Objective To explore the mechanism of electroacupuncture in alleviating hyperlipidemia in a rat model by modulating mammalian target of rapamycin complex 1(mTORC1)-mediated lipophagy in hepatocytes.Methods A total of 30 SD rats were randomly divided into blank(n=6)and modeling groups(n=24)using the random number table method.A hyperlipidemic rat model was established by feeding rats a high-fat diet(feeding for 8 weeks).After successful modeling,the modeling group was randomly divided into the model,electroacupuncture,mTORC1 inhibitor,and electroacupuncture+mTORC1 agonist groups,with six rats in each group.Except for the blank group,all other rats were fed with high fat diet.Rats in the electroacupuncture and electroacupuncture+mTORC1 agonist groups received electroacupuncture intervention at bilateral"Fenglong"(ST40)acupoints(dilatational wave 2 Hz/100 Hz,current intensity 1 mA)for 30 min once daily.Rats in the mTORC1 inhibitor group received intraperitoneal injections of the mTORC1 inhibitor,rapamycin(2 mg/kg),once daily.Rats in the electroacupuncture+mTORC1 agonist group received intraperitoneal injections of the mTORC1 agonist MHY1485(10 mg/kg)once daily.The interventions were administered for five consecutive days per week for 4 weeks.Upon completion of the intervention,the following analyses were performed:serum contents of total cholesterol(TC),triglycerides(TAG),low-density lipoprotein cholesterol(LDL-C),high-density lipoprotein cholesterol(HDL-C),free fatty acids(FFA),alanine aminotransferase(ALT),and aspartate aminotransferase(AST)were measured using a fully automated biochemical analyzer.Hepatic histopathological changes and lipid deposition were observed using hematoxylin-eosin and oil red O staining.The liver condition was observed and the liver index was calculated.Hepatic TC and TAG levels were measured using an enzyme-linked immunosorbent assay.The ultrastructure of the liver tissue was observed using transmission electron microscopy,and the mean fluorescence intensity of perilipin 2(PLIN2)and microtubule-associated protein 1 light chain 3(LC3)-Ⅱ in the liver tissue was detected using immunofluorescence.Protein expression of LC3-Ⅱ/LC3-Ⅰ,phosphorylated mammalian target of rapamycin(p-mTOR)/mTOR,and mTORC1 in liver tissue was detected using Western blotting.Results Compared to the blank group,the model group rats showed increased serum TC,TAG,LDL-C,ALT,AST,and FFA levels,along with decreased HDL-C levels(P<0.05).The liver index and hepatic TC and TAG levels were also elevated(P<0.05).Histological examination of liver tissue revealed substantial lipid accumulation,numerous lipid droplets within hepatocytes,abnormal mitochondrial morphology,and scarce autophagic vacuole.The mean fluorescence intensity of PLIN2 increased,whereas that of LC3-Ⅱ decreased(P<0.05).Additionally,the LC3-Ⅱ/LC3-Ⅰ ratio was reduced,whereas the p-mTOR/mTOR ratio and mTORC1 protein expression were increased(P<0.05).Compared to the model group,rats in the mTORC1 inhibitor and electroacupuncture groups exhibited decreased serum TC,TAG,LDL-C,ALT,AST,and FFA levels(P<0.05),along with a reduced liver index and hepatic TC and TAG levels(P<0.05).Histological examination showed markedly attenuated lipid accumulation and visible autophagic vacuole in the hepatocytes.The mean fluorescence intensity of PLIN2 decreased,whereas that of LC3-Ⅱ increased(P<0.05).Moreover,the LC3-Ⅱ/LC3-Ⅰ ratio increased,whereas the p-mTOR/mTOR ratio and mTORC1 protein expression decreased(P<0.05).In comparison with both the electroacupuncture and mTORC1 inhibitor groups,the electroacupuncture+mTORC1 agonist group demonstrated increased serum TAG,TC,LDL-C,ALT,AST,and FFA levels(P<0.05)as well as elevated liver index and hepatic TC and TAG levels(P<0.05).Liver tissues exhibited aggravated lipid deposition and absence of autophagic vacuole in liver cells.The mean fluorescence intensity of PLIN2 was enhanced,whereas that of LC3-Ⅱ was reduced(P<0.05).Furthermore,the LC3-Ⅱ/LC3-Ⅰ ratio decreased,and the p-mTOR/mTOR ratio and mTORC1 protein expression increased(P<0.05).Conclusion Electroacupuncture at"Fenglong"(ST40)may improve blood lipid levels in hyperlipidemic rats by inhibiting mTORC1 and promoting hepatocyte lipophagy.

Objective:To construct and validate a predictive model for postoperative recurrence in early non-small cell lung cancer patients.Methods:The clinical data of 252 patients with early non-small cell lung cancer admitted to the 926th Hospital of Joint Logistic Support Force of PLA from January 2016 to January 2018were retrospectively collected. All of the patients underwent surgical treatment and they were followed up for 5 years after surgery, according the recurrence after surgery, they were divided into the recurrence group (103 cases) and non- recurrence group (149 cases). The risk factors for postoperative recurrence in early non-small cell lung cancer patients were analyzed. A predictive model for postoperative recurrence in early non-small cell lung cancer patients was constructed and validated.Results:The results of Logistic regression analysis showed that tumor long diameter≥ 3 cm, lymph node metastasis, low differentiation, spicules and pleural traction were independent risk factors for postoperative recurrence in early non-small cell lung cancer patients ( P<0.05). Using R4.0.3 statistical software, the dataset was randomly divided into a training set and a validation set, with a sample size of 176 cases in the training set and 76 cases in the validation set. A prediction model was constructed, with thearea under the curve (AUC) of the receiver operating characteristic (ROC) curve of 0.754 (95% CI 0.679 - 0.828) in the training set and AUC of 0.749 (95% CI 0.634 - 0.864) in the validation set. The model was subjected to a Hosmer-Lemeshow Goodness-of-Fit Test in the validation set, χ2 = 11.31, P = 0.185. Conclusions:The predictive model base on tumor long diameter ≥ 3 cm, lymph node metastasis, low differentiation, spicules and pleural traction can identify patients at high risk of postoperative recurrence in early non-small cell lung cancer effectively.

Objectives To explore the causal relationship between asthma-related pneumonia and heart failure(HF)by using two-sample Mendelian randomization(MR)analysis.Methods The causal relationship between asthma-related pneumonia and HF were systematically evaluated through two-sample MR analysis based on publicly available Genome-Wide Association Study data.Inverse variance weighted(IVW),MR-Egger,weighted median,weighted mode,and simple mode methods were used.Different models were used to analyze sensitivity.Testing approaches were conducted to assess the robustness of the results.Results IVW analysis results showed that there was a causal relationship between asthma-related pneumonia and HF risk(OR=1.113,95％CI:1.027-1.206,P=0.009).HF was not found to have a causal effect on asthma-related pneumonia risk based on IVW analysis(OR=1.018,95％CI:0.780-1.328,P=0.893).The variance used in all MR analyses showed no heterogeneity or horizontal pleiotropy.The leave-one-out analysis revealed that no single nucleotide polymorphism disproportionately influenced the results,further confirming the credibility of the bidirectional MR findings.Conclusion This study established a causal relationship between asthma-related pneumonia and HF risk.No clear causal relationship between HF and asthma-related pneumonia risk was found.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Objective:To investigate the predictive value of systemic immune inflammation index for the efficacyof neoadjuvant chemotherapy in triple negative breast cancer patients, and analyzed the relationship between pathological complete response (pCR) and prognosis.Methods:The clinical data of 146 patients with triple-negative breast cancer admitted to the 926th Hospital of the Joint Service Support Force of the PLA from January 2018 to December 2020 were retrospectively collected. All patients received neoadjuvant chemotherapy. After chemotherapy, the patients were divided into pCR group (62 cases) and non-pCR group (84 cases) according to whether the patients achieved pCR. Pathological characteristics and systemic immunoinflammatory index levels of the two groups were compared. Receiver operating characteristic (ROC) curve was used to analyze the predictive value of systemic immunoinflammatory index for pCR after neoadjuvant chemotherapy in patients with triple-negative breast cancer, and survival curves were drawn to compare the disease-free survival of the two groups.Results:The rate of axillary lymph node metastasis in pCR group was lower than that in non-pCR group: 37.10% (23/62) vs. 64.29% (54/84), there was statistical difference ( χ2 = 10.58, P<0.01). There were no significant differences in TNM stage, Ki-67 level and histological grade between the two groups ( P>0.05). Compared with the non -pCR group, the systemic immune inflammation index in the pCR group was significantly reduced: 617.42 ± 166.40 vs. 853.67 ± 202.41, P<0.01. Systemic immune inflammation index was valuable in predicting non-pCR of triple negative breast cancer patients after neoadjuvant chemotherapy, and the area under the curve was 0.807 (95% CI: 0.738 - 0.875, P<0.01). Compared with the non-pCR group, the disease-free survival of patients in the pCR group was significantly prolonged ( P = 0.033). Conclusions:Systemic immune inflammation index was related to the efficacy of neoadjuvant chemotherapy in triple negative breast cancer patients, and can be used as a biological indicator to predict the efficacy of neoadjuvant chemotherapy in triple negative breast cancer.

Objective:To investigate the predictive value of systemic immune inflammation index for the efficacyof neoadjuvant chemotherapy in triple negative breast cancer patients, and analyzed the relationship between pathological complete response (pCR) and prognosis.Methods:The clinical data of 146 patients with triple-negative breast cancer admitted to the 926th Hospital of the Joint Service Support Force of the PLA from January 2018 to December 2020 were retrospectively collected. All patients received neoadjuvant chemotherapy. After chemotherapy, the patients were divided into pCR group (62 cases) and non-pCR group (84 cases) according to whether the patients achieved pCR. Pathological characteristics and systemic immunoinflammatory index levels of the two groups were compared. Receiver operating characteristic (ROC) curve was used to analyze the predictive value of systemic immunoinflammatory index for pCR after neoadjuvant chemotherapy in patients with triple-negative breast cancer, and survival curves were drawn to compare the disease-free survival of the two groups.Results:The rate of axillary lymph node metastasis in pCR group was lower than that in non-pCR group: 37.10% (23/62) vs. 64.29% (54/84), there was statistical difference ( χ2 = 10.58, P<0.01). There were no significant differences in TNM stage, Ki-67 level and histological grade between the two groups ( P>0.05). Compared with the non -pCR group, the systemic immune inflammation index in the pCR group was significantly reduced: 617.42 ± 166.40 vs. 853.67 ± 202.41, P<0.01. Systemic immune inflammation index was valuable in predicting non-pCR of triple negative breast cancer patients after neoadjuvant chemotherapy, and the area under the curve was 0.807 (95% CI: 0.738 - 0.875, P<0.01). Compared with the non-pCR group, the disease-free survival of patients in the pCR group was significantly prolonged ( P = 0.033). Conclusions:Systemic immune inflammation index was related to the efficacy of neoadjuvant chemotherapy in triple negative breast cancer patients, and can be used as a biological indicator to predict the efficacy of neoadjuvant chemotherapy in triple negative breast cancer.

Objective To evaluate the reliability of Vitek 2 AST-N335 card for determining the susceptibility of Acinetobacter bauman-nii(AB)to cefoperazone/sulbactam.Methods A total of 318 non-repeated clinical isolates of AB collected in 2023 were tested for antimicrobial susceptibility to cefoperazone/sulbactam using broth microdilution(BMD),the AST-N335 card,and the Kirby-Bauer(K-B)disk diffusion method.Using BMD as the reference method,the reliability of AST-N335 card was assessed,and the accuracy of K-B disk diffusion method as the confirmatory test was validated.Results Compared with BMD,the susceptibility testing of 318 AB strains to cefoperazone/sulbactam using the AST-N335 card showed categorical agreement(CA)of 87.8％(279/318),very major er-ror(VME)of 6.0％(19/318),major error(ME)of 0％(0/318),and minor error(mE)of 1.9％(6/318),which fall outside of the acceptable error range.In contrast,the K-B method achieved CA of 99.4％(316/318),VME of 0％,ME of 0.3％(1/318),and mE of 0.3％(1/318),all within acceptable limits.Of these,the errors with AST-N335 card occurred within the minimum inhibitory concentration(MIC)range of 8-32 μg/mL.Using BMD as the reference method,further analysis was performed on the 171 AB strains with AST-N335 card MIC values of 8-32 μg/mL for cefoperazone/sulbactam.It was revealed that at MIC of 32 μg/mL,the CA was 0％;at MIC of 16 μg/mL,CA was 5.3％(1/19)and VME rate was 84.2％(16/19),both of which substantially exceeded accepta-ble error ranges.At MIC of 8 μg/mL,the CA was 94.9％(131/138)and VME was 2.2％(3/138),both approaching the acceptable ranges.Conclusion The results obtained with Vitek 2 AST-N335 card in determining for cefoperazone/sulbactam are unreliable when the MIC values fall within the range of 8-32 μg/mL,which leads to an underestimation of the resistance rate to cefoperazone/sulbac-tam.This issue requires urgent attention in both laboratories and clinical practice.The K-B disk diffusion method could serve as a sup-plementary verification approach in routine laboratories.

Objective To evaluate the reliability of Vitek 2 AST-N335 card for determining the susceptibility of Acinetobacter bauman-nii(AB)to cefoperazone/sulbactam.Methods A total of 318 non-repeated clinical isolates of AB collected in 2023 were tested for antimicrobial susceptibility to cefoperazone/sulbactam using broth microdilution(BMD),the AST-N335 card,and the Kirby-Bauer(K-B)disk diffusion method.Using BMD as the reference method,the reliability of AST-N335 card was assessed,and the accuracy of K-B disk diffusion method as the confirmatory test was validated.Results Compared with BMD,the susceptibility testing of 318 AB strains to cefoperazone/sulbactam using the AST-N335 card showed categorical agreement(CA)of 87.8％(279/318),very major er-ror(VME)of 6.0％(19/318),major error(ME)of 0％(0/318),and minor error(mE)of 1.9％(6/318),which fall outside of the acceptable error range.In contrast,the K-B method achieved CA of 99.4％(316/318),VME of 0％,ME of 0.3％(1/318),and mE of 0.3％(1/318),all within acceptable limits.Of these,the errors with AST-N335 card occurred within the minimum inhibitory concentration(MIC)range of 8-32 μg/mL.Using BMD as the reference method,further analysis was performed on the 171 AB strains with AST-N335 card MIC values of 8-32 μg/mL for cefoperazone/sulbactam.It was revealed that at MIC of 32 μg/mL,the CA was 0％;at MIC of 16 μg/mL,CA was 5.3％(1/19)and VME rate was 84.2％(16/19),both of which substantially exceeded accepta-ble error ranges.At MIC of 8 μg/mL,the CA was 94.9％(131/138)and VME was 2.2％(3/138),both approaching the acceptable ranges.Conclusion The results obtained with Vitek 2 AST-N335 card in determining for cefoperazone/sulbactam are unreliable when the MIC values fall within the range of 8-32 μg/mL,which leads to an underestimation of the resistance rate to cefoperazone/sulbac-tam.This issue requires urgent attention in both laboratories and clinical practice.The K-B disk diffusion method could serve as a sup-plementary verification approach in routine laboratories.