ObjectiveTo investigate the effects of modified Buyang Huanwu Tang on cerebral ischemia-reperfusion injury （CI/RI） in mice via the PTEN-induced putative kinase 1/E3 ubiquitin ligase （PINK1/Parkin） signaling pathway-mediated mitophagy， and to explore the underlying mechanism by which modified Buyang Huanwu Tang improves CI/RI. MethodsSeventy-two male C57BL/6J mice were randomly divided into six groups （n = 12 per group）： Sham-operated group， middle cerebral artery occlusion/reperfusion （MCAO/R） model group， low-， medium-， and high-dose modified Buyang Huanwu Tang groups （8.84， 17.68， 35.36 g·kg^-1·d^-1）， and an aspirin group （13.00 mg·kg^-1·d^-1）. Neurological deficit scores were assessed using the Zea-Longa method. Cerebral infarct volume ratio was measured by 2，3，5-triphenyltetrazolium chloride （TTC） staining. Histopathological changes and neuronal injury in brain tissues were observed using hematoxylin-eosin （HE） staining and Nissl staining. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） assay. Mitochondrial ultrastructure in brain tissue was observed by transmission electron microscopy （TEM）. Serum levels of superoxide dismutase （SOD） and malondialdehyde （MDA） were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression levels of PINK1， Parkin， microtubule-associated protein 1 light chain 3B （LC3B， LC3Ⅱ/Ⅰ）， and p62 in brain tissues were detected by real-time quantitative reverse transcription PCR （Real-time PCR） and Western blot， respectively. ResultsCompared with the sham-operated group， the MCAO/R model group showed significantly increased neurological deficit scores and cerebral infarct volume ratios （P<0.01）. Severe cortical injury on the infarct side was observed， characterized by decreased neuronal density， cytoplasmic vacuolation， nuclear pyknosis， a marked reduction in Nissl bodies， dissolution of Nissl bodies in the cytoplasm of some pyramidal neurons， and blurred cellular boundaries. The number of TUNEL-positive cells increased significantly （P<0.01）. Mitochondria exhibited cristae membrane rupture and matrix vacuolation， with rupture of the outer mitochondrial membrane and formation of autophagosomes， the number of which increased significantly. Serum SOD activity decreased significantly （P<0.01）， while MDA content increased significantly （P<0.01）. In infarcted brain tissues of model mice， the relative mRNA expression and protein levels of PINK1， Parkin and LC3B were significantly increased （P<0.05， P<0.01）， whereas p62 mRNA and protein expression were significantly decreased （P<0.05， P<0.01）， showing statistical significance. Compared with the model group， all treatment groups showed significantly decreased neurological deficit scores and cerebral infarct volume ratios （P<0.01）. Neuronal density increased significantly， cytoplasmic vacuolation was alleviated， nuclear morphology tended to be more regular and clearer， Nissl body density increased significantly with reduced dissolution and improved contour clarity. The mitochondrial cristae structure was partially restored， with some mitochondria showing autophagosome encapsulation， and the degree of mitochondrial damage was alleviated. Serum SOD activity increased significantly （P<0.01）， while MDA content decreased significantly. The mRNA and protein expression levels of PINK1， Parkin， and LC3Ⅱ/Ⅰ were significantly increased （P<0.05， P<0.01）， while p62 mRNA and protein expression in the low- and medium-dose modified Buyang Huanwu Tang groups were significantly decreased （P<0.05， P<0.01）， showing statistical significance. ConclusionModified Buyang Huanwu Tang can upregulate the protein expression levels of PINK1， Parkin， and LC3Ⅱ/Ⅰ and downregulate p62 protein expression， suggesting that it may improve CI/RI by regulating the expression of proteins related to the PINK1/Parkin signaling pathway. Regulation of the mitophagy pathway may be one of the mechanisms by which modified Buyang Huanwu Tang alleviates CI/RI in mice.

Objective: To explore the independent risk factors of allogeneic blood transfusion during perioperative period of cytoreductive surgery in patients with ovarian cancer, and to construct a predictive model to facilitate clinical risk assessment and optimize perioperative blood management. Methods: Clinical data of 156 patients who underwent cytoreductive surgery for ovarian cancer in our hospital from January 2020 to December 2025 were retrospectively collected. The patients were divided into transfusion group (n=51) and non-transfusion group (n=105) according to whether they received allogeneic blood transfusion during perioperative period. The 1∶1 propensity score matching (PSM) was used to correct the confounding factors. Independent sample t test or Mann-Whitney U test was used for measurement data, and chisquare test was used for enumeration data. Variables with P<0.05 in univariate analysis were included in binary logistic regression for multivariate analysis to determine independent risk factors. A nomogram model for perioperative allogeneic blood transfusion risk prediction was constructed based on independent risk factors. Bootstrap method (100 samples) was used for internal calibration verification. ROC curve was used to evaluate the discrimination efficiency, and decision curve analysis (DCA) was used to evaluate the clinical net benefit of the model. Results: After propensity matching, the baseline data of the two groups were balanced and comparable. Multivariate logistic regression analysis showed that preoperative prothrombin time (PT) (OR=2.666, 95%CI 1.249~5.693, P=0.011), preoperative hemoglobin (Hb) (OR=0.953, 95%CI 0.923~0.984, P=0.003), intraoperative blood loss (OR=1.004, 95%CI 1.001-1.006, P=0.004), preoperative anemia grade (OR=3.052, 95%CI 1.007-9.252, P=0.049) were independent influencing factors of perioperative allogeneic blood transfusion. The nomogram model based on the above four factors was significant (LR χ =58.617, P<0.001), and the internal calibration curve showed that the predicted probability of the model was in good agreement with the actual probability (mean absolute error=0.042). The area under the ROC curve (AUC) was 0.890, indicating good discrimination efficiency. DCA showed that the clinical net benefit of the model was better than that of the unified transfusion/non-transfusion strategy in the 0-0.45 risk threshold range. Conclusion: Intraoperative blood loss, preoperative PT, preoperative Hb and preoperative anemia grade are independent risk factors for perioperative allogeneic blood transfusion in patients undergoing cytoreductive surgery for ovarian cancer. The nomogram model based on the above factors has good predictive efficacy and clinical hierarchical decision-making value, which can provide reference for clinical implementation of individualized blood management for high-risk patients and reduction of unnecessary blood transfusion rate.

Objective To analyze the external radiation dose rate and radiation protection measures during treatment of a patient with hepatocellular carcinoma (HCC) who underwent ⁹⁰Y selective internal radiotherapy (⁹⁰Y-SIRT). Methods A male HCC patient who received ⁹⁰Y-SIRT with an activity of 4.65×10⁹ Bq was selected as the research subject using retrospective analysis. External radiation dose rate meters were used to detect ambient dose equivalent rates around the radiation worker, the HCC patient, and the workplace during treatment. Surface contamination meters were used to detect surface contamination levels of the radiation worker and the workplace. Results The ambient dose equivalent rate around the interventional radiology staff during treatment ranged from 3.7 to 39.0 μSv/h. The patient's ambient dose equivalent rate of surgical site at distances of 30, 100, and 200 cm ranged from 45.0 to 5.6, 4.4 to 0.4, and 0.4 to 0.1 μSv/h respectively without protection, and 14.0 to 3.4, 3.2 to 0.3, and 0.4 to 0.1 μSv/h respectively when the surgical site was covered with a 1.0 mmPb lead rubber drape after 0.0 to 161.0 hours of the surgery. In the nuclear medicine department, ambient dose equivalent rate of the workplace ranged from 0.4 to 740.0 μSv/h. The ambient dose equivalent rate around all monitoring points in the digital subtraction angiography operating room accounted at 0.1 μSv/h, and the observation ward ranged from 0.1 to 0.2 μSv/h. The β surface contamination levels of the radiation worker and workplace were below the minimum detection limit (0.16 Bq/cm²). Conclusion Radiation doses for both HCC patients and radiation worker remained within acceptable limits when appropriate protective equipment was used. A well-designed workplace layout is essential to ensure effective implementation of radiation protection.

Objective To evaluate the safety and feasibility of remote robot-assisted thoracoscopic surgery utilizing 5G technology. Methods Clinical data from five patients who underwent 5G remote robot-assisted thoracoscopic surgery at the Thoracic Surgery Center of Gansu Provincial People's Hospital from May to October 2024 were retrospectively analyzed. Results Finally, five patients were included. There were 2 males and 3 females at median age of 50 (42-63) years. All five surgeries (including 1 patient of lobectomy, 3 patients of partial lung resection and 1 patient of mediastinal lesion resection) were successfully completed without conversion to thoracotomy, complications, or mortality. The median intraoperative signal delay across the patients was 39 (37-42) ms. The median psychological load score for the surgeons was 9 (3-13). The median operation time was 100 (80-122) minutes with a median intraoperative blood loss of 100 (30-200) mL. Catheter drainage lasted a median of 4 (3-5) days, and the median drainage volumes on the first, second, and third postoperative day were 200 (100-300) mL, 150 (60-220) mL, and 80 (30-180) mL, respectively. The median postoperative hospital stay was 4 (3-7) days, and the median pain scores on the third postoperative day were 3 (1-4), 3 (0-3), and 1 (0-3), respectively. Conclusion 5G remote robot-assisted thoracoscopic surgery is safe and effective, with good surgical experience, smooth operation and small intraoperative delay.

This case report presents a 16-year-old male patient with deficiency of adenosine deaminase 2(DADA2). The patient had a history of Raynaud′s phenomenon with digital ulcers since childhood. As the disease progressed, the patient developed retinal vasculitis, intracranial hemorrhage, skin necrosis, severe malnutrition, refractory hypertension, and gastrointestinal bleeding. Genetic testing revealed compound heterozygous mutations in the ADA2 gene (paternal c.1072G > A pathogenic mutation + maternal c.1065C > A variant of unknown clinical significance). ADA2 enzyme activity was significantly reduced (0.1 U/L). A multidisciplinary treatment team developed an individualized plan to address key issues, including nutritional support, blood pressure control, rehabilitation, pain management, and balancing anticoagulation/bleeding risks. After systematic intervention, the patient′s condition showed partial improvement. This case reveals clinical challenges such as anticoagulation decisions and nutritional support of DADA2. It also emphasizes the importance of early molecular diagnosis, tumor necrosis factor-α inhibitor targeted therapy, and multidisciplinary collaboration in management, underlining the core value of precision medicine in rare disease management.

OBJECTIVES: To explore the molecular mechanism of Jiangzhi Huaban Decoction (JZHBD) for improving atherosclerosis through the "qi meridian-blood channels" pathway. METHODS: ApoE^-/- mouse models of atherosclerosis were established by high-fat diet feeding for 8 weeks, with C57BL/6 mice on a normal diet as the controls. Forty ApoE^-/- mouse models were randomized into model group, low-, medium-, and high-dose JZHBD treatment groups, and atorvastatin treatment group (n=8) for their respective treatments for 8 weeks. The changes in body weight and overall condition of the mice were monitored weekly. After the treatments, serum levels of TC, TG, HDL-C, LDL-C, TBA, ALT, and AST of the mice were measured, pathological changes in the liver and aortic root plaques were examined with HE staining, and lipid accumulation in the liver and aortic wall was assessed using Oil Red O staining. The core molecular mechanism was studied through transcriptomics, and the expressions of the key pathway proteins were confirmed using Western blotting and immunohistochemistry. RESULTS: Treatment with JZHBD significantly reduced blood lipid and total bile acid levels, improved liver function and hepatic steatosis, and decreased aortic lipid deposition and plaque area in the mouse models of atherosclerosis. Transcriptomic analysis suggested that the therapeutic mechanism of JZHBD involved reverse cholesterol transport, PPAR signaling, and the inflammatory pathways. In atherosclerotic mice, JZHBD treatment obviously up-regulated hepatic expressions of PPARγ, LXRα, ABCA1, ABCG1, and CYP7A1, down-regulated hepatic expressions of p-p65/p65, IL-6, IL1β in the liver, increased ABCG5 and ABCG8 expressions in the intestines, and decreased ICAM-1 and VCAM-1 expressions in the aortic plaques. CONCLUSIONS JZHBD improves atherosclerotic vascular damage and plaque formation possibly by regulating hepatic reverse cholesterol transport and inflammation via modulating the hepatic PPARγ/LXRα/NF-κB signaling pathway.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Mice, Inbred C57BL ; Plaque, Atherosclerotic/metabolism* ; Liver/metabolism* ; Mice ; Atherosclerosis/metabolism* ; Cholesterol/metabolism* ; PPAR gamma/metabolism* ; Male ; Diet, High-Fat ; Biological Transport

The prelimbic cortex (PL) plays a critical role in processing both the sensory and affective components of pain. However, the underlying molecular mechanisms remain poorly understood. In this study, we observed a reduction in hyperpolarization-activated cation current (I_h) in layer V pyramidal neurons of the contralateral PL in a mouse model of spared nerve injury (SNI). The expression of hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2) channels was also decreased in the contralateral PL. Conversely, microinjection of fisetin, a partial agonist of HCN2, produced both analgesic and anxiolytic effects. Additionally, we found that cyclin-dependent kinase 5 (CDK5) was activated in the contralateral PL, where it formed a complex with HCN2 and phosphorylated its C-terminus. Knockdown of CDK5 restored HCN2 expression and alleviated both pain hypersensitivity and anxiety-like behaviors. Collectively, these results indicate that CDK5-mediated dysfunction of HCN2 in the PL underlies nerve injury-induced mechanical hypersensitivity and anxiety.
Animals ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels/metabolism* ; Hyperalgesia/metabolism* ; Cyclin-Dependent Kinase 5/metabolism* ; Neuralgia/metabolism* ; Male ; Anxiety/metabolism* ; Mice ; Potassium Channels/metabolism* ; Mice, Inbred C57BL ; Disease Models, Animal ; Pyramidal Cells/metabolism*

Protrusive facial deformities, characterized by the forward displacement of the teeth and/or jaws beyond the normal range, affect a considerable portion of the population. The manifestations and morphological mechanisms of protrusive facial deformities are complex and diverse, requiring orthodontists to possess a high level of theoretical knowledge and practical experience in the relevant orthodontic field. To further optimize the correction of protrusive facial deformities, this consensus proposes that the morphological mechanisms and diagnosis of protrusive facial deformities should be analyzed and judged from multiple dimensions and factors to accurately formulate treatment plans. It emphasizes the use of orthodontic strategies, including jaw growth modification, tooth extraction or non-extraction for anterior teeth retraction, and maxillofacial vertical control. These strategies aim to reduce anterior teeth and lip protrusion, increase chin prominence, harmonize nasolabial and chin-lip relationships, and improve the facial profile of patients with protrusive facial deformities. For severe skeletal protrusive facial deformities, orthodontic-orthognathic combined treatment may be suggested. This consensus summarizes the theoretical knowledge and clinical experience of numerous renowned oral experts nationwide, offering reference strategies for the correction of protrusive facial deformities.
Humans ; Orthodontics, Corrective/methods* ; Consensus ; Malocclusion/therapy* ; Patient Care Planning ; Cephalometry

Enamel demineralization, the formation of white spot lesions, is a common issue in clinical orthodontic treatment. The appearance of white spot lesions not only affects the texture and health of dental hard tissues but also impacts the health and aesthetics of teeth after orthodontic treatment. The prevention, diagnosis, and treatment of white spot lesions that occur throughout the orthodontic treatment process involve multiple dental specialties. This expert consensus will focus on providing guiding opinions on the management and prevention of white spot lesions during orthodontic treatment, advocating for proactive prevention, early detection, timely treatment, scientific follow-up, and multidisciplinary management of white spot lesions throughout the orthodontic process, thereby maintaining the dental health of patients during orthodontic treatment.
Humans ; Consensus ; Dental Caries/etiology* ; Dental Enamel/pathology* ; Tooth Demineralization/etiology* ; Tooth Remineralization

The prevalence of Class III malocclusion varies among different countries and regions. The populations from Southeast Asian countries (Chinese and Malaysian) showed the highest prevalence rate of 15.8%, which can seriously affect oral function, facial appearance, and mental health. As anterior crossbite tends to worsen with growth, early orthodontic treatment can harness growth potential to normalize maxillofacial development or reduce skeletal malformation severity, thereby reducing the difficulty and shortening the treatment cycle of later-stage treatment. This is beneficial for the physical and mental growth of children. Therefore, early orthodontic treatment for Class III malocclusion is particularly important. Determining the optimal timing for early orthodontic treatment requires a comprehensive assessment of clinical manifestations, dental age, and skeletal age, and can lead to better results with less effort. Currently, standardized treatment guidelines for early orthodontic treatment of Class III malocclusion are lacking. This review provides a comprehensive summary of the etiology, clinical manifestations, classification, and early orthodontic techniques for Class III malocclusion, along with systematic discussions on selecting early treatment plans. The purpose of this expert consensus is to standardize clinical practices and improve the treatment outcomes of Class III malocclusion through early orthodontic treatment.
Humans ; Malocclusion, Angle Class III/classification* ; Orthodontics, Corrective/methods* ; Consensus ; Child