81th Hospital of PLA

Parkinson’s disease (PD) represents a growing global health challenge, with prevalence doubling from 2.5 million cases in 1990 to 6.1 million in 2016, and projections suggesting it will exceed 12 million by 2040. This exponential growth has been termed the “Parkinson’s pandemic.” China and the United States, which together account for nearly half of the global PD population, have developed markedly different approaches to end-of-life (EOL) care, shaped by their distinct healthcare systems and cultural contexts. Understanding these differences is crucial for developing effective global strategies. This systematic review and meta-analysis comprehensively compares advanced-stage PD care between these two nations to quantify disparities and inform evidence-based policy interventions. We conducted a rigorous systematic review following PRISMA 2020 guidelines, searching six databases (PubMed, Embase, Scopus, Web of Science, CNKI, Wanfang) from January 2015 to October 2025. The timeframe was selected to capture contemporary care patterns following major healthcare reforms in both countries (Affordable Care Act implementation in the US; Healthy China 2030 initiative). Inclusion criteria encompassed peer-reviewed studies reporting on advanced PD (Hoehn-Yahr stage ≥ 3) with outcome measures including survival, quality of life (QoL), palliative care access, caregiver burden, rehabilitation utilization, or healthcare costs. The sample size threshold (n ≥ 100) balanced statistical power with inclusivity. Two independent reviewers screened 3,847 records with excellent agreement (Cohen’s κ = 0.82–0.89). Quality assessment employed the Newcastle-Ottawa Scale (NOS ≥ 8 indicating high quality) for observational studies and the Cochrane Risk of Bias 2.0 tool (RoB 2) for randomized controlled trials, with GRADE criteria determining evidence certainty. Meta-analyses utilized random-effects models with comprehensive heterogeneity assessment (I² statistics, meta-regression) and publication bias evaluation (Egger’s test, trim-and-fill analysis). Sensitivity analyses included high-quality studies only and examined the influence of large database studies. Our analysis of 42 high-quality studies encompassing over 125,000 patients revealed profound and systematic cross-national disparities across multiple domains. In terms of care access, US patients demonstrated significantly higher hospice enrollment rates (28–35% vs. <1% in China, p < 0.001; HIGH certainty evidence) and greater access to specialized neuropalliative programs (15% of US centers vs. <1% in China). These differences translated into measurable quality of life disparities, with Chinese patients scoring 17.6 points worse on the PDQ-39 scale (95% CI 14.8–20.4; MODERATE certainty, I²=64%), a difference exceeding the minimal clinically important difference nearly four-fold. The burden on families showed equally striking patterns: Chinese families provided 94% of EOL care compared to 61% in the US, resulting in significantly higher caregiver depression rates (47% vs. 32%, OR = 1.89, 95% CI 1.45–2.47) and burden scores (Zarit difference: 10.2 points, 95% CI 7.8–12.6). Access to interventions revealed additional gaps, with only 9.2% of Chinese patients receiving physical therapy versus 14.4% in the US (OR = 0.61, 95% CI 0.49–0.76), and a 5.25-fold disparity in deep brain stimulation access (4.2% vs. 0.8%). Economic analysis demonstrated substantial out-of-pocket burden differences: Chinese families paid 58% of total costs ($4,200 annually) versus 12% for US families ($2,800). Meta-regression identified healthcare system characteristics as the primary driver of these disparities (R²=0.42, p < 0.001). This comprehensive analysis reveals that systematic differences in healthcare infrastructure, insurance coverage, and cultural care models are associated with markedly divergent EOL experiences for PD patients in China versus the United States. These findings have policy implications. For China, our findings suggest consideration of: (1) establishing pilot neuropalliative programs in tertiary centers with phased national expansion; (2) developing caregiver support infrastructure including respite care and training programs; (3) leveraging telemedicine platforms to address urban-rural disparities. For the United States, priorities may include: (1) addressing racial disparities in rehabilitation access through culturally competent outreach; (2) expanding Medicare coverage for maintenance therapy; (3) earlier integration of neuropalliative care. Implementation science research would strengthen the evidence base for culturally adapted interventions. As global PD prevalence accelerates, lessons from this bilateral comparison provide a framework for other nations confronting similar challenges in neurological care delivery.

Objective: The purpose of this study is to explore the application advantages and nursing effects of external fixator combined with negative pressure closed drainage in the treatment of patients with open tibia and fibula fractures accompanied by soft tissue defects. Methods: The study included 46 patients with open tibia and fibula fractures and soft tissue defects who were treated with an external fixator combined with negative pressure closed drainage in our hospital from January 2024 to June 2025 as research samples. They were divided into an experimental group and a conventional group of 23 cases each using the random number table method. The conventional group received routine nursing measures. The experimental group adopted an individualized nursing intervention plan. The two groups of cases were compared in terms of fracture healing time, soft tissue repair time, probability of complications, and total effectiveness of treatment.&amp;nbsp;Results:&amp;nbsp;The fracture healing time and soft tissue repair time in the experimental group were shorter than those in the conventional group (P&amp;nbsp;&lt; 0.05). At the same time, the probability of complications in the experimental group was lower than that in the conventional group, and the total clinical nursing effectiveness of patients in the experimental group was higher than that in the conventional group (P&amp;nbsp;&lt; 0.05). Conclusion: Individualized nursing intervention for patients with open tibia and fibula fractures and soft tissue defects who are treated with external fixator combined with negative pressure closed drainage can speed up the patient&amp;rsquo;s recovery process and reduce the risk of complications, improve the efficiency of clinical care for patients, and has good clinical research value.

Autoantibody- and complement-mediated cytotoxicity can cause autoimmune astrocytopathy that leads to CNS inflammatory demyelination. Formyl peptide receptor 2 (FPR2/ALX) governs the activation and propagation of immune response. However, the precise role of FPR2/ALX in neuroinflammation and the effect of FPR2/ALX stimulation on autoimmune astrocytopathy are poorly understood. Using a mouse model of autoimmune astrocytopathy induced by AQP4-IgG- and complement-mediated cytotoxicity, we found that the stimulation of FPR2/ALX with the small-molecule agonist Quin-C1 led to reduced brain lesion volume, astrocyte loss and demyelination. This was accompanied by enhanced anti-inflammatory activity of microglia and reduced infiltration of lymphocytes in the brain. FPR2/ALX stimulation also led to increased phosphorylation of SYK and AKT in mice with autoimmune astrocytopathy. Notably, the benefits of FPR2/ALX stimulation were attenuated in mice with autoimmune astrocytopathy after microglial depletion using the CSF1R inhibitor PLX5622 or natural killer (NK) cell depletion using an anti-NK1.1 monoclonal antibody. Additionally, the protective effects of FPR2/ALX stimulation were diminished in mice with autoimmune astrocytopathy that received the SYK inhibitor R406. Collectively, our findings demonstrate that FPR2/ALX stimulation may represent a promising therapeutic strategy to attenuate detrimental neuroinflammation in autoimmune astrocytopathy by modulating microglia and NK cells. FPR2/ALX stimulation suppresses autoimmune astrocytopathy: Using a mouse model of autoimmune astrocytopathy, we demonstrated that FPR2/ALX stimulation with the small molecule Quin-C1 reduces the CNS infiltration of lymphocytes and augments the anti-inflammatory activity of microglia, leading to attenuated astrocyte pathology induced by AQP4-IgG and complement-mediated attacks. Mechanistically, the benefits of FPR2/ALX stimulation using Quin-C1 involve microglia, natural killer (NK) cells, and SYK-AKT signaling.

Stable fixation of Schatzker IV tibial plateau fractures is crucial for functional recovery. Conventional plating techniques can compromise the pes anserinus tendon. This study biomechanically evaluates a novel hockey-stick locking plate (NHLP), which features a pes anserinus sparing design, against a traditional T-shaped locking plate (TTLP) and a double reconstruction locking plate (DRLP). Eighteen synthetic tibiae (Sawbones) with a standardized Schatzker IV fracture model were randomly assigned to three fixation groups (NHLP, TTLP, DRLP; n = 6/group). All constructs underwent quasi-static compression, cyclic loading, and load to failure testing. Construct stiffness, interval and cumulative displacement, changes in fracture gap and articular step-off, and ultimate failure load were measured. The NHLP construct demonstrated significantly lower stiffness and a lower ultimate failure load compared to the TTLP and DRLP. During cyclic loading, no significant differences were observed in interval displacement among the groups; however, the cumulative displacement of the NHLP group was significantly greater than the other two (P < 0.001). All three constructs effectively maintained the articular surface, with no significant differences in fracture gap or anterior/central step-off. For posterior articular step-off, the NHLP provided superior control compared to the TTLP (P < 0.001) and was comparable to the DRLP. In this biomechanical study of a Schatzker IV fracture model, the NHLP demonstrated lower overall stiffness and strength than conventional plates but provided superior stabilization of the posterior articular surface. The construct's ultimate strength was found to be sufficient for expected early postoperative physiological loads. The NHLP represents a biomechanically viable option for this fracture pattern, particularly given its design feature of sparing the pes anserinus. Not applicable.

This investigation seeks to assess the efficacy and safety profile of drug-coated balloon (DCB) and drug-eluting stent (DES) throughout primary percutaneous coronary intervention (PCI) among individuals with ST-segment elevation myocardial infarction (STEMI). The medical records of 142 STEMI patients receiving emergency PCI in our hospital between January 2019 and April 2024 underwent retrospective examination. Per the intervention strategy, patients were split into the observation group (n = 85, DCB therapy) and the control group (n = 131, DES therapy). The study compared several parameters between these cohorts: the occurrence of target lesion revascularization and major adverse cardiovascular events (MACE) within one week, measurements of left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDd), and the frequency of slow-flow post-PCI. Additionally, these parameters (excluding slow-flow), along with late lumen loss (LLL) and bleeding incidents, were evaluated during a nine-month follow-up period. There were no notable variations in postoperative LVEDd, LVEF, incidence rates of slow-flow, target lesion revascularization, and MACE within one week between the two groups. After the ten-month follow-up, there were no notable variations in LLL, incidence rates of target lesion revascularization (6.87% VS. 4.71%), MACE (35.11% VS. 31.76%), and hemorrhage (8.40% VS. 2.35%) between the control group and observation group. In individuals with STEMI undergoing emergency percutaneous coronary intervention, the short and long-term prognoses of drug-coated balloons are not inferior to those of drug-eluting stents, which are safe and effective.

Despite cultural preferences for organ preservation in East Asia, choledochoscopic gallbladder-preserving surgery (CGPS) remains controversial given high recurrence rates. This study objectively quantified the increased technical complexity of laparoscopic cholecystectomy (LC) for recurrent cholecystolithiasis after prior CGPS using the Tokyo Guidelines 2018 (TG18). In this propensity-matched study (1:1, n = 220) conducted between 2020 and 2025, patients requiring LC due to recurrent cholecystolithiasis after prior CGPS were compared with patients with primary cholecystolithiasis undergoing LC. Investigators matched groups for TG18 severity grading, BMI, and biliary anomalies. Two blinded surgeons assessed the intraoperative findings using TG18 Delphi scoring (7-point scale). Primary outcomes included difficulty scores, critical view of safety (CVS) achievement, and bile duct injury. The CGPS group demonstrated significantly higher median TG18 scores (34 [IQR 30–39] vs. 21 [18–24]; adjusted mean difference: Δ 14.0 points, 95% CI: 11.2–16.8; p < 0.001), primarily due to fibrotic adhesions: Calot’s triangle dense fibrosis (49.1% vs. 6.4%), partial scarring (21.8% vs. 0.9%), and diffuse scarring (15.5% vs. 0%; all p < 0.001). Surgeons achieved CVS less frequently in the CGPS group (83.6% vs. 98.2%, p < 0.001). TG18 scores > 25 predicted a fivefold increased conversion risk (aOR = 4.9, 95% CI: 2.3–10.6). Prior CGPS induces irreversible fibrosis that significantly increases reoperative difficulty (Δ 14 TG18 points), highlighting the need for careful patient selection in organ-preserving procedures. Definitive management with primary cholecystectomy remains the gold standard.

The repair of large cranial defects remains a major clinical challenge, as conventional materials primarily act as inert fillers and fail to meet the complex biological requirements of cranial bone regeneration. In particular, they lack the ability to temporally coordinate angiogenesis and osteogenesis. This study aimed to develop a temporally functional composite scaffold to dynamically modulate the regenerative microenvironment and promote sequential vascularized bone regeneration. Methods: A silk fibroin-based hydrogel system was designed, incorporating salvianolic acid B (SalB)-loaded sustained-release hydrogel and mineralized silk fibroin hydrogel microspheres (MSFM). Material characterization was performed to evaluate the structural and mechanical properties of the scaffold, as well as the drug release behavior. In vitro assays were conducted to assess endothelial cell migration, tube formation, and the expression of angiogenesis-related genes, along with the osteogenic differentiation potential of bone marrow-derived mesenchymal stem cells (BMSCs). In vivo reparative efficacy was further validated using a rat cranial defect model through morphological and histological analyses. Results: Characterization confirmed that OSFM microgels were uniformly spherical with a porous internal structure and exhibited sustained release of OGP. In vitro, OSFM showed excellent cytocompatibility with BMSCs, significantly enhancing cell proliferation, ALP activity, and mineralized nodule formation compared with SFM (p < 0.05). Tube formation and scratch assays demonstrated that OSFM-conditioned medium promoted HUVEC migration and angiogenesis. In vivo, implantation of OSFM+PCL scaffolds into rat calvarial defects resulted in markedly superior bone regeneration compared with control, PCL, and SFM+PCL groups. The bone volume fraction in the OSFM+PCL group reached 52.31 ± 4.27% at the 8th weeks, significantly higher than 23.65 ± 3.81%, 30.42 ± 3.96%, and 37.86 ± 4.12% in the other groups (p < 0.05). Histological staining confirmed more mature bone formation, abundant collagen deposition, and tight integration between new bone and scaffold. Immunohistochemistry revealed upregulated expression of RUNX2, OCN, and CD31, indicating enhanced osteogenesis and angiogenesis. Conclusions: This temporally functional composite scaffold achieved a sequential "angiogenesis first, osteogenesis later" strategy by leveraging the differential degradation kinetics of its components. The findings demonstrate a biomimetic and temporally regulated approach with strong bioactivity and translational potential for cranial bone regeneration.

Intervertebral disc degeneration (IVDD), a primary cause of debilitating low back pain, is driven by a vicious cycle involving a harsh microenvironment (“soil”) and dysfunctional nucleus pulposus cells (“seeds”), which together promote pathological neurovascular ingrowth (“weeds”) and pain. A therapeutic strategy that can simultaneously “condition the soil” and “modulate the seed” is therefore paramount. Thus, we engineered a biomimetic intelligent nanoliposome (NM-LPTK/RSV-MnCDs) for this dual purpose. The platform is camouflaged with NPC membranes for precise “seed”-homing and incorporates a reactive oxygen species (ROS)-responsive linker for on-demand drug release within the degenerative “soil.” It co-delivers carbonized Mn-containing nanodots (MnCDs) to “condition the soil” by scavenging ROS, and resveratrol (RSV) to “modulate the seed” by suppressing pro-neurovascular signaling. The nanoplatform demonstrated outstanding efficacy in vitro and in two distinct murine IVDD models. It effectively scavenged ROS, inhibited axonal and vascular growth, and preserved matrix synthesis. In vivo, it significantly attenuated disc degeneration, suppressed pathological neurovascular ingrowth, and alleviated pain-related behaviors. Mechanistically, we found this synergistic “soil-conditioning” and “seed-modulating” effect was mediated through the inactivation of the Hippo-YAP signaling pathway, which restored redox homeostasis and blocked aberrant remodeling. This study establishes a targeted, intelligent nanoplatform that synergistically alleviates IVDD and discogenic pain by restoring the disc ecosystem via Hippo pathway inhibition, presenting a precise therapeutic paradigm for degenerative disc disease and its associated neuropathic pain.

Psychological problem and physical–psychological multimorbidity is rising among middle-aged and older adults in China. Whether residential greenness, air pollution and systemic inflammation jointly influence psychiatric outcomes remains unclear. Using a retrospective cross-sectional design based on 2015 China Health and Retirement Longitudinal Study (CHARLS) data, we investigated the link between the Normalized Difference Vegetation Index (NDVI) and psychiatric problems/comorbidities, and evaluated the roles of ambient pollutants (PM₂.₅, PM₁₀) and the inflammatory biomarker C-reactive protein (CRP). The final sample included 6900 adults aged ≥ 45 years. Key findings revealed that a 0.1-unit increase in NDVI was associated with an 18% lower risk of psychiatric problems (OR = 0.82, 95% CI 0.68–0.97, P = 0.024) and a 19% lower risk of physical–psychological multimorbidity (OR = 0.81, 95% CI 0.67–0.99, P = 0.035). Conversely, each unit increase in PM₂.₅ and PM₁₀ was linked to a 1% higher risk of psychiatric problems (PM₂.₅: OR = 1.01, 95% CI: 1.00–1.02, P = 0.033; PM₁₀: OR = 1.01, 95% CI 1.00–1.02, P = 0.042) and multimorbidity (PM₂.₅: OR = 1.01, 95% CI 1.00–1.03, P = 0.048; PM₁₀: OR = 1.01, 95% CI 1.00–1.02, P = 0.052). Inflammatory marker analysis showed that a 10-unit increase in CRP was associated with a 20% higher risk of psychiatric problems (OR = 1.20, 95% CI 1.04–1.39, P = 0.013) and a 22% higher risk of comorbidities (OR = 1.22, 95% CI 1.06–1.42, P = 0.007). Pathway analysis confirmed no significant evidence of mediation effects of PM₂.₅, PM₁₀, or CRP on the association between NDVI and physical–psychological multimorbidity. Cross-sectional analyses indicate an inverse association between residential greenness and psychiatric morbidity, yet longitudinal or interventional evidence is required to establish the clinical significance of this relationship and to determine whether air pollution or inflammation represents a causal mediator before findings can guide policy or practice.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-24005-8.

BackgroundMajor depressive disorder (MDD) poses a significant global public health challenge. Although the Patient Health Questionnaire-9 (PHQ-9) is widely used for MDD screening, its validation in psychiatric samples is limited. Additionally, variability in cut-off values across populations may lead to diagnostic inaccuracies. This study aims to develop a highly accurate nomogram tailored to improve MDD screening precision in psychiatric samples.MethodsFrom March 2024 to February 2025, participants were consecutively recruited from psychiatric outpatient clinics at Xijing Hospital and the 904 Hospital, assigned to training and validation cohorts. Using Least Absolute Shrinkage and Selection Operator regression for dimensionality reduction and predictor identification, we then weighted key factors via multivariable logistic regression to construct a clinically interpretable nomogram. The model’s discriminative ability, calibration, clinical utility and improvement metrics underwent rigorous evaluation.FindingsIn the training cohort (n=519) and validation cohort (n=225), 53.95% and 53.33% of participants were diagnosed with MDD. We constructed a nomogram using 11 predictors selected from 20 variables. In internal validation, the nomogram’s area under the curve (AUC) (95% CI) surpassed the PHQ-9’s (0.932 (0.910–0.954) vs 0.874 (0.844–0.905), p<0.001). Similarly, in external validation, the nomogram’s AUC (95% CI) was higher than the PHQ-9’s (0.935 (0.902–0.968) vs 0.888 (0.844–0.932), p<0.001). Moreover, the nomogram demonstrated better performance than the PHQ-9 in calibration and clinical utility during both internal and external validation. These improvements suggest that the nomogram has the potential to reduce false-positive and false-negative rates in MDD screening.ConclusionThis study developed a novel tool for MDD screening in psychiatric samples by integrating weighted relevant factors, which demonstrates significantly improved accuracy in identifying MDD.