Liuyang City Maternal and Child Health Hospital

Introduction: This study aimed to assess the association of Geriatric Nutritional Risk Index (GNRI) with cognitive function level and cognitive impairment risk among older adults with cardiometabolic disease using data from the National Health and Nutrition Examination Survey (NHANES). Methods: Using cross-sectional data from the NHANES, this research included 1,937 participants aged 60 years or older with at least one cardiometabolic disease (diabetes, hypertension, stroke, or congestive heart failure). Cognitive function was assessed using the CERAD tests, Animal Fluency Test (AFT), and Digit Symbol Substitution Test (DSST). Multivariable linear and logistic regression analyses were used to estimate the β coefficients and odds ratios (ORs) with 95% confidence intervals (CIs) for the associations of GNRI with cognitive function level and risk of cognitive impairment. Results: A total of 1937 participants aged≥60 years with cardiometabolic disease were included. The results showed that per 1-SD increase in GNRI was associated with increased cognitive function levels, including CERAD: Trial 1 (β=0.11, 95% CI: 0.03-0.19), CERAD: Trial 3 (β=0.12, 95% CI: 0.04-0.21), CERAD: Delayed Recall (β=0.21, 95% CI: 0.11-0.32), CERAD test (β=0.53, 95% CI: 0.23-0.82), and AFT (β=0.34, 95% CI: 0.11-0.57) scores. Restricted cubic splines showed significantly positive linear dose-response associations between GNRI and cognitive function. Compared to participants with the lowest quartile (Q1) of GNRI, those with the highest quartile (Q4) had a lower cognitive impairment risk (OR=0.59, 95% CI: 0.41-0.85). Discussion: Potential mechanisms underlying GNRI’s protective effect against cognitive impairment may involve the pleiotropic neuroprotection of albumin and body mass index-mediated brain structural changes. Conclusion: Higher GNRI is independently associated with better cognitive function and reduced risk of cognitive impairment in older adults with cardiometabolic diseases. To mitigate cognitive risk, implementing GNRI screening may identify high-risk older adults with cognitive impairment, prompting timely nutritional support that improves cognitive health and disease management.

BackgroundAsthma is a prevalent chronic respiratory, significantly impacting their quality of life. Omalizumab, an anti-IgE monoclonal antibody, was approved for children aged 6 to 11 years in 2016, but its safety and efficacy in this age group have not been thoroughly studied.MethodsWe conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) published before October 20, 2024, that evaluated the safety and efficacy of omalizumab in pediatric patients aged 6 to 11 years. The review adhered to the PRISMA guidelines and was registered with PROSPERO (CRD42024531092).ResultsOur systematic review and meta-analysis included 4 RCTs with a total of 1078 pediatric patients. Adverse events did not significantly increase with omalizumab compared to placebo. Omalizumab reduced asthma exacerbations (risk ratio (RR) 95% confidence interval (CI) = 0.60 [0.52,0.69], P < 0.01), particularly during the steroid reduction phase (RR 95%CI = 0.52 [0.43,0.64], P < 0.01). Omalizumab also decreased the need to inhaled corticosteroid (ICS) doses and increased the number of patients completely stopping ICS compared to placebo (RR 95%CI = 1.44 [1.10,1.88], P < 0.01). Improvements in pulmonary function indices were observed in the omalizumab group, and analysis of fractional exhaled nitric oxide (FeNO) levels indicated reduced airway inflammation.ConclusionThese results advocate for the use of omalizumab as an effective therapeutic option for children with allergic asthma aged 6–11 years, highlighting its potential to optimize asthma management and enhance clinical outcomes in this vulnerable age group. Further research is warranted to confirm these findings and explore long-term outcomes.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12887-026-06595-y.

Background:The THBS gene family plays key functions in various diseases; however, its specific roles in colorectal cancer (CRC) have not been systematically characterized.Methods:Multi-omics data and online databases were used to analyze the mRNA expression levels of the THBS gene family in CRC and their correlations with clinicopathological features and survival. This analysis identified THBS3 as a potential oncogene closely linked with CRC progression. Then, the relationship between THBS3 expression and the immune landscape was assessed. Single-cell RNA sequencing analyzed THBS3 distribution in CRC subtypes. Additionally, GO, KEGG, and GSEA enrichment analyses investigated the mechanisms of THBS3 in CRC. Molecular docking identified anticancer compounds with high affinity for THBS3. Lastly, in vitro experiments examined THBS3’s function in CRC.Results:THBS3 was significantly upregulated in CRC and correlated with poor prognosis. Elevated THBS3 correlated with increased infiltration of M2 macrophages and regulatory T cells (Treg cells), as well as higher expression of immune checkpoint molecules, suggesting its role in shaping an immunosuppressive microenvironment. THBS3 promoted CRC cell proliferation and metastasis, through activation of the PI3K-AKT and EMT pathways.Conclusion:THBS3 facilitates the progression of CRC and may serve as a novel prognostic biomarker and therapeutic target.

Hand rehabilitation exoskeletons represent a critical advancement in restoring motor function for patients with neurological impairments, offering quantifiable and repetitive training to address deficits caused by stroke, spinal cord injuries, or trauma. However, existing systems struggle to simultaneously integrate lightweight construction, multi-joint coordination, and multi-directional haptic feedback, limiting their clinical utility and user engagement. To bridge this gap, this study develops a multi-link underactuated finger exoskeleton using a single miniature geared motor with cascaded four-bar linkages to drive MCP, PIP, and DIP joints, coupled with orthogonally arranged Linear Resonant Actuators (LRAs) for directional tactile feedback. Kinematic analysis via closed-loop vector methods and SolidWorks Motion simulations validated natural flexion trajectories, while 3D-printed resin components achieved a total weight of 220 g. Key findings demonstrate: (1) MCP-PIP joint motion exhibits linear correlation <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">$\left(0-50^{\circ} \text{MCP} \rightarrow 72^{\circ} \text{PIP}\right)$</tex>; (2) MCP-DIP kinematics follow a nonlinear profile with peak DIP flexion preceding MCP; (3) the orthogonal LRA configuration enables spatially distinct vibrotactile cues; and (4) modular design accommodates anthropometric variations across all five fingers. This work uniquely converges underactuation, haptic feedback, and additive manufacturing to advance functional integration in rehabilitation robotics, offering a clinically viable solution that enhances training efficacy and patient immersion.

ObjectiveTo analyze and discuss the clinical characteristics of carbapenem-induced platelet abnormalities.MethodsThe databases of CNKI, Wanfang Data, Chinese VIP, Web of science, PubMed, Embase and Elsevier were searched (up to June 30,2025), and the case reports of carbapenem-induced platelet abnormalities were collected and descriptively analyzed.ResultsA total of 42 patients (21 males and 21 females) were included, with a median age of 64 years (range:0–96 years). Thrombocytosis was observed in 20 patients, while thrombocytopenia occurred in 22 patients. Platelet abnormality most often occurred in patients receiving meropenem (64.3%) followed by imipenem (26.2%). All cases occurred during carbapenem therapy. The median time to platelet count abnormality was 3 days (range 0.125–12), with 79.5% of cases occurring within one week. Specifically, the median time to carbapenem-induced thrombocytopenia was 2.5 days (range 0.125–9), while the median time to carbapenem-induced thrombocytosis was 3 days (range 3–12). The nadir of platelet count was reached at 5 days (range 1–10) after medication, with a median platelet count nadir of 21.5×109 /L (range 0–136). The peak of platelet count was reached at 8 days (range 3–18), with a median platelet count peak of 900×109 /L (range 570–1,440). Complications occurred in 10 thrombocytopenia cases, all of which were bleeding events. After discontinuation of the drug and symptomatic treatment, all cases showed significant improvement in platelet counts and resolution of complications, except for one patient who died from multiple organ dysfunction syndrome.ConclusionCarbapenem-induced platelet abnormalities appear to be more frequent than previously recognized, predominantly occurring within the first week of therapy. This potentially severe adverse drug reaction should be particularly considered in elderly patients receiving meropenem therapy.

BackgroundPrevious studies have shown an association between frailty and multimorbidity, but the underlying mechanisms are still unclear. Therefore, this study aimed to investigate the potential chain mediating roles of sleep quality and anxiety in the relationship between frailty and multimorbidity.MethodsThis cross-sectional study used data from the first follow-up of the Liyang cohort study on chronic diseases and risk factors monitoring in China (Liyang Study), which comprised 2874 participants aged ≥ 60 years from 17 health centres in Liyang City. Multimorbidity was defined based on 13 self-reported chronic conditions. A modified version of the frailty phenotype was used to assess frailty. Sleep quality and anxiety were assessed using the Pittsburgh Sleep Quality Index and the 7-item Generalized Anxiety Disorder Scale, respectively. Spearman correlation analysis was employed to examine the correlations between frailty, sleep quality, anxiety, and multimorbidity. A chain mediation analysis of sleep quality and anxiety on the relationship between frailty and multimorbidity was conducted using the SPSS PROCESS macro (Model 6).ResultsIn this study, significant correlations were observed between frailty, sleep quality, anxiety, and multimorbidity (P < 0.01). Frailty had a direct impact on multimorbidity (unstandardised coefficient [B] = 0.196, bootstrap 95% confidence interval [CI] = [0.146, 0.246]). The association was mediated by three important pathways. (1) Sleep quality contributes 26.53% of the total effect (B = 0.052, bootstrap 95% CI = [0.038, 0.068]). (2) Anxiety accounts for 20.92% of the total effect (B = 0.041, bootstrap 95% CI = [0.025, 0.060]). (3) Sleep quality and anxiety represent 5.10% of the total effect (B = 0.010, bootstrap 95% CI = [0.006, 0.015]). The overall mediation effect was 52.55%.ConclusionsFrailty was positively associated with multimorbidity, and sleep quality and anxiety were important mediators of the association between frailty and multimorbidity. Addressing frailty, enhancing sleep quality, and promoting a positive mood may help reduce multimorbidity and enhance the overall well-being of elderly individuals. This study could potentially contribute to the development of more effective strategies to prevent multimorbidity.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12877-025-06490-8.

BackgroundCongenital disorders of glycosylation (CDG) are a group of multi-systemic genetic disorders. Over 100 monogenic human diseases were known related with defects in glycosylation process. Defects of SSR4 gene lead to a rare X linked pattern of CDG which has been rarely reported.MethodWe reported a Chinese boy with developmental delay, microcephaly, and epileptic seizures. Whole exome sequencing and Sanger sequencing were performed in the family.ResultA novel maternal splice variant c.351+1del in SSR4 gene was identified by trio-exome sequencing, and confirmed by Sanger sequencing. The functional effect of the variant was further investigated by minigene. The minigene results showed three abnormal splice forms: (1) 1 bp deletion in 3′ end of exon 4; (2) 42 bp deletion in 3′ end of exon 4; (3) skipping of exon 4. All three forms resulted in truncated proteins. c.351+1del in SSR4 gene causes congenital disorder of glycosylation, type Iy, consisted with the proband's phenotype. Up to date, all of the pathogenic SSR4 gene variants were null variants. The most variants were reported in exon 4. Patients (within or between families) carrying the same variants exhibited phenotypic heterogeneity.ConclusionThe current study expanded the pathogenic variant spectrum of SSR4 gene and revealed the impact of c.351+1del on SSR4 splicing. Standardizing the transcript and naming conventions of variants were crucial for the study of SSR4 genotypes and phenotypes.

Background and objectiveThis study aimed to elucidate the role of insulin resistance in the progression from non-alcoholic fatty liver disease (NAFLD) to cardiovascular-kidney-metabolic (CKM) diseases, and to explore the potential influence of lifestyle factors.MethodsThis study included participants free of NAFLD and CKM diseases from the UK Biobank. Insulin resistance was assessed using the TyG index. CKM diseases include ischemic stroke (IS), ischemic heart disease (IHD), type 2 diabetes (T2D), and chronic kidney disease (CKD). Markov multi-state models were used to assess the associations between the TyG index and disease transitions.ResultsAmong 377,757 participants (median age 57 years), 4949 developed NAFLD over a median follow-up of 13.6 years. Of these, 12.65% progressed to T2D, 9.11% to IHD, 8.63% to CKD, and 4.61% to IS. Elevated TyG levels significantly accelerated transitions from NAFLD to first-onset CKM disease (HR = 1.25, 95% CI 1.05–1.49), double CKM disease (HR = 1.46, 95% CI 1.19–1.80), and triple CKM disease (HR = 1.81, 95% CI 1.28–2.55). Similar progression risk increases were observed for individual CKM components: T2D (HR = 1.41, 95% CI 1.11–1.78), CKD (HR = 1.37, 95% CI 1.08–1.75), and IS (HR = 1.70, 95% CI 1.27–2.27). A J-shaped dose–response relationship was identified. Transitions risk remained pronounced among individuals with healthy sleep and regular physical activity.ConclusionsInsulin resistance independently accelerated the progression from NAFLD to CKM diseases, particularly ischemic stroke. Healthy sleep and regular physical activity failed to offset this detrimental impact.Graphical abstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s12933-025-02953-9.