ObjectiveTo develop a community-family management model for older adults with mild cognitive impairment (MCI) and to formulate detailed application specifications, and to fully leverage the initiative of communities and families under limited resource conditions, for achieving community-based early detection and early intervention for older adults with MCI. MethodsA systematic literature review was conducted to identify pertinent publications. Corpus-based research methodologies were employed to extract, refine, integrate and synthesize management elements, thereby establishing the specific content and service processes for each stage of the management model. Utilizing the 5W2H analytical framework, essential elements such as management stakeholders, target populations, content and methods for each stage were delineated. The model and its application guidelines were finalized through expert consultation and demonstration. ResultsAn expert evaluation of the management model yielded mean scores of 4.84, 4.32 and 4.84 for acceptability, feasibility and systematicity, respectively. By integrating the identified core elements with expert ratings and feedback, the final iteration of the community-family management model for older adults with MCI was formulated. This model comprised of five stages: screening and identification, comprehensive assessment, intervention planning, monitoring and referral pathways to ensure implementation, and enhanced support for communities, family members and caregivers. Additionally, it included 18 specific application guidelines. ConclusionThe proposed management model may theoretically help delay cognitive decline, improve cognitive function and potentially promote reversal from MCI to normal cognition. It may also enhance the awareness and coping capacity of older adults and their families, strengthen community healthcare professionals' ability to early identify and manage MCI.

Myasthenia gravis is an autoimmune disorder characterized by impaired neuromuscular transmission. Thymectomy is one of the therapeutic options for acetylcholine receptor antibody-positive myasthenia gravis patients. The quality of perioperative care is directly associated with surgical safety and patient outcomes. However, there is currently a lack of specialized nursing consensus or guidelines specifically addressing the care of these patients domestically or internationally. To promote the standardization and normalization of perioperative nursing care for myasthenia gravis patients undergoing thymectomy and to ensure treatment efficacy, a panel of 57 experts from relevant fields was convened. Based on evidence-based medicine and clinical practice experience, discussions were held on various aspects including condition assessment, nutritional support, medication management, and airway care, resulting in a consensus with 18 final recommendations by using the Delphi method through two rounds of expert consultation. This consensus aims to provide a scientific reference for the perioperative nursing care of myasthenia gravis patients undergoing thymectomy.

OBJECTIVE To formulate Guidelines for the standardized implementation of pharmacist-managed clinics （ 2026 edition ） in response to the challenges faced by such clinics in China， including uneven development， large discrepancies in service specifications， insufficient patient awareness， and limited medical insurance coverage. METHODS Led by the Pharmaceutical Affairs Professional Committee of the Chinese Hospital Association， the Evidence-based Pharmacy Professional Committee of the Chinese Pharmaceutical Association， and the Hospital Pharmacy Professional Committee of the Cross-strait Medical and Health Exchange Association， a total of 19 domestic hospital pharmacy experts were organized. Through a systematic review of national policies and literature research， current practical experience was summarized. Consensus on the contents of the guidelines was reached after in-depth discussions. RESULTS &CONCLUSIONS The guidelines covered five sections： definition and connotation of pharmacist-managed clinics， establishment requirements， implementation and management， post competency， and practical research. Firstly， the definition and connotation included three operational forms of pharmacist-managed clinics （independent mode， physician-pharmacist joint mode， and online pharmacist-managed clinic mode） and classified service modes （specialty-specific， drug-specific， and disease-specific pharmacist-managed clinics）. The establishment requirements were further refined， covering system construction （pharmaceutical service management system， quality control and assessment mechanism）， personnel qualifications （professional credentials， continuing education and professional training， etc）， service recipients， as well as service venues and facilities. Subsequently， the implementation and management of pharmacist-managed clinics were proposed， involving service procedures， intervention measures， documentation and records， patient education and follow-up， humanistic care， as well as risk management and quality control. Finally， post competency encompassed the competency requirements for pharmacists providing services in pharmacist-managed clinics， as well as the suggestions on teaching methods； practical research encouraged the conduct of high-quality pharmaceutical practice in the setting of pharmacist-managed clinics. The guidelines provide valuable guidance for the standardized implementation of pharmacist-managed clinics in China in terms of establishment， management， teaching， and research， fill the guideline gap in this field， and can promote the high-quality development of pharmacist-managed clinics.

"Sinew prescription correspondence" is the principle of selecting prescriptions for channel sinew diseases. On the basis of the theory of syndrome differentiation and treatment， the pulse manifestation corresponds to the channel sinew syndrome， which can improve the flexibility and standardization of clinical prescriptions. From the perspective of systematic dialectical sphygmology， this paper explains the dialectical relationship between channel sinew theory and pulse body elements， pulse wall elements， pulse elements and blood flow elements， and clarifies the internal relationship between pulse manifestation and prescriptions at the level of channel sinew disease. The prescription is derived from the method， while the method is established with the syndrome， and the prescription is unified by the method. According to the theory of "sinew prescription correspondence"， the treatment ideas of channel sinew diseases were analyzed from the perspective of channel sinew distribution， functional characteristics and structural changes. On this basis， the diagnosis of channel sinew disease and the application of prescriptions are expanded， and the research on the internal treatment and diagnosis mode of "pulse manifestation-channel sinew-zang fu （脏腑）" is prospected， so as to expand the differentiation and treatment methods of channel sinew theory.

Background: and Purpose Vertebrobasilar fusiform aneurysms (VBFAs) carry substantial morbidity and mortality, but optimal management for unruptured VBFAs remains unclear. We compared the safety and efficacy of conservative management (CM), stent-assisted coiling (SAC), and flow diverters (FDs) in patients with unruptured VBFAs, focusing on long-term prognosis. Methods: This study included data from a nationwide Chinese cohort of patients with vertebrobasilar dissecting aneurysms. Inverse probability of treatment weighting (IPTW) balanced confounders across groups. The primary outcome was poor prognosis (modified Rankin Scale score >2). Secondary outcomes included aneurysm rupture, ischemic stroke, compression symptoms, and VBFA-related deaths. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup and sensitivity analyses were performed. Results: Among 1,115 patients with unruptured VBFAs, 838 (median age, 54 years; 655 men) were included. After IPTW, baseline characteristics were balanced. Median follow-up was 54 months. FD was associated with a lower risk of poor prognosis than CM (OR, 0.48 [95% CI, 0.30 to 0.77]; p=0.002), with no difference between CM and SAC. FD also reduced aneurysm rupture (OR, 0.20 [95% CI, 0.07 to 0.60]; p=0.004) and compression symptoms (OR, 0.30 [95% CI, 0.13 to 0.68]; p=0.004) versus CM. Time-to-event analyses further revealed significant differences in vertebral artery lesions and Type I–II VBFAs, whereas no significant differences were observed in basilar or vertebrobasilar junction lesions or in Type III–IV VBFAs. Conclusions Compared with CM, FD was associated with improved long-term outcomes in unruptured VBFAs, particularly in vertebral artery lesions and Type I–II VBFAs, although residual confounding cannot be excluded.

Objective To explore the feasibility of magnetic compression technique (MCR) in the treatment of severe single mid-ureteral stricture in a rabbit model. Methods After 10 female New Zealand rabbits were selected, the distal end of the right ureter was ligated with silk thread. Two weeks after the operation, when the right ureter was dilated, the mid-ureter was ligated again with silk thread to create a severe single mid-ureteral stricture animal model. Longitudinal incisions were made at the upper and lower ends of the ligation site, and cylindrical NdFeB magnets with central holes (sub-magnets and main magnets) were placed to anastomose and recanalize the mid-ureteral stricture. The magnets were adjusted to the appropriate position to automatically align and attract each other. The longitudinal incision sites of the ureter were sutured with 6-0 Prolene thread, and the abdominal cavity was closed layer by layer. The operation time was recorded. X-ray films were taken every two days to confirm the position of the magnets and record the time of magnet detachment. Three weeks after the operation, the anastomotic specimens were obtained, and the formation of the anastomosis was evaluated with gross observation and histological staining. Results Two weeks after ligation, all experimental rabbits showed obvious dilation of the right ureter. The mid-ureteral ligation and placement of the male and female magnets were successfully completed in all 10 experimental rabbits, with an operation time of (24.00±5.15)minutes. The male and female magnets attracted each other well. X-ray examination showed that the magnets detached and entered the distal ureter (14.0±1.9) days after magnetic compression. The recanalization of the severe single mid-ureteral stricture was successfully achieved. The gross specimens and histological examination of the anastomosis showed that the anastomosis remained patent and the mucosal healing was good. All experimental rabbits survived well after the operation without serious complications. Conclusion MCT provides a new idea and novel method for the treatment of mid-ureteral stricture. This study confirmed the feasibility of this technique in treating severe single mid-ureteral stricture in a rabbit model. The operation is relatively simple and has potential for clinical application.

BackgroundNon-suicidal self-injury （NSSI） has become a public health concern of wide interest. Adolescents with depressive disorder are at high risk of NSSI behaviors. Previous studies have mostly focused on analyzing factors associated with NSSI behaviors， while research on developing visual models that are intuitive， quantifiable， and suitable for rapid clinical assessment is relatively limited. ObjectiveTo investigate the risk factors for NSSI behaviors in adolescents with depressive disorder， and to construct a nomogram prediction model for the risk of NSSI behaviors occurrence， so as to provide a quantitative tool for clinical rapid assessment of the occurrence risk of NSSI behaviors in this population. MethodsA cross-sectional study was conducted. A total of 448 adolescent patients diagnosed with depressive disorder who attended the Mental Health Department of The Second Hospital， Lanzhou University from February to December 2025 and met the diagnostic criteria for depressive disorder as specified in the Diagnostic and Statistical Manual of Mental Disorders， fifth edition （DSM-5） were enrolled. All participants were randomly divided into the modeling group （n=313） and the validation group （n=135） at a ratio of 7∶3. Assessments were performed using the Self-rating Depression Scale （SDS）， the Self-rating Anxiety Scale （SAS）， the Barratt Impulsiveness Scale-11 （BIS-11）， the Childhood Trauma Questionnaire-short form （CTQ-SF）， and the Pittsburgh Sleep Quality Index （PSQI）. Binary Logistic regression analysis was applied to screen independent predictors of NSSI behaviors in the modeling group， and a nomogram was constructed accordingly. The receiver operating characteristic （ROC） curve， calibration curve， and decision curve analysis （DCA） were used to evaluate the discrimination， calibration and clinical utility of the model， respectively. ResultsBinary Logistic regression analysis revealed that younger age， female sex， higher SDS score， higher BIS-11 score， higher CTQ-SF score， and higher PSQI score were risk factors for NSSI behaviors in adolescent patients with depressive disorder （OR=0.816， 2.671， 1.131， 1.030， 1.064， 1.102， P<0.05 or 0.01）. The Hosmer-Lemeshow test of the nomogram prediction model constructed based on these six indicators showed a good fit （χ²=15.144， P=0.056）. Model validation showed that the AUC was 0.895 for the modeling group and 0.891 for the validation group. The calibration curves suggested that the mean absolute errors between the actual values and the predicted values were 0.043 and 0.023， respectively. Decision curve analysis indicated that the model provided a clear net clinical benefit when the risk threshold was greater than 0.11. ConclusionThe nomogram model based on six indicators （age， sex， depressive symptom severity， impulsivity， childhood trauma， and sleep quality） for predicting NSSI risk in adolescent patients with depressive disorder exhibits good discrimination， calibration， and clinical application value. ［Funded by National Natural Science Foundation of China （number， 82560281）； Gansu Provincial Science and Technology Program （number， 25JRRA618）； Gansu Provincial Health Industry Research Project （number， GSWSKY2025-13）； The College Students' Innovation and Entrepreneurship Training Program of the Second Clinical Medical College of Lanzhou University （number， 20250050060）］

ObjectiveTo develop and validate a nomogram for predicting the risk of concurrent cognitive impairment in older adults with heart disease. MethodsSelf-reported data from 2 673 respondents in the 2020 China Health and Retirement Longitudinal Study were analyzed. The participants were randomly divided into a training set (n = 1 871) and a validation set (n = 802). Heart disease status was determined using a self-report questionnaire. Logistic regression analysis was performed to identify predictors, and a nomogram for predicting the risk of concurrent cognitive impairment in older adults with heart disease was developed using R software. Bootstrap resampling was used for internal validation, and model performance was further evaluated in the randomly split validation set. The predictive performance of the model was assessed using the area under the receiver operating characteristic curve (AUC) and calibration curves.. ResultsA total of 2 673 older adults with heart disease were included, out of whom 315 participants in the training set had cognitive impairment. Lasso regression analysis identified age, education level, place of residence, instrumental activities of daily living and depression as predictors of concurrent cognitive impairment. A prediction model incorporating these five variables was constructed. The AUC were 0.827 (95%CI 0.804 to 0.850) in the training set and 0.847 (95%CI 0.812 to 0.882) in the validation set. The Hosmer-Lemeshow test yielded P = 0.154 and P = 0.716 in the training and validation sets, respectively. Calibration curves showed good agreement between predicted and observed probabilities. Decision curve analysis indicated that the model provided favorable net benefit and predictive performance. ConclusionThe nomogram may provide a useful reference for risk screening and early intervention for cognitive impairment in older adults with heart disease.

Renal fibrosis is the common pathological endpoint of many forms of chronic kidney disease (CKD), yet the mechanisms determining effective repair versus persistent fibrotic remodeling remain incompletely understood. Peritubular capillaries (PTCs) are not merely passive targets of fibrotic injury, but form a dynamic vascular microenvironment linking regional perfusion, oxygen delivery, tubular metabolism, endothelial barrier integrity, pericyte support, immune-cell trafficking, and extracellular matrix (ECM) remodeling. We propose that PTC abnormalities should not be interpreted simply as reduced capillary density, but as a multidimensional disturbance of microvascular structure and function. Structural vascular preservation does not necessarily indicate effective microcirculation: anatomically detectable capillaries may still exhibit impaired perfusion, barrier dysfunction, abnormal endothelial-pericyte interactions, disturbed oxygen metabolism, or reduced network connectivity. Conversely, increased angiogenesis does not necessarily signify successful vascular repair if vessels remain immature, poorly perfused, or inadequately integrated into the existing network. To organize these abnormalities, we conceptualize PTC remodeling into four predominant but nonexclusive states: endothelial barrier disruption with inflammatory adhesion; endothelial-pericyte uncoupling with no-reflow; dysregulated angiogenesis with network simplification; and capillary rarefaction with fibrotic matrix locking. These states are not sequential stages of CKD. They may coexist within the same kidney, overlap within the same anatomical region, and vary with disease etiology, injury phase, vascular compartment, and treatment exposure. We further propose six dimensions for evaluating PTC status—structural presence, functional perfusion, barrier integrity, pericyte coupling, oxygen metabolism, and network connectivity—so that vascular quantity, function, and reparative capacity are assessed separately rather than inferred from a single endothelial marker or capillary-density measurement. Mechanistically, these states converge on a bidirectional microvascular-fibrotic feedback loop. Barrier disruption facilitates leukocyte recruitment and alters vascular paracrine signaling. Endothelial-pericyte uncoupling compromises capillary stability, whereas abnormal pericyte contraction may increase local vascular resistance and contribute to no-reflow before overt capillary loss. Dysregulated angiogenesis may generate vessels that fail to mature or connect to an effective perfusion network. Progressive capillary rarefaction compromises oxygen delivery, while sustained tubular transport demand and mitochondrial dysfunction may aggravate regional oxygen supply-demand mismatch. Injured tubules, immune cells, endothelial cells, pericytes, and fibroblasts communicate through soluble mediators, extracellular vesicles, direct cell contact, and cell-matrix signaling. Importantly, fibrosis is not merely a downstream consequence of microvascular injury. Altered ECM may increase diffusion distance, modify mechanotransduction, impair endothelial survival and migration, and restrict capillary reopening and regeneration. We use the term matrix locking to describe this sustained constraint on vascular repair, while emphasizing that current evidence does not establish irreversible disease in humans. This framework also has therapeutic implications. PTC-directed treatment should not be reduced to increasing vessel number or uniformly promoting angiogenesis. Instead, intervention should be matched to the dominant and potentially reversible abnormality: preserving endothelial barrier function; restoring endothelial-pericyte stability and reducing pathological microvascular resistance; normalizing angiogenesis so that vascular growth is accompanied by maturation, barrier competence, network integration, and effective perfusion; and, in advanced rarefaction, relieving matrix-related constraints while supporting vascular regeneration. The context- and time-dependent effects of signaling through VEGF, Tie2, PDGF-B/PDGFRβ, eNOS/NO, and related pathways indicate that the same molecular signal may exert different effects depending on disease context and timing. Therapeutic efficacy should therefore be evaluated by restoration of effective microcirculation and tissue function rather than by isolated molecular changes or capillary counts alone. Despite increasing mechanistic evidence, the translational basis for this framework remains limited. Most causal and interventional data derive from animal or cell models, whereas human evidence is largely limited to pathological observations, patient-sample associations, and prognostic studies. Currently available circulating and urinary candidate biomarkers generally lack sufficient specificity for PTC injury or state assignment, and no standardized quantitative thresholds have been externally validated. The four-state model should therefore be regarded as a hypothesis-generating analytical framework rather than a clinicopathological classification system. Future studies should integrate spatially resolved tissue phenotyping, blood and urine biomarkers, and dynamic microcirculatory assessment in longitudinal cohorts. They should test reproducibility, assess prognostic value beyond conventional pathology, estimated glomerular filtration rate, and proteinuria, and determine whether changes in PTC status precede or mediate therapeutic benefit. Linking reproducible microvascular phenotypes to defined mechanisms, treatment response, and long-term renal outcomes will be essential to determine whether state-directed assessment and restoration of the PTC microenvironment can ultimately inform patient stratification and therapeutic decision-making.

Inflammatory bowel disease (IBD) is a chronic disorder characterized by recurrent mucosal inflammation. Although biologics and small-molecule therapies can effectively suppress inflammation, only 13%-34% of patients achieve deep histological remission, and most experience relapse within 2-3 years. Existing biomarkers, including C-reactive protein (CRP), fecal calprotectin, and endoscopic measures, have limited ability to detect subclinical molecular abnormalities, suggesting that disease-driving factors may persist even during clinical remission. Recently, Pang et al. reported a study in Science that investigated the role of epithelial cell-death signaling using a prospective adult IBD cohort comprising 80 participants and more than 900 biopsy specimens. By integrating bulk and spatial transcriptomics, patient-derived organoids, and 24-36 months of longitudinal follow-up, the authors characterized epithelial cell-death programs associated with IBD persistence. They found that the necroptosis-associated marker pRIPK3 could be detected in the absence of overt histological inflammation and persisted during advanced therapy. IFN‑γ and TNF reshaped the transcriptional landscape of specific colonic epithelial cells, inducing an inflammatory macrophage-like program termed cluster B and triggering RIPK1-independent RIPK3 signaling. This was followed by NOS2/iNOS-mediated mitochondrial apoptosis driving colonocyte death, whereas PUMA-dependent apoptosis contributed to intestinal stem-cell loss. Higher baseline pRIPK3 levels were associated with subsequent disease activity, although their independent predictive value remains to be established. These findings suggest that persistent IBD may reflect not only residual immune inflammation but also inflammation-induced pathological epithelial states. Future therapeutic strategies may therefore need to extend beyond inflammation control toward “molecular repair”, including targeting noncanonical RIPK3 signaling, modulating iNOS/PUMA-dependent mitochondrial apoptosis, and developing relapse-risk stratification strategies based on tissue biomarkers such as pRIPK3. Such approaches may help shift the therapeutic goal from “clinical remission” toward “molecular healing”.