EDIL3) and 16 peak genes (ENSGALG00000051843, ENSGALG00000053498, ENSGALG00000054800, KIF27, PTPRD, ENSGALG00000047579, ENSGALG00000041052, ARHGEF28, CAMK4, SERINC5, ENSGALG00000050776, ERCC8, MCC, ADAMTS19, ENSGALG00000053322, CHRNA8) located on the Z chromosome was associated with the rumpless trait. The results of this study furtherly revealed the molecular mechanism of the rumpless trait in Hongshan chickens, and identified the candidate genes associated with this trait. Our results will help to improve the shape of chicken tail feathers and to rise individual economic value in some specific market in China.