Lung cancer constitutes the most prevalent and lethal malignant tumor in China. Approximately 85% of lung cancer diagnoses correspond to the non-small cell histological subtype [non-small cell lung cancer (NSCLC)]. Despite surgery being the mainstay for early-stage disease, postoperative recurrence remains high and adjuvant chemotherapy offers limited benefit. In recent years, targeted therapy has demonstrated substantial advantages in driver mutation-positive NSCLC. To this end, the Lung Cancer Medical Education Committee of the Chinese Medical Education Association developed guidelines based on a systematic review of evidence through November 2025, using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and a modified Delphi method. Focusing on epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and addressing ROS proto-oncogene 1 (ROS1), B-Raf proto-oncogene serine/threonine kinase (BRAF) V600E mutation, and mesenchymal-epithelial transition factor (MET) exon 14 (METex14) skipping, the guideline covers molecular testing, neoadjuvant/adjuvant therapy, perioperative strategies, minimal residual disease monitoring, and postoperative surveillance. It defines testing requirements, specifies stage-directed and subtype-specific treatments, and standardizes minimal residual disease monitoring. These recommendations emphasize precision and feasibility to improve survival and quality of life.

As a physical treatment technique, modified electro-convulsive therapy (MECT) is used to treat mental and certain neurological disorders by causing seizures with short, suitable electrical currents applied to the brain while the patient is under general anesthesia and muscle relaxants. MECT is recognized for its therapeutic efficacy and clinical safety, rendering it one of the most prevalent interventions in psychiatric care. To enhance clinical outcomes and minimize adverse effects, this consensus document delineates the indications, therapeutic parameters, therapeutic procedures, potential adverse effects, and associated management strategies for MECT. These guidelines are informed by the latest clinical research and expert consensus, integrating evidence-based medicine methodologies. The objective is to furnish clinicians with precise operational guidelines and to advance the standardization of MECT practices in clinical settings.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.

Objective To explore the genes related to the pathogenesis of polycystic ovary syndrome(PCOS)through bioinformatics methods and verify them in ovarian granulosa cells,providing a reference for screening potential molecular markers of PCOS.Methods The GSE34526 and GSE137684 datasets were re-spectively used as the training set and validation set.The inflammation-related genes potentially associated with the onset of PCOS were explored through differential expression analysis and weighted gene co-expres-sion network analysis.Subsequently,their predictive value was verified through the receiver operating charac-teristic(ROC)curve.Thirty patients with PCOS(the PCOS group)and 27 patients without PCOS(the con-trol group)who were treated in Affiliated Hospital of Youjiang Medical University for Nationalities were se-lected as the research objects.RT-qPCR was applied to verify the expression level of core genes in granular cells.Spearman correlation and multiple linear regression were used to analyze the correlation between the ex-pression level of core genes and various clinical parameters,and the ROC curve was used to analyze the diag-nostic efficacy of the expression level of core genes for PCOS.Finally,the protein expression level of core genes was verified on animal models.Results A total of 1 888 differentially expressed genes,89 module-relat-ed genes and 366 inflammatory response-related genes were identified.The core gene phosphatidylinositol-4,5-diphosphate 3-kinase catalytic subunit γ(PIK3CG)was ultimately obtained by taking co-expressed genes and verifying with the ROC curve.RT-qPCR results showed that the expression level of PIK3CG in granulosa cells of the PCOS group was higher than that of the control group(P<0.05).Spearman correlation analysis showed that the expression level of PIK3CG was positively correlated with BMI,testosterone(T),fasting in-sulin(FINS),and insulin resistance index(HOMA-IR,P<0.05).Multivariate linear regression analysis showed that FINS,HOMA-IR and BMI were increased with the increasing of PIK3CG expression level(P<0.05).ROC curve analysis showed that the area under the curve for diagnosing PCOS patients with PIK3CG mRNA expression levels in granulosa cells was 0.659 3.The immunohistochemical results showed that the ex-pression of PIK3CG protein in the ovarian tissues of mice in the PCOS group was significantly increased.Con-clusion PIK3CG may be potentially associated with the pathogenesis of PCOS.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.

As a physical treatment technique, modified electro-convulsive therapy (MECT) is used to treat mental and certain neurological disorders by causing seizures with short, suitable electrical currents applied to the brain while the patient is under general anesthesia and muscle relaxants. MECT is recognized for its therapeutic efficacy and clinical safety, rendering it one of the most prevalent interventions in psychiatric care. To enhance clinical outcomes and minimize adverse effects, this consensus document delineates the indications, therapeutic parameters, therapeutic procedures, potential adverse effects, and associated management strategies for MECT. These guidelines are informed by the latest clinical research and expert consensus, integrating evidence-based medicine methodologies. The objective is to furnish clinicians with precise operational guidelines and to advance the standardization of MECT practices in clinical settings.

Objective:To establish and validate a fluorescence PCR with internal positive control for rapid Mycoplasma detection. Methods:A fluorescence PCR with internal positive control for Mycoplasma detection was developed and verified for its specificity, limit of detection, and robustness. A sample of fever with thrombocytopenia syndrome (SFTSV) virus strains was tested with this method, and the result was compared with those of culture method and indicator cell culture method. Results:The established fluorescence PCR had good specificity and could amplify 11 kinds of plasmids containing Mycoplasma 16S rRNA gene with high efficiency. There was no cross reaction with the genomic DNAs of Clostridium sporogenes, Clostridium acetobutylicum, Lactobacillus acidophilus, Streptococcus pneumoniae, Bacillus subtilis, Staphylococcus aureus, Salmonella enteritidis, Escherichia coli, Pseudomonas aeruginosa, Aspergillus niger, Candida albicans, Vero cells, RD cells, and SF9 cells. The amplification efficiency of the internal positive control was basically consistent with that of the target gene of Mycoplasma, suggesting that the internal positive control could be used to detect the presence of PCR inhibitors. The sensitivity of the established method was high, and the detection limit was 10 colony-forming unit (CFU)/ml for Mycoplasma fermentans, 5 CFU/ml for Mycoplasma arginine, 5 CFU/ml for Mycoplasma gallisepticum, 5 CFU/ml for Mycoplasma hyorhinis, 5 CFU/ml for Acholeplasma laidlawii, 5 CFU/ml for Mycoplasma orale, 5 CFU/ml for Mycoplasma pneumoniae, 5 CFU/ml for Mycoplasma synoviae, and 1 CFU/ml for Spiroplasma citri by 7500 Fast real-time PCR system. At the detection limit of each species, there was no significant difference in the positive detection rate using different thermal cycler types. The established fluorescence PCR, culture method, and indicator cell culture were performed to detect Mycoplasma in the sample of SFTSV virus strains, and the results all showed Mycoplasma contamination. Conclusions:The established fluorescence PCR has high specificity, sensitivity, and robustness, and can be used as an alternative method for rapid detection of Mycoplasma.

Objective To evaluate the economic value of using glucagon-like peptide-1 receptor agonist(GLP-1RA)in combination with metformin for the treatment of type 2 diabetes mellitus(T2DM).Methods Based on 7 randomized controlled clinical trials(RCTs),Markov model was built to simulate the dynamic changes of metformin alone or combined with GLP-1RA in the treatment of T2DM patients without or with complications and death from the perspective of China's health system.Quality-adjusted life years(QALYs)was used as a health output indicator and 3 times China's per capita gross domestic product(GDP)in 2023 was set as the willingness-to-pay(WTP)threshold.The cycle was at the rate of 1 year and a total of 20 years cohort simulation in Markov model was applied to obtain long-term cost and effect of each treatment strategy.The incremental cost-utility ratio(ICUR)was analyzed as the primary evaluation indicator and the sensitivity of cost,utility and discount was performed to test the stability of the results.Results Compared with metformin alone,the ICUR of GLP-1RA including liraglutide,dulaglutide,exenatide,loxenatide,semaglutide combined with metformin were all below the WTP threshold,and the increased cost was acceptable.Extending the simulation time to 30 years or 50 years had no effect on results.The results of probability sensitivity analysis showed that the cost effect of semaglutide 0.5 mg combined with metformin had the highest probability of a cost-utility advantage of 99.7％among all the treatment strategies when WTP threshold was 3 times China's per capita GDP in 2023(268 074 yuan).Conclusion GLP-1RA,including liraglutide,dulaglutide,exenatide,lixisenatide,and semaglutide,at the regular recommended dose combined with metformin,would present higher cost-utility compared to metformin monotherapy.

Objective To evaluate the efficacy and safety of glucagon-like peptide 1 receptor agonists(GLP-1RA)in type 2 diabetes mellitus(T2DM)patients with overweight or obese.Methods PubMed,Embase,Cochrane Library,Ovid,ClinicalTrial.gov,SinoMed,CNKI,WanFang Data and VIP databases were electronically searched to collect randomized controlled trials(RCTs)on the efficacy of GLP-1RA in the treatment of T2DM patients with overweight or obese from January 1,2005 to November 1,2023.Two researchers independently screened the literature,extracted data and evaluated the risk of bias of the included studies.R software was then used for meta-analysis.The level of evidence was assessed by using the GRADE system.Results A total of 71 RCTs were included,including 29 476 patients.The results of Meta-analysis showed that compared with other hypoglycemic drugs,GLP-1RA showed superior effects in improving HbAlc status(WMD=-0.55,95％CI-0.65 to-0.45,P＜0.001)and weight loss(WMD=-2.61,95％CI-3.25 to-1.97,P＜0.001),while the effect on fasting plasm glucose was time-dependent(within 16 weeks:WMD=0.25,95％CI-0.17 to 0.66,P=0.250;16 to 52 weeks:WMD=-0.06,95％CI-0.32 to 0.20,P=0.650;over 52 to 104 weeks:WMD=-1.67,95％CI-1.91 to-1.43,P＜0.001).In terms of safety,the incidence of GLP-1RA's adverse reactions was higher than other hypoglycemic drugs(RR=1.11,95％CI 1.07 to 1.15,P＜0.001);the incidence of hypoglycemia was lower with GLP-1RA than with insulin(RR=0.58,95％CI 0.48 to 0.71,P＜0.001)and similar to oral hypoglycemic drugs(RR=0.83,95％CI 0.58 to 1.19,P=0.310).According to the GRADE assessment,only the certainty of the evidence for the results of the incidence of hypoglycemia was moderate,and the certainty of the evidence for the other results was low.Conclusion Current evidence shows that for T2DM patients with overweight or obese,GLP-1RA especially semaglutide,was more effective in lowering blood glucose,controlling body weight and reducing the occurrence of hypoglycemia than placebo,insulin and oral hypoglycemic drugs.

Oncolytic virus is a unique anti-tumor immunotherapy that can specifically infect and lyse tumor cells,while inducing and activating the body's own anti-tumor immune response to attack tumors.So far,three oncolytic viruses have been approved for marketing.In 2005,China first approved recombinant human adenovirus type 5(H101/Oncorine)combined with chemotherapy for the treatment of advanced nasopharyngeal cancer patients.In 2015,the US Food and Drug Administration(FDA)approved herpes simplex virus type I(T-VEC)for the treatment of recurrent melanoma after primary surgery,T-VEC was subsequently approved in Europe.In 2021,Japan's Ministry of Health,Labour and Welfare approved third-generation recombinant herpes simplex virus type I(Delytact/G47Δ)for the treatment of malignant glioma.Although the approval of H101 in China marks a breakthrough in the development of oncolytic viruses,compared to T-VEC and Delytact,H101 has not significantly impacted the treatment of patients with advanced nasopharyngeal carcinoma.This may be due to its inability to provide a complete tumor response as a monotherapy,and the fact that most nasopharyngeal carcinoma patients in China undergo radiotherapy,making it difficult for them to benefit from chemotherapy combined with H101.Therefore,this treatment regimen still needs improvement.In recent years,with the maturity of genetic engineering technology,oncolytic viruses have been continuously improved and refined.This review summarizes the clinical research progress of oncolytic viruses and discusses their characteristics and development prospects.