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Summary: The relation between hepatitis B virus (HBV) infection and fatty liver has been addressed by several observational studies, but their results remain controversial. To date, no study has precisely investigated the association of current and past HBV infection with the risk of nonalcoholic fatty liver disease (NAFLD) in the Chinese population. Therefore, we conducted a hospital‐based case‐control study in southwestern China to clarify this issue. A total of 631 newly ultrasound‐diagnosed NAFLD cases and 2357 controls were selected from 123 243 consecutive patients admitted to a tertiary‐care hospital between January 2015 and December 2016. Multivariate logistic regression was employed to calculate adjusted odds ratios (ORs) and 95% confidence intervals (CIs). A propensity score was developed for adjustment and matching. Subgroup analysis was conducted to identify potential effect modifiers. Current and past HBV infection had an overall prevalence of 9.7% and 55.2%, respectively. In the fully adjusted model, current HBV infection was associated with a decreased risk of NAFLD (OR 0.64; 95% CI 0.42‐0.95). A similar inverse association was observed in both propensity‐score‐adjusted (OR 0.58; 95% CI 0.40‐0.86) and propensity‐score‐matched analyses (OR 0.61; 95% CI 0.40‐0.92).The inverse association was stronger in patients with hypertension than in those without (Pinteraction = .018).No significant association between past HBV infection and NAFLD risk was found. In conclusion, current but not past HBV infection is associated with a decreased risk of NAFLD in the Chinese population. The corresponding biological mechanisms remain to be elucidated. [ABSTRACT FROM AUTHOR]

Abstract: Aim: This study aimed to analyse the potential significance of metastasis to the inferior mesenteric artery lymph node (IMA‐LN) in patients with malignancy of the left colon and rectum. Method: A retrospective analysis of a cohort of 890 patients collected prospectively who underwent radical resection of a primary tumour of the descending colon, sigmoid colon and rectum in our department from 1 January 2009 to 31 December 2015 was performed. Patients were divided into an IMA‐LN metastasis (IMA‐LN (+)) group (n = 51) and a non IMA‐LN metastasis (IMA‐LN (‐)) group (n = 839). A total of 801 patients were followed by a designated member of the study staff. Clinical features, pathological characteristics, recurrence patterns and survival rates were compared between the two groups. Results: In the IMA‐LN (+) group, the risk ratio of overall recurrence and tumour related death was 7.786 (95% CI 4.142–14.637) and 7.756 (95% CI 4.142–14.525) respectively. Significant differences were found in overall survival (log‐rank: χ2 = 69.06, P < 0.0001) and disease‐free survival (log‐rank: χ2 = 69.06, P < 0.0001) between the two groups. Furthermore, there were significant differences in overall survival (log‐rank: χ2 = 18.47, P < 0.0001) and disease‐free survival (log‐rank: χ2 = 16.99, P < 0.0001) between the IMA‐LN (−) and IMA‐LN (+) subgroups of patients with Stage N2 disease. Multivariate survival analysis indicated that IMA‐LN (+) was an independent risk factor of poor prognosis. There was no difference in the prognosis between high tie and low tie with IMA‐LN dissection. Conclusion: Inferior mesenteric artery lymph node metastasis was an independent predictive factor for high systemic recurrence. Low ligation of the IMA with IMA‐LN dissection was not inferior to high ligation. [ABSTRACT FROM AUTHOR]

Peptidoglycan is the major bacterial component recognized by the insect immune system. Peptidoglycan recognition proteins (PGRPs) are a family of patternrecognition receptors that recognize peptidoglycans and modulate innate immune responses. Some PGRPs retain N-acetylmuramoyl-L-alanine amidase (Enzyme Commission number: 3.5.1.28) activity to hydrolyse bacterial peptidoglycans. Others have lost the enzymatic activity and work only as immune receptors. They are all important modulators for innate immunity. Here, we report the cloning and functional analysis of PGRP-S4, a short-form PGRP from the domesticated silkworm, Bombyx mori. The PGRP-S4 gene encodes a protein of 199 amino acids with a signal peptide and a PGRP domain. PGRP-S4 was expressed in the fat body, haemocytes and midgut. Its expression level was significantly induced by bacterial challenges in the midgut. The recombinant PGRP-S4 bound bacteria and different peptidoglycans. In addition, it inhibited bacterial growth and hydrolysed an Escherichia coli peptidoglycan in the presence of Zn2+. Scanning electron microscopy showed that PGRP-S4 disrupted the bacterial cell surface. PGRP-S4 further increased prophenoloxidase activation caused by peptidoglycans. Taken together, our data suggest that B. mori PGRP-S4 has multiple functions in immunity. [ABSTRACT FROM AUTHOR]

A broadband left-handed parallel-line microstrip coupler is implemented by both electromagnetic simulation and actual fabrication. The circuit dimensions are smaller and more compact than those in previous studies and a thinner Duroid substrate of thickness h = 0.635 mm is used. Parametric studies were performed using IE3D, and fabrication was done via a Quick Circuit 7000 prototyping machine. The network-analyser measurements indicate broad bandwidth coupling in the 6.5–7.7-Ghz region. © 2005 Wiley Periodicals, Inc. Microwave Opt Technol Lett 45: 255–258, 2005; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.20788 [ABSTRACT FROM AUTHOR]

The nonlinear response of a high-temperature superconductor hairpin-comb filter in a perpendicular dc magnetic field was examined through measurement of its insertion loss and center frequency. The effect of the applied field on the insertion loss at low field regime is small, and increases gradually with respect to the field. A hysteretic effect as well as a linear relationship of the center frequency and the applied dc magnetic field were also observed. ©1999 John Wiley & Sons, Inc. Microwave Opt Technol Lett 22: 192–194, 1999. [ABSTRACT FROM AUTHOR]

Aim: To ascertain the connection between normal-range urinary albumin-to-creatinine ratio (UACR) and all-cause mortality (ACM) among diabetic adults with preserved eGFR., Methods: We used data from the 2003-2018 National Health and Nutrition Examination Survey. Nationally representative cross-sectional survey data linked with mortality outcomes from the National Death Index. Restricted cubic spline curves (RCS) and multivariable Cox regression models alongside subgroup analyses were utilised for estimating hazard ratios (HRs) and 95% confidence intervals (Cls) for UACR-ACM interplay, adjusting for demographic, socioeconomic, biochemical, medication and medical history factors. The UACR's predictive accuracy for survival outcomes was determined through receiver operating characteristic analysis., Results: The RCS regression analysis showcased that there was no significant evidence to support a nonlinear relationship between normal-range UACR and ACM (p = 0.080 for nonlinearity) in participants with diabetes mellitus (DM). In the model 2 adjusted for multiple confounding variables, the HR for ACM was 1.22 (95% CI, 1.06-1.40) per 10 mg/g raise in continuous UACR and 1.50 (95%CI, 1.18-1.91) for the high UACR tertile compared to the low. Kaplan-Meier analysis showed significantly lower survival rates in the medium and high UACR groups (p < 0.001). Subgroup analysis manifested a significant UACR-body mass index (BMI) interaction (p = 0.033 for interaction)., Conclusions: In DM adults without overt kidney dysfunction, elevated normal-range UACR was independently related to escalated ACM, particularly in those with normal BMI. To conclude, we underscore the significance of early risk assessment in DM patients with normal-range albuminuria, even without overt kidney dysfunction., (© 2025 The Author(s). Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.)

The role of KIAA0040 role in glioma development is not yet understood despite its connection to nervous system diseases. In this study, KIAA0040 expression levels were evaluated using qRT-PCR, WB and IHC, and functional assays were conducted to assess its impact on glioma progression, along with animal experiments. Moreover, WB was used to examine the impact of KIAA0040 on the JAK2/STAT3 signalling pathway. Our study found that KIAA0040 was increased in glioma and linked to tumour grade and poor clinical outcomes, serving as an independent prognostic factor. Functional assays showed that KIAA0040 enhances glioma growth, migration and invasion by activating the JAK2/STAT3 pathway. Of course, KIAA0040 enhances glioma growth by preventing tumour cell death and promoting cell cycle advancement. Our findings suggest that targeting KIAA0040 could be an effective treatment for glioma due to its role in promoting aggressive tumour behaviour and poor prognosis., (© 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Background: Alzheimer's disease (AD) is a neurodegenerative disorder distinguished by a swift cognitive deterioration accompanied by distinctive pathological hallmarks such as extracellular Aβ (β-amyloid) peptides, neuronal neurofibrillary tangles (NFTs), sustained neuroinflammation, and synaptic degeneration. The elevated frequency of AD cases and its proclivity to manifest at a younger age present a pressing challenge in the quest for novel therapeutic interventions. Numerous investigations have substantiated the involvement of C/EBPβ in the progression of AD pathology, thus indicating its potential as a therapeutic target for AD treatment., Aims: Several studies have demonstrated an elevation in the expression level of C/EBPβ among individuals afflicted with AD. Consequently, this review predominantly delves into the association between C/EBPβ expression and the pathological progression of Alzheimer's disease, elucidating its underlying molecular mechanism, and pointing out the possibility that C/EBPβ can be a new therapeutic target for AD., Methods: A systematic literature search was performed across multiple databases, including PubMed, Google Scholar, and so on, utilizing predetermined keywords and MeSH terms, without temporal constraints. The inclusion criteria encompassed diverse study designs, such as experimental, case-control, and cohort studies, restricted to publications in the English language, while conference abstracts and unpublished sources were excluded., Results: Overexpression of C/EBPβ exacerbates the pathological features of AD, primarily by promoting neuroinflammation and mediating the transcriptional regulation of key molecular pathways, including δ-secretase, apolipoprotein E4 (APOE4), acidic leucine-rich nuclear phosphoprotein-32A (ANP32A), transient receptor potential channel 1 (TRPC1), and Forkhead BoxO (FOXO)., Discussion: The correlation between overexpression of C/EBPβ and the pathological development of AD, along with its molecular mechanisms, is evident. Investigating the pathways through which C/EBPβ regulates the development of AD reveals numerous multiple vicious cycle pathways exacerbating the pathological progression of the disease. Furthermore, the exacerbation of pathological progression due to C/EBPβ overexpression and its molecular mechanism is not limited to AD but also extends to other neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and multiple sclerosis (MS)., Conclusion: The overexpression of C/EBPβ accelerates the irreversible progression of AD pathophysiology. Additionally, C/EBPβ plays a crucial role in mediating multiple pathways linked to AD pathology, some of which engender vicious cycles, leading to the establishment of feedback mechanisms. To sum up, targeting C/EBPβ could hold promise as a therapeutic strategy not only for AD but also for other degenerative diseases., (© 2024 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)

Pseudomonas aeruginosa is an important opportunistic human pathogen, which raises a worldwide concern for its increasing resistance. Nonthermal plasma, which is also called cold atmospheric plasma (CAP), is an alternative therapeutic approach for clinical infectious diseases. However, the bacterial factors that affect CAP treatment remain unclear. The sterilization effect of a portable CAP device on different P. aeruginosa strains was investigated in this study. Results revealed that CAP can directly or indirectly kill P. aeruginosa in a time-dependent manner. Scanning electron microscopy and transmission electron microscope showed negligible surface changes between CAP-treated and untreated P. aeruginosa cells. However, cell leakage occurred during the CAP process with increased bacterial lactate dehydrogenase release. More importantly, pigmentation of the P. aeruginosa culture was remarkably reduced after CAP treatment. Further mechanical exploration was performed by utilizing mutants with loss of functional genes involved in pyocyanin biosynthesis, including P. aeruginosa PAO1 strain-derived phzA1::Tn, phzA2::Tn, ΔphzA1/ΔphzA2, phzM::Tn and phzS::Tn, as well as corresponding gene deletion mutants based on clinical PA1 isolate. The results indicated that pyocyanin and its intermediate 5-methyl phenazine-1-carboxylic acid (5-Me-PCA) play important roles in P. aeruginosa resistance to CAP treatment. The unique enzymes, such as PhzM in the pyocyanin biosynthetic pathway, could be novel targets for the therapeutic strategy design to control the growing P. aeruginosa infections., (© 2022 The Authors. Microbial Biotechnology published by Society for Applied Microbiology and John Wiley & Sons Ltd.)

Background: Helicobacter pylori (H. pylori) is a carcinogenic factor for gastric cancer. Our previous study demonstrated that H. pylori decreased the expression of micro-RNA (miRNA)-30a to promote the tumorigenesis of gastric cancer. However, the upstream regulatory molecules of miR-30a are not well elucidated. In this study, we found the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) may sponge miR-30a to regulate COX-2/BCL9 pathway., Methods: The expression of NEAT1 was detected in gastric cancer tissues and tumor-adjacent tissues by fluorescence in situ hybridization (FISH) analysis and RT-qPCR. LncRNA-miRNA interaction networks were constructed using the RNAhybrid and starBase v.2.0. and then validated using a dual-luciferase reporter assay. The effects of NEAT1 dysregulation on the proliferative, migratory, and invasive abilities of H. pylori filtrate-infected gastric cancer cells were observed by cell counting kit-8 (CCK-8), colony formation, wound healing test, and transwell assays. Western blot and RT-qPCR were performed to detect protein and RNA expression. Immunohistochemistry (IHC) was carried out to analyze the localization and expression of COX-2 and BCL9., Results: FISH and RT-qPCR demonstrated that the expression of NEAT1 was up-regulated in gastric cancer tissues, especially in H. pylori-infected gastric cancer tissues, and the expression of NEAT1 was negatively correlated with miR-30a (miR-30a-3p and miR-30a-5p). The upregulation of NEAT1 enhanced proliferation, migration, and invasion of H. pylori filtrate-infected gastric cancer cells, while the downregulation of NEAT1 decreased these abilities, and miR-30a could reverse the effect of NEAT1 on these abilities. The dual-luciferase reporter assay identified that NEAT1 directly targeted miR-30a (miR-30a-3p and miR-30a-5p). Because miR-30a (miR-30a-3p and miR-30a-5p) negatively regulates the expression of downstream COX-2 and BCL9, NEAT1 was identified to upregulate indirectly the expression of COX-2 and BCL9. IHC showed that the expression of COX-2 and BCL9 was increased in H. pylori gastric cancer tissues., Conclusion: The study demonstrated that lncRNA NEAT1 may act as a promoter of tumorigenesis in H. pylori gastric cancer, by sponging miR-30a (miR-30a-3p and miR-30a-5p) to regulate the COX-2/BCL9 pathway., (© 2021 John Wiley & Sons Ltd.)

Metformin, a drug widely used for treating diabetes, can prolong the lifespan in several species. Metformin also has the promise to slow down age-related cognitive impairment. However, metformin's therapeutic use as an anti-aging drug is yet to be accepted because of conflicting animal and human studies results. We examined the effects of metformin treatment in late middle age on cognitive function in old age. Eighteen-month-old male C57BL6/J mice received metformin or no treatment for 10 weeks. A series of behavioral tests revealed improved cognitive function in animals that received metformin. Such findings were evident from a better ability for pattern separation, object location, and recognition memory function. Quantification of microglia revealed that metformin treatment reduced the incidence of pathological microglial clusters with alternative activation of microglia into an M2 phenotype, displaying highly ramified processes in the hippocampus. Metformin treatment also seemed to reduce astrocyte hypertrophy. Additional analysis demonstrated that metformin treatment in late middle age increased adenosine monophosphate-activated protein kinase activation, reduced proinflammatory cytokine levels, and the mammalian target of rapamycin signaling, and enhanced autophagy in the hippocampus. However, metformin treatment did not alter neurogenesis or synapses in the hippocampus, implying that improved cognitive function with metformin did not involve enhanced neurogenesis or neosynaptogenesis. The results provide new evidence that metformin treatment commencing in late middle age has promise for improving cognitive function in old age. Modulation of microglia, proinflammatory cytokines, and autophagy appear to be the mechanisms by which metformin facilitated functional benefits in the aged brain., (© 2021 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.)

The level of response (LR) to alcohol as measured with the Self-Report of the Effects of Alcohol Retrospective Questionnaire (SRE) evaluates the number of standard drinks usually required for up to four effects. The need for a higher number of drinks for effects is genetically influenced and predicts higher risks for heavy drinking and alcohol problems. We conducted genome-wide association study (GWAS) in the African-American (COGA-AA, N = 1527 from 309 families) and European-American (COGA-EA, N = 4723 from 956 families) subsamples of the Collaborative Studies on the Genetics of Alcoholism (COGA) for two SRE scores: SRE-T (average of first five times of drinking, the period of heaviest drinking, and the most recent 3 months of consumption) and SRE-5 (the first five times of drinking). We then meta-analyzed the two COGA subsamples (COGA-AA + EA). Both SRE-T and SRE-5 were modestly heritable (h 2 : 21%-31%) and genetically correlated with alcohol dependence (AD) and DSM-IV AD criterion count (r g : 0.35-0.76). Genome-wide significant associations were observed (SRE-T: chromosomes 6, rs140154945, COGA-EA P = 3.30E-08 and 11, rs10647170, COGA-AA+EA P = 3.53E-09; SRE-5: chromosome13, rs4770359, COGA-AA P = 2.92E-08). Chromosome 11 was replicated in an EA dataset from the National Institute on Alcohol Abuse and Alcoholism intramural program. In silico functional analyses and RNA expression analyses suggest that the chromosome 6 locus is an eQTL for KIF25. Polygenic risk scores derived using the COGA SRE-T and SRE-5 GWAS predicted 0.47% to 2.48% of variances in AD and DSM-IV AD criterion count in independent datasets. This study highlights the genetic contribution of alcohol response phenotypes to the etiology of alcohol use disorders., (© 2019 Society for the Study of Addiction.)

The most important task of the olfactory system is to generate a precise representation of odour information under different brain and behavioural states. As the first processing stage in the olfactory system and a crucial hub, the olfactory bulb plays a key role in the neural representation of odours, encoding odour identity, intensity and timing. Although the neural circuits and coding strategies used by the olfactory bulb for odour representation were initially identified in anaesthetized animals, a large number of recent studies focused on neural representation of odorants in the olfactory bulb in awake behaving animals. In this review, we discuss these recent findings, covering (a) the neural circuits for odour representation both within the olfactory bulb and the functional connections between the olfactory bulb and the higher order processing centres; (b) how related factors such as sniffing affect and shape the representation; (c) how the representation changes under different states; and (d) recent progress on the processing of temporal aspects of odour presentation in awake, behaving rodents. We highlight discussion of the current views and emerging proposals on the neural representation of odorants in the olfactory bulb., (© 2019 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)

The global epidemic features of enteric fever have changed greatly in recent years. The incidence of enteric fever caused by Salmonella enterica serovar Paratyphi A has progressively increased. In some areas of Asia, infections with S. Paratyphi A have exceeded those with S. Typhi, resulting in S. Paratyphi A becoming the main causative agent of enteric fever. However, two currently licensed typhoid vaccines do not confer adequate cross-protection against S. Paratyphi A infection. Therefore, development of specific vaccines against enteric fever caused by S. Paratyphi A is urgently needed. In the present study, an attenuated strain was constructed by double deletion of the htrA and yncD genes in a wild-type strain of S. Paratyphi A and its safety and immunogenicity assessed. In a mouse model, the 50% lethal dose of the double deletion mutant and the wild-type strain were 3.0 × 10(8) CFU and 1.9 × 10(3) CFU, respectively, suggesting that the double deletion resulted in remarkably decreased bacterial virulence. Bacterial colonization of the double deletion mutant in the livers and spleens of infected mice was strikingly less than that of the wild-type strain. A single nasal administration of the attenuated vaccine candidate elicited high concentrations of anti-LPS and anti-flagellin IgG in a mouse model and protected immunized mice against lethal challenge with the wild-type strain. Thus, our findings suggest that the attenuated vaccine strain is a promising candidate worthy of further evaluation both as a human enteric fever vaccine and as a vaccine delivery vector for heterologous antigens., (© 2015 The Societies and Wiley Publishing Asia Pty Ltd.)

Background: The density of Helicobacter pylori is thought to correlate with the degree of inflammation and thus indirectly with the outcome of the infection. Rapid quantitative assays of H. pylori in gastric or duodenal mucosa are lacking. The aim was to develop quantitative assays using the polymerase chain reaction to assess the quantity of H. pylori in the gastric mucosa., Methods: Competitive PCR was based on coamplification of a segment of the ureC sequence and an internal control using a single set of primers. PCR products were quantified colorimetrically by an enzyme-linked immunosorbent assay and compared with known quantities of the internal control standard added to the PCR reaction. The highly sensitive, noncompetitive PCR assay does not use coamplification and measures the amplified DNA sequence using a flash-type luminescent tag and a specific probe. The mouse infected model using H. pylori strain SS-1 was used to develop the assays., Results: Quantification of H. pylori using either the competitive or noncompetitive PCR was reliable, highly sensitive and specific., Conclusions: The ability to rapidly quantitate H. pylori from gastric mucosa should be useful to investigate the role of H. pylori density and infection outcome, as well as to monitor the effectiveness of antibiotic treatment or vaccines against H. pylori.

Background: A murine model for Helicobacter pylori infection could facilitate vaccine development. This study was designed to determine the effect of various conditions of dose, frequency of administration, and fasting on H. pylori infection of mice., Materials and Methods: Balb/c and C3H/HeN mice were inoculated orogastrically with clinical isolates of H. pylori grown in liquid culture. At 2-week intervals, the stomachs were removed for secondary culture on horse blood agar and for histological analysis. H. pylori from secondary cultures or homogenized stomach tissue from infected mice was inoculated a second time in naïve animals., Results: H. pylori was cultured with high frequency only from the stomachs of C3H/HeN mice. Fasting the mice and increasing the number of organisms inoculated did not increase the rate of infection. Histological analysis detected no inflammation, but mucus depletion and erosion were present in the stomachs of C3H/HeN mice. H. pylori organisms were not observed. Secondary cultures of H. pylori or homogenized infected stomach tissue did not cause infection when inoculated in naïve mice., Conclusions: Clinical isolates of H. pylori transiently infect C3H/HeN mice. This murine model is suitable for testing oral vaccines. Effective vaccination against H. pylori could prevent transient infection and reduce subsequent gastritis.