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Background Lipid accumulation product (LAP) and cardiometabolic index (CMI) are two novel obesity-related indexes associated with enhancing metabolic disease (MD) risk. Current evidences suggest that the differences in sex hormones and regional fat distribution in both sexes are directly correlated with MD and nonalcoholic fatty liver disease (NAFLD) risk. Hence, NAFLD incidences reflect sex differences. Herein, we examined the accuracy of LAP and CMI in diagnosing NAFLD in both sexes. Methods Overall, 14,407 subjects, who underwent health check-up in the northeastern China, were enrolled in this study, and their corresponding LAP and CMI were calculated. Abdominal ultrasonography was employed for NAFLD diagnosis. Multivariate analyses were analyzed potential correlations between LAP and/or CMI and NAFLD. Odds ratios (ORs) and 95% confidence intervals (CIs) were evaluated. Receiver operating characteristic curve analyses was executed for the exploration of the diagnostic accuracies. Areas under the curves (AUCs) with 95%CIs were calculated. Results NAFLD prevalence increased with elevated quartiles of LAP and CMI in both sexes. In multivariate logistic regression analyses, LAP and CM expressed as continuous variables or quartiles, significantly correlated with NAFLD. The ORs for the top versus bottom quartile of LAP and CMI for NAFLD were 13.183 (95%CI = 8.512–20.417) and 8.662 (95%CI = 6.371–11.778) in women and 7.544 (95%CI = 5.748–9.902) and 5.400 (95%CI = 4.297–6.786) in men. LAP and CMI exhibited larger AUCs, compared to other obesity-related indexes in terms of discriminating NAFLD. The AUCs of LAP and CMI were 0.860 (95%CI = 0.852–0.867) and 0.833 (95%CI = 0.825–0.842) in women and 0.816 (95%CI = 0.806–0.825) and 0.779 (95%CI = 0.769–0.789) in men. Conclusions LAP and CMI are convenient indexes for the screening and quantification of NAFLD within a Chinese adult population. Their associations with NAFLD are substantially greater in women than men.

Objective The aim of this study was to evaluate the safety and efficacy of biological mesh in laparoscopic intraperitoneal onlay mesh plus (IPOM plus) repair of abdominal wall hernias. Methods From January 2021 to January 2022, the clinical data of 30 patients with various types of abdominal wall hernias were analyzed. All patients underwent laparoscopic IPOM plus repair, during which the hernia defect was closed with non-absorbable sutures prior to placement of the biological mesh. Preoperative general information, as well as complications, adverse events, and hospitalization costs, were monitored and analyzed. Results In this study, the patients’ ages ranged from 28 to 65 years, and the length of their hospital stays ranged from 4 to 10 days. The surgical method employed was laparoscopic IPOM plus repair, with operation times ranging from 50 to 80 min. Follow-up evaluations were conducted at 7 days, 1 month, 3 months, 6 months, 1 year, and 2 years post-operation. No patients were lost to follow-up during this period. Additionally, there were no cases of abdominal hernia recurrence, intestinal fistula, intestinal obstruction, wound infection, mesh infection, chronic pain, or foreign body sensation. One patient developed seroma, which was cured via drainage. The patients’ hospitalization costs ranged from $4,211 to $8,307 USD. Conclusion The use of biological mesh for laparoscopic IPOM plus repair with non-absorbable suture closure of the hernia defect is both effective and safe, making it a valuable option for clinical application, especially for young patients.

Although the neurobiological basis for autism spectrum disorder (ASD) has not yet been fully clarified, converging lines of evidence implicated a role of neuroinflammation in the etiological pathway of this disorder. The present article provided a systematic review of publications regarding the involvement of different components of neuroinflammation in postmortem brain samples of subjects diagnosed with ASD. A systematic search of PubMed, Embase, and Web of Science was conducted, which was supplemented by manual searching of reference lists of included articles. The screening for study and extraction of data were conducted by two independent authors after reviewing the abstract and full text. Of 356 articles identified in the literature search, 27 articles comprising 685 subjects (ASD = 313, controls = 351, schizophrenia = 10, epilepsy = 11) covering 19 brain regions met the eligibility criteria for this review. The search yielded 11 studies that estimated astrocyte-related changes, 8 studies that reported microglia-related changes, 2 studies that evaluated oligodendrocyte-related changes, 3 studies that examined changes in glial cells without differentiating cell types, 6 studies that evaluated the levels of cytokines and chemokines, and 7 studies that measured other inflammatory parameters in postmortem brain samples of subjects with ASD compared with controls. Although a few studies noted a lack of changes in neuroinflammatory markers in postmortem brain samples of ASD subjects, the majority of studies supported the presence of neuroinflammation in the neurobiological pattern of ASD as shown by activation of astrocytes and microglia together with abnormal levels of cytokines and chemokines.

The non-structural (NS) NS4A protein in flaviviruses has three predicted transmembrane domains, is critical for virulence and participates in membrane morphogenesis. In Dengue virus (DENV), both hydrophylic N-terminal tail and its first transmembrane domain participate in the formation of oligomers which are important for pathogenicity. However, the relative importance of the N-terminal domain in oligomerization has been under debate. In particular, since in the absence of detergent or lipids, this domain (residues 1–48) in both DENV and Zika virus (ZIKV) NS4A, was found to be disordered. Recently, however, we reported preliminary data that showed that peptide ZIKV NS4A 4–58 adopts a defined secondary structure in aqueous solution and forms oligomers, signaling its importance for full length NS4A oligomerization. Herein we have performed detailed analytical ultracentrifugation experiments to further characterize the oligomerization of this peptide and also a shorter variant (residues 4–44). In both cases, sedimentation velocity produced a single species with concentration-dependent sedimentation coefficient, consistent with a fast equilibrium between at least two species. Combining sedimentation velocity and equilibrium experiments, data is best fitted to a monomer–dimer–trimer equilibrium. Possible models of NS4A oligomers obtained with AlphaFold-2 predict the stabilizing role for residues in this N-terminal domain, such as Arg20, Asn27, Ala44 and Glu50, all at highly conserved positions in flavivirus NS4A proteins. Our results are thus consistent with N-terminal domain interactions acting as one of the driving forces for NS4A homo-oligomerization.

Oligodendroglia support axon survival and function through mechanisms independent of myelination, and their dysfunction leads to axon degeneration in several diseases. The cause of this degeneration has not been determined, but lack of energy metabolites such as glucose or lactate has been proposed. Lactate is transported exclusively by monocarboxylate transporters, and changes to these transporters alter lactate production and use. Here we show that the most abundant lactate transporter in the central nervous system, monocarboxylate transporter 1 (MCT1, also known as SLC16A1), is highly enriched within oligodendroglia and that disruption of this transporter produces axon damage and neuron loss in animal and cell culture models. In addition, this same transporter is reduced in patients with, and in mouse models of, amyotrophic lateral sclerosis, suggesting a role for oligodendroglial MCT1 in pathogenesis. The role of oligodendroglia in axon function and neuron survival has been elusive; this study defines a new fundamental mechanism by which oligodendroglia support neurons and axons. Disruption of the lactate transporter monocarboxylate transporter 1 (MCT1), which is highly enriched within oligodendroglia and reduced in patients with amyotrophic lateral sclerosis (ALS), causes axon damage and neurodegeneration in animal and cell culture models, suggesting a fundamental role for MCT1 in metabolic support of axons and ALS pathogenesis. Oligodendroglial cell function Oligodendroglial dysfunction leads to axon degeneration in several human diseases. These cells support axon survival and function in part by myelination, as well as by other means that are less well defined. Myelinated axons can use lactate when energy-deprived. This study shows that oligodendrocytes express monocarboxylate transporter 1 (MCT1), which transports lactate, and therefore seems to be the prime metabolic supplier of lactate to axons and neurons. Downregulation of MCT1 in oligodendroglia results in axon pathology and neuron loss. Moreover, MCT1 is downregulated in affected regions in patients with amyotrophic lateral sclerosis (ALS) and in mouse models of ALS. Thus MCT1-regulated lactate export from oligodendroglia is crucial for local energy supply to axons, and disruption of this transport leads to axon dysfunction and, ultimately, neuron degeneration.

The combination of astrocyte, oligodendroglial, and neuronal pathology likely limit remyelination through diverse mechanisms: (i) inhibition of oligodendroglial differentiation; (ii) inhibition of oligodendrocyte progenitor migration due to blood-brain barrier injury; and (iii) impaired myelin wrapping secondary to irreversible axonal destruction (Weber et al., 2018). Remyelination failure results from impaired recruitment of OPCs into the lesion site and inhibition of OPC differentiation into new mature remyelinating oligodendrocytes. [...]current approaches to enhance remyelination have been focused on promoting the recruitment or stimulating the proliferation and differentiation of OPCs (Plemel et al., 2017). Transcriptomics and functional assays implicate that microglia function in remyelination likely involves phagocytosis of myelin debris, the secretion of growth factors and remodeling of the extracellular matrix to recruit OPCs and promote oligodendrocyte regeneration (Lloyd et al., 2017). [...]microglia activation may play an important role in advancing oligodendrocytes to a mature myelinating stage.

Objective The purpose of this study was to investigate the associations between mobile phone dependency, bedtime procrastination, FoMO, and sleep quality among college students during the COVID-19 outbreak. Specifically, we examined whether bedtime procrastination and FoMO mediate the relationship between mobile phone dependency and sleep quality. Methods A total of 881 college students completed an online survey in May 2022 in Shanghai, China. Mobile Phone Involvement Questionnaire, Bedtime Procrastination Scale, Fear of Missing Out Scale and Pittsburgh Sleep Quality Index were used to assess mobile phone dependency, bedtime procrastination, fear of missing out, and sleep quality, respectively. Multiple linear regression and mediation analysis were conducted. Results The correlation analyses indicated mobile phone dependency was positively associated with fear of missing out, bedtime procrastination, and poor sleep quality among college students. The structural equation modeling analyses revealed that mobile phone dependency had significant indirect effects on sleep quality through bedtime procrastination (indirect effect: 0.030, 95%CI: 0.022–0.041) and fear of missing out (indirect effect: 0.013, 95%CI: 0.003–0.023). Conclusion The findings indicated that bedtime procrastination and fear of missing out are mediators mediating the relationship between mobile phone dependency with sleep quality. Bedtime procrastination and fear of missing out should be considered as potential intervention targets for reducing mobile phone dependency and improving sleep quality in college students.

The Autonomous Underwater Vehicle (AUV) is usually equipped with multiple sensors, such as an inertial navigation system (INS), ultra-short baseline system (USBL), and Doppler velocity log (DVL), to achieve autonomous navigation. Multi-source information fusion is the key to realizing high-precision underwater navigation and positioning. To solve the problem, a fusion scheme based on factor graph optimization (FGO) is proposed. Due to multiple iterations and joint optimization of historical data, FGO could usually show a better performance than the traditional Kalman filter. In addition, considering that USBL and DVL are usually heavily influenced by the environment, outliers are often present. A robust integrated navigation algorithm based on a maximum correntropy criterion and FGO scheme is proposed. The proposed algorithm solves the problem of multi-sensor fusion and non-Gaussian noise. Numerical simulations and field tests demonstrate that the proposed FGO scheme shows a better performance and robustness than the traditional Kalman filter. Compared with the traditional Kalman filtering, the positioning accuracy is improved by 5.3%, 9.1%, and 5.1% in the east, north, and height directions. It can realize a more accurate navigation and positioning of underwater multi-sensors.

Angle-of-arrival (AOA) measurements are often used in underwater acoustical localization. Different from the traditional AOA model based on azimuth and elevation measurements, the AOA model studied in this paper uses bearing measurements. It is also often used in the Ultra-Short Baseline system (USBL). However, traditional acoustical localization needs additional range information. If the range information is unavailable, the closed-form solution is difficult to obtain only with bearing measurements. Thus, a localization closed-form solution using only bearing measurements is explored in this article. A pseudo-linear measurement model between the source position and the bearing measurements is derived, and considering the nonlinear relationship of the parameters, a weighted least-squares optimization equation based on multiple constraints is established. Different from the traditional two-step least-squares method, the semidefinite programming (SDP) method is designed to obtain the initial solution, and then a bias compensation method is proposed to further minimize localization errors based on the SDP result. Numerical simulations show that the performance of the proposed method can achieve Cramer–Rao lower bound (CRLB) accuracy. The field test also proves that the proposed method can locate the source position without range measurements and obtain the highest positioning accuracy.

Allergic rhinitis is a global illness that puzzles many researchers. Most patients with allergic rhinitis also have lower airway hyperresponsiveness, and an allergic rhinitis attack can increase lower airway hyperresponsiveness. However, the mechanism of the effect of allergic rhinitis on the lower airways is still unclear. In this paper, the effects of allergic rhinitis on the lower airways are studied in terms of epidemiology, anatomy, pathophysiology, nasal function loss, inflammation drainage, nasobronchial reflex, and whole-body circulatory flow to determine the mechanism involved and provide ideas for future diagnosis, treatment, and experiments.