Stroke is the leading cause of death and disability among adults in China， and its common complications include digestive system abnormalities， cognitive impairment， depression， stroke-associated pneumonia， and hemiplegia. The combination of traditional Chinese and Western medicine has great potential in treating post-stroke complications. Xinglou Chengqitang （XLCQT） is a representative prescription of alleviating the disease in the upper part by treating the lower part. It has definite therapeutic effect and high safety. Clinically， XLCQT is often used to treat stroke and its complications. However， the quantity and quality of clinical trials of XLCQT in treating post-stroke complications need to be improved. Additionally， since the basic research is weak， the material basis and multi-target mechanism for the efficacy of this prescription are unknown. This article reviews XLCQT in terms of the pharmacodynamic basis， medicinal properties， safety evaluation， and progress in clinical research and mechanisms in treating post-stroke complications. This article summarizes 22 key active ingredients of XLCQT in treating acute stroke complicated with syndrome of phlegm heat and fu-organ excess. Among these key active ingredients， resveratrol， kaempferol， luteolin， chrysoeriol， apigenin， （+）-catechin， and adenosine have good pharmacokinetic properties and high bioavailability. The mechanisms of XLCQT in treating post-stroke complications are complex， including inflammatory response， brain-gut axis， hypothalamic-pituitary-adrenal （HPA） axis， intestinal flora， neurotrophic factors， autophagy， oxidative stress， and free radical damage. This review helps to deeply understand the pharmacodynamic basis and mechanisms of XLCQT in treating post-stroke complications and provides a theoretical basis for the clinical application of XLCQT against post-stroke complications and the development of drugs.

OBJECTIVE: To delineate the clinical and genetic features of a Chinese girl harboring a rare de novo variant of SYNGAP1 associated with Mental retardation, autosomal dominant 5 (MRD5), and to conduct a comprehensive genotype-phenotype correlation analysis within the Chinese population through an extensive literature review. METHODS: A 5-year-old girl presenting with seizures without an obvious cause was enrolled in September 2020. Genomic DNA was extracted from the patient and her parents. Whole exome sequencing (WES) was performed on the proband to identify suspected pathogenic variants based on her clinical phenotype. Sanger sequencing was used for validation, followed by bioinformatic analysis of the variant. Additionally, data from 54 previously reported Chinese cases with SYNGAP1 variants were integrated to summarize the distribution of variant types and clinical characteristics. Ethical approval was obtained from the Ethics Committee of Kunming Children's Hospital (Ethics No.: 2021-03-055-K01). RESULTS: WES identified a heterozygous nonsense variant, SYNGAP1 c.725G>A (p.Trp242*), in the proband. Sanger sequencing confirmed it was a de novo variant. According to the ACMG guidelines, this variant was classified as pathogenic (PVS1+PS2). Based on the clinical manifestations, the patient was diagnosed with MRD5. Bioinformatic analysis suggested that this variant introduces a premature stop codon at tryptophan 242, disrupting the PH domain and leading to the loss of the C2, Ras-GAP, and C-terminal domains. The pooled analysis of Chinese cases revealed that nonsense (38.2%) and frameshift (36.4%) variants were the predominant types. Intellectual disability/developmental delay was present in 100.0% of patients, epilepsy in 83.6%, and autism spectrum disorder in 41.3%. The incidence of epilepsy differed significantly among variant types (P = 0.045). Exons 8 and 15 were identified as mutation hotspots. CONCLUSION This study has identified a SYNGAP1 c.725G>A variant in the Chinese population and confirmed it as a potential cause of MRD5, which expanded the mutational spectrum of this disorder.
Humans ; Female ; Child, Preschool ; Intellectual Disability/genetics* ; ras GTPase-Activating Proteins/genetics* ; Phenotype ; Exome Sequencing ; Genetic Association Studies

With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

ObjectiveTo investigate the impact of a cold environment on the pathophysiological changes in dogs after abdominal gastrointestinal blast injury. MethodsEight healthy common-grade adult male Beagles were selected and randomly divided into a cold group and a normal temperature group, with 4 dogs in each group. Prior to surgery, Beagles dogs were fasted and deprived of water for 12 hours; after establishing a vein at the edge of the ear, propofol （2 mg·kg^-1·min^-1） was continuously infused using a microinfusion pump to maintain anesthesia. Tracheal intubation was performed while preserving spontaneous breathing, and the electroencephalogram bifrequency index was maintained at 40-60 to ensure stable anesthesia. A model of abdominal gastrointestinal blast injury in Beagle dogs was established using a multifunctional combat trauma modeling platform. After blast injury, the cold group was exposed to a cold chamber at -20 ℃ combined with 10% body surface area ice water immersion for 40 min, while the normal temperature group was kept in an environment at (25±2) ℃ for 40 min after blast injury. Vital signs such as heart rate, blood pressure, and blood oxygen saturation were monitored in both groups before blast injury, immediately after blast injury, and 40 min after blast injury. And arterial blood gas parameters, including pH, partial pressure of oxygen in arterial blood (PaO₂), partial pressure of carbon dioxide in arterial blood (PaCO₂), actual bicarbonate radical (HCO₃^-), lactic acid (Lac), and blood base excess (BEb), were measured. After the experiment, gastrointestinal tissues (gastric antrum and upper jejunum 5 cm distal to the suspensory ligament of the duodenum) were harvested for pathological analysis via hematoxylin-eosin (HE) staining combined with semi-quantitative scoring. ResultsPhysiological indicators showed that the body temperature of the cold group was significantly lower than that of the normal temperature group (P<0.01), and the heart rate and systolic blood pressure of the cold group were significantly higher than those of the normal temperature group (P<0.000 1). PaCO₂ was markedly elevated and BEb was markedly decreased in the cold group relative to the normal temperature group (P<0.000 1), suggesting aggravated respiratory acidosis and metabolic acidosis. Pathological analysis showed that gastro-intestinal tissue damage was more severe in the cold group: the gastric mucosal epithelial shedding rate was > 60% (vs. <25% in the normal temperature group), the necrosis rate of the epithelial cells at the tips of intestinal villi reached more than 70% (vs. < 30% in the normal temperature group), and inflammatory cell infiltration involved the submucosa (vs. limited to the superficial mucosa in the normal temperature group). The semi-quantitative scoring results were consistent with the pathological analysis results, further confirming that the cold environment exacerbated gastrointestinal tissue damage caused by abdominal gastrointestinal blast injury. ConclusionA cold environment can exacerbate circulatory dysfunction and gastrointestinal tissue damage in Beagle dogs after blast injury, providing experimental evidence for early rewarming intervention for combat trauma in cold regions.

With the widespread adoption of low-dose CT screening and the extensive application of high-resolution CT, the detection rate of sub-centimeter lung nodules has significantly increased. How to scientifically manage these nodules while avoiding overtreatment and diagnostic delays has become an important clinical issue. Among them, lung nodules with a consolidation tumor ratio less than 0.25, dominated by ground-glass shadows, are particularly worthy of attention. The therapeutic challenge for this group is how to achieve precise and complete resection of nodules during surgery while maximizing the preservation of the patient's lung function. The "watershed topography map" is a new technology based on big data and artificial intelligence algorithms. This method uses Dicom data from conventional dose CT scans, combined with microscopic (22-24 levels) capillary network anatomical watershed features, to generate high-precision simulated natural segmentation planes of lung sub-segments through specific textures and forms. This technology forms fluorescent watershed boundaries on the lung surface, which highly fit the actual lung anatomical structure. By analyzing the adjacent relationship between the nodule and the watershed boundary, real-time, visually accurate positioning of the nodule can be achieved. This innovative technology provides a new solution for the intraoperative positioning and resection of lung nodules. This consensus was led by four major domestic societies, jointly with expert teams in related fields, oriented to clinical practical needs, referring to domestic and foreign guidelines and consensus, and finally formed after multiple rounds of consultation, discussion, and voting. The main content covers the theoretical basis of the "watershed topography map" technology, indications, operation procedures, surgical planning details, and postoperative evaluation standards, aiming to provide scientific guidance and exploration directions for clinical peers who are currently or plan to carry out lung nodule resection using the fluorescent microscope watershed analysis method.

AIM: To investigate the research status and hotspots in the field of ocular trauma over the past two decades using bibliometric software CiteSpace and VOSviewer.METHODS: A bibliometric study. Relevant literature on ocular trauma published in the past 20 a was retrieved from the CNKI database and Web of Science Core Collection in June 2025. EndNote X9 was used for literature management and verification. Microsoft Office Excel 2019 was employed for data management and statistics, with graphical representations created for frequency data. CiteSpace and VOSviewer were utilized to construct and analyze visual maps of authors, institutions, countries/regions, journals, and keywords.RESULTS: A total of 3 437 valid articles were included(911 in Chinese, 2 526 in English). English publications grew at an average annual rate of 12.7%(peak: 289 articles in 2021), while Chinese articles decreased from 31.2% in 2005(peak: 149 articles)to 6.3% in 2024. Chinese scholars showed an early surge in output but a subsequent declining trend, necessitating enhanced sustained research investment and translational outcomes. The United States(682 articles), China(272 articles), and India(206 articles)formed a core collaborative triangle, with a transnational collaboration rate of 68.2%. Six author clusters(e.g., Yan Hua/Zhang Maonian, et al.)demonstrated strong intra-group collaboration but minimal inter-group cooperation. Analysis of high-frequency keywords and burst terms revealed six global research hotspots: 1)ocular trauma score and minimally invasive vitrectomy; 2)optical coherence tomography(OCT)/ultrasound biomicroscopy(UBM)-guided diagnosis and management of intraocular foreign bodies; 3)amniotic membrane transplantation for chemical injury repair; 4)multimodal assessment of corneal perforation injuries; 5)inflammatory indicators for diagnosing endophthalmitis as a traumatic complication; 6)family-based interventions for preventing and controlling pediatric ocular trauma. Trends indicate a shift in research focus from emergency care toward artificial substitutes and full-cycle nursing rehabilitation.CONCLUSION: Differences in research outputs between China and other countries reflect imbalances in prevention policies and medical resource allocation. China should strengthen sustained investment and overcome collaboration barriers to jointly advance ocular trauma research toward full-cycle precision management.

Objective: To classify the ABO blood group phenotypes of 5 cases from a family, and to explore the molecular mechanism for reduced B antigen expression in ABO blood group system. Methods: Serological identification of the ABO blood group was performed using microcolumn gel assay and saline tube method. The soluble antigens in saliva were detected by the agglutination inhibition assay. The full-length sequences and upstream promoter regions of ABO gene were sequenced for genotyping using PacBio SMRT sequencing technology. Results: The results of serological tests indicated the expression of B antigen decreased in 3 out of 5 blood samples. A mixed-field agglutination was observed with anti-B antibody. B antigen was not detected in all 5 saliva samples. The ABO genotype for all samples were ABO B.01/ABO O.01.02, and a novel mutation c. 28+5875C>T within the DNA-binding region of RUNX1 in +5.8-kb site were found in the B allele for 3 samples with reduced expression of B antigen. Conclusion: Results of serological and genetic analyses classify the 3 cases with reduced B antigen expression as B phenotype. The novel mutation c. 28+5875C>T of RUNX1 could be the key reason for reduced B antigen expression in 3 cases with B phenotype.

Microglial functions are linked to Ca²⁺ signaling, with endoplasmic reticulum (ER) calcium stores playing a crucial role. Microglial abnormality is a hallmark of Alzheimer's disease (AD), but how ER Ca²⁺ receptors regulate microglial functions under physiological and AD conditions remains unclear. We found reduced ryanodine receptor 2 (Ryr2) expression in microglia from an AD mouse model. Modulation of RyR2 using S107, a RyR-Calstabin stabilizer, blunted spontaneous Ca²⁺ transients in controls and normalized Ca²⁺ transients in AD mice. S107 enhanced ATP-induced migration and phagocytosis while reducing ramification in control microglia; however, these effects were absent in AD microglia. Our findings indicate that RyR2 stabilization promotes an activation state shift in control microglia, a mechanism impaired in AD. These results highlight the role of ER Ca²⁺ receptors in both homeostatic and AD microglia, providing insights into microglial Ca²⁺ malfunctions in AD.
Animals ; Microglia/pathology* ; Alzheimer Disease/pathology* ; Phagocytosis/drug effects* ; Ryanodine Receptor Calcium Release Channel/metabolism* ; Disease Models, Animal ; Mice ; Cell Movement/drug effects* ; Mice, Transgenic ; Calcium Signaling/physiology* ; Calcium/metabolism* ; Mice, Inbred C57BL ; Male ; Endoplasmic Reticulum/metabolism*

Objective:To understand the basic situation of occupational internal exposure to 131I among nuclear medicine staff in Jiangsu province, and to analyze the relevant factors that contribute to the formation of internal exposure. Methods:A four-year external direct measurement of thyroid organ counting was conducted on nuclear medicine staff who underwent 131I treatment in Jiangsu province. The result were statistically analyzed, and the effective dose of accumulated internal exposure was estimated. The relationship between the detection rate of internal exposure and 10 possible factors was analyzed. Results:A total of 847 person-times were monitored during the monitoring period, of which 345 person-times were detected for 131I, with a detection rate of 40.7%. The highest individual monitoring result for internal exposure was 24.83 kBq, with an average value of 77.3 Bq and a median of 28.3 Bq among the detected individuals. The average committed effective dose of internal exposure for staff was 0.201 mSv, with a median of 0.074 mSv among the detected individuals. Conclusions:There is statistically significant difference in the detection rate of individual doses of internal exposure among nuclear medicine staff in each year. It has been observed that the main factors related to the detection rate are age, hospital grade, job position, location, whether there is an automatic dispensing operation, operating method, exposure level and length of exposure. Sufficient attention should be given to the situation of internal exposure, and further effective monitoring should be conducted on all such staff members.

Keratoconus is a progressive eye disease that primarily affects individuals in adolescence and early adult-hood.Dilating changes in the cornea cause it to thin and become steeper,resulting in irregular astigmatism and decreased vision.Keratoconus has multiple etiologies and pathogenic factors,including genetic,environmental,biomechanical and cellular factors.Environmental factors encompass eye rubbing,UV exposure,and wearing contact lenses.At the cellular level,the interaction of complex factors such as hormonal changes,extracellular enzyme activity,and changes in biochemi-cal and biomechanical signaling pathways disrupts collagen crosslinking within the stroma,leading to the loss and distortion of the integrity of normal corneal anatomical structures.Detection of keratoconus in its early stages remains a challenge,and corneal topographic maps are the primary diagnostic tool for keratoconus.However,in early cases,the use of a single parameter to diagnose keratoconus is not sufficient.In addition to corneal topographic maps,corneal thickness measure-ments and high-order aberration data are now commonly used detection methods.Clinically,keratoconus is diagnosed by clinical examination and corneal imaging.Advanced imaging platforms can improve the detection rate of keratoconus,facil-itating early diagnosis and monitoring of disease progression.Treatment strategies for keratoconus are tailored to the severi-ty and progression of the disease.In the early stages,glasses or soft contact lenses for vision correction are sufficient.As the disease progresses,rigid breathable contact lenses or scleral contact lenses may be needed.Corneal crosslinking has emerged as a key treatment aimed at stopping the progression of corneal dilation.The epidemiology,pathogenesis and treatment of keratoconus will be comprehensively reviewed in this paper.