Objectives: Vertebral fractures are associated with disability and mortality, but most vertebral fractures are asymptomatic. The present study aimed to determine the incidence of and develop a predictive nomogram for asymptomatic vertebral fractures in Vietnamese adults. Methods: This cohort study as a part of the Vietnam Osteoporosis Study involved 168 men and 287 women aged 50 years and older without a clinically diagnosed vertebral fracture. Their spine x-rays were taken at the recruitment and subsequent 2-year visit. Vertebral fractures were ascertained using the Genant’s semiquantitative method. We employed the Bayesian Model Averaging method to search for the optimal model for predicting asymptomatic vertebral fractures. A predictive nomogram was also developed to facilitate risk prediction. Results: During a median of 2.38 years of follow-up, 13 men and 16 women developed an asymptomatic vertebral fracture, yielding the overall incidence rate of 28 fractures per 1000 person-years, or 33 fractures/1000 personyears in men and 24 fractures/1000 person-years in women, respectively. Most asymptomatic vertebral fractures were moderate, almost 1.5 times more common than mild fractures. The optimal model for predicting incident asymptomatic vertebral fractures included age, male sex and lower femoral neck T-score. The area under the receiver’s operating characteristic curve was 0.91, with 95% CI ranging from 0.86 to 0.96. Conclusions Asymptomatic vertebral fractures were relatively common among adults in Vietnam. A simple model with sex, age and femoral neck T-score is helpful for selective screening of asymptomatic vertebral fractures in Vietnamese individuals.

Chronic cerebral hypoperfusion leads to white matter injury (WMI), which plays a significant role in contributing to vascular cognitive impairment. While 13-docosenamide is a type of fatty acid amide, it remains unclear whether it has therapeutic effects on chronic cerebral hypoperfusion. In this study, we conducted bilateral common carotid artery stenosis (BCAS) surgery to simulate chronic cerebral hypoperfusion-induced WMI and cognitive impairment. Our findings showed that 13-docosenamide alleviates WMI and cognitive impairment in BCAS mice. Mechanistically, 13-docosenamide specifically binds to cannabinoid receptor 1 (CNR1) in oligodendrocyte precursor cells (OPCs). This interaction results in an upregulation of ubiquitin-specific peptidase 33 (USP33)-mediated CNR1 deubiquitination, subsequently increasing CNR1 protein expression, activating the phosphorylation of the AKT/mTOR pathway, and promoting the differentiation of OPCs. In conclusion, our study suggests that 13-docosenamide can ameliorate chronic cerebral hypoperfusion-induced WMI and cognitive impairment by enhancing OPC differentiation and could serve as a potential therapeutic drug.
Animals ; Oligodendrocyte Precursor Cells/metabolism* ; Mice ; Cell Differentiation/drug effects* ; Male ; Receptor, Cannabinoid, CB1/metabolism* ; Mice, Inbred C57BL ; Ubiquitin Thiolesterase/metabolism* ; Ubiquitination/drug effects* ; Carotid Stenosis/complications* ; Cognitive Dysfunction/drug therapy*

Hypertrophic cardiomyopathy (HCM) is a major contributor to cardiovascular diseases (CVD), the leading cause of death globally. HCM can precipitate heart failure (HF) by causing the cardiac tissue to weaken and stretch, thereby impairing its pumping efficiency. Moreover, HCM increases the risk of atrial fibrillation, which in turn elevates the likelihood of thrombus formation and stroke. Given these significant clinical ramifications, research into the etiology and pathogenesis of HCM is intensifying at multiple levels. In this review, we discuss and synthesize the latest findings on HCM pathogenesis, drawing on key experimental studies conducted both in vitro and in vivo. We also offer our insights and perspectives on these mechanisms, while highlighting the limitations of current research. Advancing fundamental research in this area is essential for developing effective therapeutic interventions and enhancing the clinical management of HCM.
Cardiomyopathy, Hypertrophic/physiopathology* ; Humans ; Animals

OBJECTIVE: Patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection frequently develop central nervous system damage, yet the mechanisms driving this pathology remain unclear. This study investigated the primary pathways and key factors underlying brain tissue damage induced by the SARS-CoV-2 beta variant (lineage B.1.351). METHODS: K18-hACE2 and C57BL/6 mice were intranasally infected with the SARS-CoV-2 beta variant. Viral replication, pathological phenotypes, and brain transcriptomes were analyzed. Gene Ontology (GO) analysis was performed to identify altered pathways. Expression changes of host genes were verified using reverse transcription-quantitative polymerase chain reaction and Western blot. RESULTS: Pathological alterations were observed in the lungs of both mouse strains. However, only K18-hACE2 mice exhibited elevated viral RNA loads and infectious titers in the brain at 3 days post-infection, accompanied by neuropathological injury and weight loss. GO analysis of infected K18-hACE2 brain tissue revealed significant dysregulation of genes associated with innate immunity and antiviral defense responses, including type I interferons, pro-inflammatory cytokines, Toll-like receptor signaling components, and interferon-stimulated genes. Neuroinflammation was evident, alongside activation of apoptotic and pyroptotic pathways. Furthermore, altered neural cell marker expression suggested viral-induced neuroglial activation, resulting in caspase 4 and lipocalin 2 release and disruption of neuronal molecular networks. CONCLUSION These findings elucidate mechanisms of neuropathogenicity associated with the SARS-CoV-2 beta variant and highlight therapeutic targets to mitigate COVID-19-related neurological dysfunction.
Animals ; COVID-19/genetics* ; Mice ; Brain/metabolism* ; Apoptosis ; Mice, Inbred C57BL ; SARS-CoV-2/physiology* ; Pyroptosis ; Gene Expression Profiling ; Transcriptome ; Male ; Female

Objectives: Vertebral fractures are associated with disability and mortality, but most vertebral fractures are asymptomatic. The present study aimed to determine the incidence of and develop a predictive nomogram for asymptomatic vertebral fractures in Vietnamese adults. Methods: This cohort study as a part of the Vietnam Osteoporosis Study involved 168 men and 287 women aged 50 years and older without a clinically diagnosed vertebral fracture. Their spine x-rays were taken at the recruitment and subsequent 2-year visit. Vertebral fractures were ascertained using the Genant’s semiquantitative method. We employed the Bayesian Model Averaging method to search for the optimal model for predicting asymptomatic vertebral fractures. A predictive nomogram was also developed to facilitate risk prediction. Results: During a median of 2.38 years of follow-up, 13 men and 16 women developed an asymptomatic vertebral fracture, yielding the overall incidence rate of 28 fractures per 1000 person-years, or 33 fractures/1000 personyears in men and 24 fractures/1000 person-years in women, respectively. Most asymptomatic vertebral fractures were moderate, almost 1.5 times more common than mild fractures. The optimal model for predicting incident asymptomatic vertebral fractures included age, male sex and lower femoral neck T-score. The area under the receiver’s operating characteristic curve was 0.91, with 95% CI ranging from 0.86 to 0.96. Conclusions Asymptomatic vertebral fractures were relatively common among adults in Vietnam. A simple model with sex, age and femoral neck T-score is helpful for selective screening of asymptomatic vertebral fractures in Vietnamese individuals.

Objective To investigate the status of hearing impaired children's hearing device independence skills,and to explore the ways to improve their self-use of hearing equipment.Methods This study surveyed 64 re-habilitation teachers and 411 parents of children with hearing impairment aged 0-12 years.Through face-to-face or remote telephone interview,3 good habits(A asking parents for advice before removing the HA,B putting the de-vice into a moisture-proof box after removing it,C bringing batteries to school and knowing where are them)and 3 key abilities[D wearing the device independently,E replacing the battery independently,and F independently handle foreign bodies in the ear mold(Fa)and water vapor(Fb)]was investigated.The age when mastering skills or de-veloping habits difference of hearing impaired children in different groups were compared.Results ① The ratio of ability D in the bilateral CI group and the bilateral HA group of preschool children was 30.97％and 18.57％respec-tively.Among elementary school children,85.29％and 90.70％had this ability respectively.② The ratio of ability E in the bilateral CI group,the bilateral HA group and the bimodel group were 11.50％,15.71％and 16.49％,re-spectively.Among elementary school children,64.71％,53.49％and 68.52％had this ability,respectively.③Among preschool children,there was no statistical difference in age when different equipment groups developed the three good habits and acquired ability D and E(P＞0.05).④ Among primary school children,there was a statisti-cal difference in the age when different equipment groups formed habit A(P＜0.05),and the age when double CI group had this ability was slightly earlier than the double HA group.There was no significant difference in other abilities among age groups(P＞0.05).Conclusion The age at which hearing impaired children develop the three good habits precedes the age at which they master the key skills,which accords with the law of skill acquisition and development of ordinary children.Corresponding teaching process should be based on the age and ability of hearing-impaired children without considering the type of equipment.

Type 2 diabetes mellitus(T2DM)is a chronic metabolic disorder characterized primarily by pancreatic β-cell dysfunction and insulin resistance.Beyond impaired glucose homeostasis,the glucotox-icity resulting from dysregulated glucose metabolism can lead to complications such as diabetic nephropa-thy,diabetic coronary heart disease,and diabetic cognitive dysfunction,posing severe threats to patients' health.Therefore,enhancing glucose metabolism and improving insulin resistance are critical strategies for T2DM prevention and treatment.Currently,the primary therapeutic approaches for T2DM include oral hypoglycemic agents and exogenous insulin injections.However,these methods face challenges such as unclear diagnostic markers,suboptimal therapeutic efficacy,and drug-related side effects.Consequently,the development of more precise and effective treatment strategies remains a top priority in clinical re-search.MicroRNA(miRNA)is a short non-coding RNA that regulates gene transcription.It has been reported to exhibit significant alterations even before the onset of overt pathological features like hypergly-cemia,suggesting their potential as early diagnostic biomarkers for T2DM to address current issues like delayed diagnosis and disease progression due to missed optimal treatment windows.Moreover,miRNAs can modulate the expression of pathways involved in glucose metabolism,thereby improving insulin resist-ance and maintaining glucose homeostasis while avoiding side effects associated with conventional thera-pies,such as reduced bone density and localized fat accumulation.This positions miRNAs as a promising avenue for precise and efficient T2DM management.This article systematically elucidates the molecular mechanisms by which miRNAs regulate glucose metabolism-related pathways,providing a theoretical foundation and reference for future clinical research.

Objective:To explore the mechanism of long non-coding RNA nuclear-enriched transcript 1(LncRNA NEAT1)on improving myocardial injury in rats with myocardial infarction(MI)mechanism through miR-136/extracellular signal-regulated kinase 1/2(ERK1/2)axis.Methods:Using the random number table method,120 male SD rats were divided into 6 groups(n=20):sham group,myocardial infarction group(MI group),control interference group(sh-NC group),NEAT1 interference group(sh-NEAT1 group),NEAT1 interference+miR-136 control inhibition group(sh-NEAT1+antagomiR-NC group)and NEAT1 interference+miR-136 suppression group(sh-NEAT1+antagomiR-136 group).Seven days before MI operation,100 μl of corresponding adenovirus vector was injected into the myocardium.Rats in each group were ligated the left anterior descending vessel to establish MI model.In sham group,only the left chest was opened and the heart was exposed without ligation.H9C2 cardiomyocyte were divided into:control group,vehicle group,sh-NC group,sh-NEAT1 group,sh-NEAT1+antagomiR-NC group and sh-NEAT1+antagomiR-136 group.Car-diomyocyte were transfected with corresponding NEAT1 interference vector and negative control,miR-136 inhibitor and negative con-trol.StarBase prediction and dual luciferase report experiment verify the targeted regulation of LncRNA NEAT1 on miR-136;myocar-dial infarct size was measured by TTC staining,and myocardial histopathological changes were observed by HE staining;Echocardiog-raphy was used to detect rat cardiac function;detection of apoptosis in rat myocardial tissue and H9C2 cells by flow cytometry.ELISA method was used to detect serum oxidative stress,corresponding indexes of myocardial enzymes and the contents of inflammatory fac-tors in myocardial tissue and H9C2 cells.CCK8 and EdU staining were used to detect the proliferation ability of H9C2 cells.RT-qPCR was used to detect the expressions of miR-136,SIRT1 mRNA in myocardial tissue and H9C2 cells.Western blot was used to detect the expressions of ERK1/2,p-ERK1/2,B-cell lymphoma-2(Bcl-2),Bcl2-related X protein(Bax)protein in rat myocardial tissue and H9C2 cells.Results:The expression of LncRNA NEAT1 was up-regulated in injured myocardial tissues and cells,and the expression of miR-136 was down-regulated(P<0.05).At the same time,NEAT1 targets and regulates the level of miR-136.Inhibition of NEAT1 expression could increase left ventricular ejection fraction(LVEF),left ventricular fraction shortening(LVFS),Bcl-2 level,and de-crease the activities of creatine kinase(CK),lactate dehydrogenase(LDH),and aspartame Acid transaminase(AST),superoxide dismutase(SOD),reduce Bax,troponin Ⅰ(cTnⅠ),malondialdehyde(MDA),TNF-α,IL-1β,IL-6,ERK1/2/p-ERK1/2 levels(P<0.05),promote the proliferation of myocardial cells,inhibit cell apoptosis,reduce the area of myocardial infarction,inhibit oxida-tive stress and inflammation,and improve myocardial damage Inhibiting miR-136 can save the above effects.Conclusion:The expres-sion of LncRNA NEAT1 is up-regulated and the expression of miR-136 is down-regulated in injured myocardial tissue and cells.Inhibi-tion of LncRNA NEAT1 expression inhibits apoptosis,oxidative stress and inflammation through miR-136/ERK1/2 axis,thus improving myocardial injury.

OBJECTIVE: To compare clinical efficacy of tibial transverse transport (TTT) microcirculation reconstruction and periosteal distraction in treating patients with early diabetic foot(DF). METHODS: From June 2021 to June 2024, 60 patients with DF were admitted and divided into bone transport group and stretch group according to different treatment methods. There were 30 patients in bone transport group, including 16 males and 14 females;aged from 48 to 65 years old with an average of (55.59±3.78) years old;the course of disease ranged from 2 to 9 months with an average of(5.95±1.32) months;TTT microcirculation reconstruction surgery was performed. There were 30 patients in distraction group, including 17 males and 13 females;aged from 47 to 67 years old with an average of (55.24±3.81) years old;the course of disease ranged from 2 to 10 months with an average of (5.68±1.54) months;periosteal distraction surgery was performed. The skin temperature of the affected feet, the time of getting out of bed and walking after operation, the time of full weight-bearing, the wound healing time and complications were compared between two groups;the pain was evaluated by visual analogue scale (VAS) before operation and one month after operation respectively;the changes of blood flow velocity of dorsal foot arteries, ankle brachial index(ABI), epidermal growth factor (EGF), and basic fibroblast growth factor (bFGF) before and after operation at 3 months were compared between two groups. RESULTS: All patients were followed up for 3 to 4 months with an average of (3.52±0.12) months. There were no statistically significant differences in comparison of foot skin temperature, postoperative walking time, full weight-bearing time and complications between two groups (P>0.05). The wound healing time of bone transport group (61.26±7.31) days was shorter than that of distraction group (70.17±7.15) days, and the difference was statistically significant (P<0.05). Postoperative VAS at 1 month of bone transport group (2.19±0.21) was lower than that of distraction group (2.55±0.20), and the difference was statistically significant (P<0.05). At 3 months after operation, the blood flow velocity of dorsal foot artery, ankle-brachial index, EGF and bFGF in bone transport group were(34.73±4.18) cm·s^-1, (0.95±0.13), (716.61±71.13) pg·ml^-1 and (175.69±31.28) pg·ml^-1, respectively;which were higher than that of distraction group (31.86±3.23) cm·s^-1, (0.84±0.11), (677.37±70.21) pg·ml^-1, (149.26±30.13) pg·ml^-1, and the differences were statistically significant (P<0.05). There was no recurrence of ulcers in situ or at other sites in both groups during follow-up. CONCLUSION Compared with periosteal distraction, TTT microcirculation reconstruction surgery has a definite effect in the treatment of early DF. It could effectively reduce pain level, improve blood flow indicators and vascular endothelial function of the foot, and has a relatively high safety.
Humans ; Male ; Female ; Middle Aged ; Aged ; Tibia/blood supply* ; Diabetic Foot/physiopathology* ; Microcirculation ; Periosteum/surgery* ; Plastic Surgery Procedures/methods* ; Osteogenesis, Distraction

Objective:To explore the independent risk factors for uremic encephalopathy(UE)in maintenance hemodialysis(MHD)patients and provide evidence for early clinical warning and intervention.Methods:A case-control study was conducted,enrolling 67 MHD patients diagnosed with UE(UE group)at Laibin People's Hospital from January 2010 to December 2024,and 67 non-UE patients during the same period(control group).Demographic characteristics,dialysis parameters,laboratory indicators,and infection events were collected.Univariate and multivariate logistic regression analyses were used to identify independent risk factors for UE.Results:The UE group had significantly higher rates of infection(58.2％vs.29.9％),serum creatinine(789 vs.702 μmol/L),and iPTH levels(568 vs.385 pg/mL)compared to the control group(P＜0.05).Multivariate analysis revealed that concurrent infection(OR=3.022,95％CI:1.312-6.958),elevated serum creatinine(OR=1.004,95％CI:1.000-1.008),and elevated iPTH(OR=1.002,95％CI:1.001-1.003)were independent risk factors for UE(P＜0.05).The combined prediction model achieved an AUC of 0.878(95％CI:0.822-0.934),with 82.1％sensitivity and 80.6％specificity.Conclusion:Infection,elevated serum creatinine,and elevated iPTH significantly increase the risk of UE in MHD patients.Clinical management should emphasize infection prevention,toxin clearance optimization,and parathyroid function regulation to reduce UE incidence.