BACKGROUND:Naringin has been shown to promote the proliferation and osteogenic differentiation of bone marrow derived mesenchymal stem cells,making it a potential candidate for treating osteoporosis andenhancing fracture healing.However,its clinical application is limited by its low bioavailability.OBJECTIVE:To prepare chitosan/β-tricalcium phosphate scaffolds loaded with naringin and characterize their biological properties.METHODS:Chitosan/β-tricalcium phosphate scaffolds were prepared by freeze-drying and chemical crosslinking.The chitosan/β-tricalcium phosphate scaffolds were immersed in anhydrous ethanol solution containing naringin for 3 hours.After vacuum cold drying,chitosan/β-tricalcium phosphate/naringin scaffolds were obtained.The pore size,porosity,swelling rate,degradation rate,mechanical properties,and in vitro release capacity of naringin of the scaffolds were characterized.Rat bone marrow mesenchymal stem cells were inoculated on the surface of chitosan/β-tricalcium phosphate scaffolds and chitosan/β-tricalcium phosphate/naringin scaffolds,respectively,and cell proliferation,adhesion,activity and alkaline phosphatase activity after osteogenic differentiation were detected.RESULTS AND CONCLUSION:(1)The results of scanning electron microscopy showed that the naringin-chitosan/β-tricalcium phosphate composite scaffold had a porous mesh structure.The average pore diameter was(106.82±25.22)μm;the porosity was(76.26±4.81)％;24-hour swelling rate was(796.17±31.76)％;in vitro degradation rate of 7.71％at 4 weeks,and naringin could be slowly released in vitro for 9 days.There was no significant difference in the average pore size,porosity,24-hour swelling rate,in vitro degradation rate,compression strength and compression modulus at 4 weeks between the chitosan/β-tricalcium phosphate scaffold and the chitosan/β-tricalcium phosphate scaffold(P＞0.05).(2)Rat bone marrow mesenchymal stem cells adhered well to the surfaces of the two scaffolds and had good activity.Compared with the chitosan/β-tricalcium phosphate scaffold,the chitosan/β-tricalcium phosphate/naringin scaffold promoted the proliferation of rat bone marrow mesenchymal stem cells(P＜0.05),and increased the alkaline phosphatase activity of bone marrow mesenchymal stem cells after osteogenic differentiation(P＜0.05).(3)The results show that the chitosan/β-tricalcium phosphate/naringin scaffolds exhibit favorable physical properties and can effectively promote the adhesion,proliferation,and osteogenic differentiation of bone marrow-derived mesenchymal stem cells.

BACKGROUND:Naringin has been shown to promote the proliferation and osteogenic differentiation of bone marrow derived mesenchymal stem cells,making it a potential candidate for treating osteoporosis andenhancing fracture healing.However,its clinical application is limited by its low bioavailability.OBJECTIVE:To prepare chitosan/β-tricalcium phosphate scaffolds loaded with naringin and characterize their biological properties.METHODS:Chitosan/β-tricalcium phosphate scaffolds were prepared by freeze-drying and chemical crosslinking.The chitosan/β-tricalcium phosphate scaffolds were immersed in anhydrous ethanol solution containing naringin for 3 hours.After vacuum cold drying,chitosan/β-tricalcium phosphate/naringin scaffolds were obtained.The pore size,porosity,swelling rate,degradation rate,mechanical properties,and in vitro release capacity of naringin of the scaffolds were characterized.Rat bone marrow mesenchymal stem cells were inoculated on the surface of chitosan/β-tricalcium phosphate scaffolds and chitosan/β-tricalcium phosphate/naringin scaffolds,respectively,and cell proliferation,adhesion,activity and alkaline phosphatase activity after osteogenic differentiation were detected.RESULTS AND CONCLUSION:(1)The results of scanning electron microscopy showed that the naringin-chitosan/β-tricalcium phosphate composite scaffold had a porous mesh structure.The average pore diameter was(106.82±25.22)μm;the porosity was(76.26±4.81)％;24-hour swelling rate was(796.17±31.76)％;in vitro degradation rate of 7.71％at 4 weeks,and naringin could be slowly released in vitro for 9 days.There was no significant difference in the average pore size,porosity,24-hour swelling rate,in vitro degradation rate,compression strength and compression modulus at 4 weeks between the chitosan/β-tricalcium phosphate scaffold and the chitosan/β-tricalcium phosphate scaffold(P＞0.05).(2)Rat bone marrow mesenchymal stem cells adhered well to the surfaces of the two scaffolds and had good activity.Compared with the chitosan/β-tricalcium phosphate scaffold,the chitosan/β-tricalcium phosphate/naringin scaffold promoted the proliferation of rat bone marrow mesenchymal stem cells(P＜0.05),and increased the alkaline phosphatase activity of bone marrow mesenchymal stem cells after osteogenic differentiation(P＜0.05).(3)The results show that the chitosan/β-tricalcium phosphate/naringin scaffolds exhibit favorable physical properties and can effectively promote the adhesion,proliferation,and osteogenic differentiation of bone marrow-derived mesenchymal stem cells.

Objective: To retrospectively investigate the clinical efficacy, safety, and management experience of a patient diagnosed with polycythemia vera (PV) at the age of 3 who underwent regular erythrocytapheresis for 7 years starting at the age of 10. Methods: Treatment was initiated when the patient's hematocrit was≥50%. The goal was to reduce the hematocrit to below 40%; the removal volume was calculated as 10%-15% of the total red blood cell mass, and an equal volume of normal saline was supplemented during the procedure. Pre-treatment precautions included avoiding fasting and high-fat diets. Post-treatment measures included lying flat for 30 minutes, reducing strenuous exercise for 2–3 days, and rechecking complete blood count 2–5 days after the procedure. During the procedure, adverse reactions such as palpitations, dyspnea, hypotension, and convulsions were monitored. Follow-up was conducted after 3 days to assess any delayed adverse effects. Results: As of August 2025, the patient had undergone a total of 16 erythrocytapheresis sessions. The average volume ranged from 212 to 500 mL. The frequency was 1 to 4 times annually. Post-procedure, hemoglobin (Hb) and hematocrit (Hct) were effectively controlled. Conclusion: Continuous erythrocytapheresis can effectively control Hb and Hct levels in PV patients, preventing adverse effects from the primary disease. Erythrocytapheresis demonstrates efficacy with minimal adverse reactions and can be used as a routine therapeutic technique for PV patients.

ObjectiveTo investigate the association between insulin resistance （IR） and cardiovascular metabolic indicators， including blood pressure， blood lipids， and serum uric acid， in a middle-aged population. MethodsBased on the baseline survey of the Hong Sifang cohort of China National Salt Industry Group， a total of 575 participants were included. According to the homeostasis model assessment of insulin resistance， the participants were divided into an IR group （n=116） and a non-IR group （n=459）. Differences between the two groups were compared using the t-test and chi-square test. Multivariate logistic regression analysis was performed to evaluate the associations between IR and abnormalities in metabolic indicators. ResultsA total of 575 participants were included， including 390 men and 185 women， with a mean age of （48.58 ± 5.14） years and a mean body mass index （BMI） of （24.16 ± 2.97） kg/m². Blood pressure， serum uric acid， and blood lipid levels were significantly higher in the IR group than in the non-IR group （P<0.001）. After adjusting for potential confounders including age， sex， and BMI， IR was independently associated with hypertension， dyslipidemia， and hyperuricemia， with odds ratios （OR） and 95% confidence intervals （CI） of 2.57 （1.61-4.09）， 3.81 （2.36-6.17）， and 2.68 （1.53-4.71）， respectively （all P<0.001）. ConclusionInsulin resistance is significantly associated with multiple cardiovascular metabolic risk factors in the middle-aged population. Monitoring IR may contribute to the early prevention and control of cardiovascular diseases.

Peripheral nerve injury (PNI) severs peripheral connections and induces profound reorganization of primary somatosensory (S1) and motor (M1) cortical maps, a dynamic process that critically shapes the extent and quality of functional recovery. Brain-derived neurotrophic factor (BDNF) has emerged as a central molecular hub linking the initial peripheral insult to subsequent central plastic changes. This review systematically examines BDNF-mediated cortical remodeling following PNI, with a particular emphasis on its spatiotemporally specific regulatory mechanisms and the therapeutic opportunities they present. Immediately after PNI, deafferented cortical territories undergo rapid functional silencing and, over time, become progressively encroached upon by adjacent intact representations. This maladaptive reorganization—characterized by sensory map fusion and motor compensatory invasion—actively impedes successful reinnervation and optimal recovery. Such phenomena have been consistently documented in both non-human primate models and human fMRI studies, spanning sensory and motor modalities. Motor remapping is also prominently observed in facial nerve injury and chronic nerve compression models, underscoring the universality of these plastic changes. Notably, a range of interventions including regional local anesthesia, auditory-tactile substitution, and guided tactile imagery can effectively mitigate this aberrant remodeling, revealing promising avenues for the therapeutic modulation of cortical plasticity during critical post-injury windows. BDNF coordinates post-PNI cortical remodeling through three mechanistically interconnected pathways. First, BDNF drives dendritic and axonal growth via TrkB receptor signaling: retrogradely transported axonal signaling endosomes integrate CREB-dependent transcriptional programs with mTOR-mediated local protein synthesis to bolster dendritic arborization and axonal elongation, while BDNF-induced Limk1 translation precisely fine-tunes actin cytoskeletal dynamics, thereby stabilizing dendritic spine morphology. Second, BDNF governs GABAergic interneuron maturation and perineuronal net formation through the JNK signaling cascade, thereby acting as a “plasticity brake” that preserves the delicate excitatory/inhibitory balance and constrains indiscriminate, maladaptive rewiring. Third, BDNF robustly potentiates NMDAR-dependent long-term potentiation (LTP) by elevating NMDA channel open probability and increasing synaptic receptor density, thus tightly coupling structural remodeling with functional synaptic strengthening. Concurrently, long-term depression pathways are subject to modulation, with NMDAR antagonism exerting time-dependent, bidirectional effects that vary with the post-injury phase. Superimposed on these mechanisms, the functionally antagonistic actions of proBDNF/p75NTR (favoring pruning and growth cone collapse) and mature BDNF/TrkB (promoting survival and stabilization) add further layers of regulatory complexity, highlighting the absolute necessity for precise spatiotemporal control in any therapeutic strategy. Extending our previous experimental findings, we introduce a “cortical reclamation threshold” model. In this framework, early upregulation of BDNF-TrkB signaling enhances inhibitory tone to restrict cortical encroachment by neighboring intact regions, whereas delayed but precisely timed BDNF delivery following surgical nerve repair actively facilitates the reclamation of the original, deafferented cortical maps by regenerating afferent fibers. Importantly, the common BDNF Val66Met polymorphism may significantly modulate individual thresholds, providing a biologically grounded rationale for patient stratification and personalized timing of intervention. Despite this mechanistic promise, clinical translation faces considerable hurdles. These include inherently poor pharmacokinetics of BDNF, severely limited penetration across the blood-brain barrier, dose-dependent neurotoxicity mediated through the p75NTR receptor, and the overarching dual-edged nature of BDNF signaling, which can simultaneously promote both adaptive and maladaptive plasticity. Emerging delivery platforms——including engineered exosomes, polymeric nanoparticles, cryogel microcarriers, and adeno-associated virus (AAV)-based gene therapy——offer potential solutions, but all require rigorous pharmacokinetic, toxicological, and functional validation. Future research priorities should encompass: (1) comprehensive single-cell and spatial transcriptomic mapping to resolve BDNF cellular sources and real-time signaling dynamics across distinct cortical layers and cell types; (2) genotype-stratified dose-response studies to establish safe, effective, and personalized delivery protocols; and (3) large-scale multicenter clinical trials that seamlessly integrate BDNF-targeted interventions with multimodal rehabilitation strategies, such as repetitive transcranial magnetic stimulation and mirror therapy, with longitudinal neuroimaging serving as a biomarker for cortical reclamation. By systematically addressing these priorities, we aim to transform BDNF from a critical endogenous regulator into a precisely controllable and titratable therapeutic target, ultimately enabling a paradigm shift from mere structural repair to true functional neural reconstruction following PNI.

BACKGROUND:Some studies have found that ferroptosis of osteoblasts can be an important mechanism to induce the occurrence and development of hormone-induced femoral head necrosis.With the development of Chinese medicine,some scholars have found that some Chinese medicine monomer,Chinese medicine compound and Chinese patent medicine can regulate the ferroptosis of osteoblasts through various pathway mechanisms,and finally play a role in the treatment of steroid-induced avascular necrosis of femoral head. OBJECTIVE:To investigate the relationship between ferroptosis and steroid-induced avascular necrosis of femoral head and the mechanism of Chinese medicine regulating ferroptosis of osteoblasts in the treatment of steroid-induced avascular necrosis of femoral head,so as to provide new ideas for the diagnosis and treatment of steroid-induced avascular necrosis of femoral head. METHODS:With"ferroptosis,steroid-induced avascular necrosis of femoral head,osteoblast,Chinese herbal medicine,glucocorticoid,iron metabolism,reactive oxygen species,glutathione peroxidase"as Chinese search terms,and"ferroptosis,hormonal necrosis of the femoral head,osteoblast,Chinese herbal medicine,glucocorticoid,iron metabolism,ROS,GPX4"as English search terms,the search was conducted on CNKI,PubMed,WanFang,VIP and other databases.The relevant articles on osteoblast ferroptosis and steroid-induced avascular necrosis of femoral head and the regulation of Chinese herbal medicine intervention from the establishment of each database to 2023 were screened.Finally,76 articles were systematically analyzed. RESULTS AND CONCLUSION:(1)Ferroptosis of osteoblasts plays an important role in the pathogenesis of steroid-induced avascular necrosis of femoral head.(2)The occurrence of ferroptosis in osteoblasts is regulated by a variety of mechanisms,such as intracellular iron overload causing ferroptosis.Lipid peroxidation damages cell membrane and causes ferroptosis.Cystine/glutamate reverse transporter induced ferroptosis by influencing glutathione level and glutathione peroxidase 4 activity.Fenton reaction in the cell produces a large number of reactive oxygen species and causes ferroptosis.(3)Chinese medicine monomer icariin,Chinese medicine compound Qinge pills and Chinese patent medicine Bushen Huoxue granules can regulate the occurrence of osteoblast ferroptosis,and help to prevent and treat steroid-induced avascular necrosis of femoral head.(4)The mechanism of ferroptosis in osteoblasts is still unclear.Further investigation on the mechanism of action of both is expected to provide a new choice for clinical treatment of steroid-induced avascular necrosis of femoral head.

Objective: To investigate the status of salt-restriction spoons use among residents in Zhejiang Province, so as to provide evidence for optimizing salt-reduction intervention strategies and preventing chronic disease. Methods: Residents aged 18-69 from five counties (cities/districts) in Zhejiang Province were selected using a multi-stage stratified random sampling method. Demographic characteristics, dietary habits, and salt-restriction spoons use were collected using questionnaires. The rate of salt-restriction spoons use and correct rate of salt-restriction spoons use were analyzed. Factors affecting salt-restriction spoons use among residents were analyzed by multivariable logistic regression model. Results: Totally 7 601 questionnaires were allocated, and 7 509 valid questionnaires were recovered, with an effective recovery rate of 98.79%. The respondents included 3 744 males (49.86%) and 3 765 females (50.14%). The mean age was (44.81±14.03) years. The rate of salt-restriction spoons use was 11.97%, the correct rate of salt-restriction spoon use was 52.73%. Multivariable logistic regression analysis showed that rural (OR=0.851, 95%CI: 0.731-0.991), education level of primary school and below (illiterate or semi-literate, OR=0.269, 95%CI: 0.172-0.420; primary school, OR=0.595, 95%CI: 0.436-0.811), and excessive dietary salt intake (OR=0.718, 95%CI: 0.559-0.922) were inhibiting factors for salt-restriction spoons use among residents; physical exercise (OR=1.581, 95%CI: 1.362-1.836) and received health education on a low-salt diet (OR=2.082, 95%CI: 1.790-2.421) were promoting factors for salt-restriction spoons use among residents. Conclusions The rate of salt-restriction spoons use among residents in Zhejiang Province was relatively low, primarily influenced by region, educational level, physical activity, dietary salt intake, and health education on a low-salt diet. It is recommended that propose a multi-component intervention strategy centered on skill enhancement and health education, delivered through progressive staged implementation, to promote sustained adoption of salt-restriction spoons among residents.

Objective To verify the safety and effectiveness of a new percutaneous controllable curved plasma radiofrequency instrument for nucleus pulposus ablation. Methods A new percutaneous controllable curved plasma radiofrequency instrument were designed (controllable curved group), and its ablation effect was compared with the currently used straight head non-bendable plasma ablation instrument (non-bendable group) on gross specimens. The ablation instrument was placed through the right intervertebral foramen, and continuous ablation on the same intervertebral disc was conducted for three times. The ablation range and trajectory were recorded, and the temperature changes in the front, back, left, and right of the ablation center during and 15 seconds after ablation were monitored by the inserted temperature probe. Results There were no difference in temperature changes in the front, back, right regions of the ablation center during and 15 seconds after ablation between the two groups. The temperature changes in the left region of the ablation center both during and 15 seconds after 3rd ablation were larger than those in the non-bendable group (P＜0.01). Compared with the non-bendable group, the controllable curved group achieved angle control and larger single ablation area (2.282 5 mm² vs 1.135 8 mm², P＜0.000 1). Conclusions This new percutaneous controllable curved plasma ablation instrument can achieve angle control and ablation on the side opposite to the puncture site, increase ablation volume, and is safe.

BACKGROUND: Generalized pustular psoriasis (GPP), a rare and recurrent autoinflammatory disease, imposes a substantial burden on patients and society. Awareness of GPP in China remains limited. METHODS: This cross-sectional survey, conducted between September 2021 and May 2023 across 14 hospitals in China, included GPP patients of all ages and disease phases. Data collected encompassed demographics, clinical characteristics, economic impact, disease severity, quality of life, and treatment-related complications. Risk factors for GPP recurrence were analyzed. RESULTS: Among 127 patients (female/male ratio = 1.35:1), the mean age of disease onset was 25 years (1st quartile [Q1]-3rd quartile [Q3]: 11-44 years); 29.2% had experienced GPP for more than 10 years. Recurrence occurred in 75.6% of patients, and nearly half reported no identifiable triggers. Younger age at disease onset ( P  = 0.021) and transitioning to plaque psoriasis ( P  = 0.022) were associated with higher recurrence rates. The median diagnostic delay was 8 months (Q1-Q3: 2-41 months), and 32.3% of patients reported misdiagnoses. Comorbidities were present in 53.5% of patients, whereas 51.1% experienced systemic complications during treatment. Depression and anxiety affected 84.5% and 95.6% of patients, respectively. During GPP flares, the median Dermatology Life Quality Index score was 19.0 (Q1-Q3: 13.0-23.5). This score showed significant differences between patients with and without systemic symptoms; it demonstrated correlations with both depression and anxiety scores. Treatment costs caused financial hardship in 55.9% of patients, underscoring the burden associated with GPP. CONCLUSIONS The substantial disease and economic burdens among Chinese GPP patients warrant increased attention. Patients with early onset disease and those transitioning to plaque psoriasis require targeted interventions to mitigate the high recurrence risk.
Humans ; Male ; Female ; Psoriasis/pathology* ; Adult ; Cross-Sectional Studies ; Adolescent ; Child ; Young Adult ; Quality of Life ; Middle Aged ; China/epidemiology* ; Recurrence ; Risk Factors ; Surveys and Questionnaires ; East Asian People