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 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.

Objective To investigate the clinicopathological characteristics and prognostic factors of hepatoid adenocarcinoma of the stomach (HAS).Methods From Jan 2006 to Jan 2016,the clinical pathological data of 15 HAS cases in our hospital were analyzed retrospectively.60 TNM stage matched cases of non-HAS gastric cancer served as the control group.The clinical pathology factors and prognosis were compared between the two groups.Results Serum AFP positive HAS patients accounted for 87％.The serum level of AFP in HAS were significantly higher than that in controls (P ＜0.001).HAS was more prone to lymphatic invasion (73％ vs.33％,x2 =7.918,P =0.005) and vascular invasion (40％ vs.10％,x2 =8.036,P =0.005) than control gastric cancer.The immunohistochemistry positive rates of AFP,Glypican3,Hepatocyte and CEA in HAS were 87％,87％,33％,53％ respectively.Liver metastasis (53％ vs.12％,P =0.001) and other distant metastases (53％ vs.15％,P =0.004) were higher in the HAS.HAS median survival time was significantly lower (28.0 months vs.50.7 months,x2 =4.350,P =0.037).Postoperative HAS 1,3 and 5 years survival rates were 80％,33％ and 20％,respectively,significantly worse than 97％,78％ and 33％ in control group (x2 =5.525,17.198,5.472,P =0.019,0.000,0.019 respectively).The independent risk factor influencing the prognosis of HAS included TNM stage,vascular invasion,distant metastasis.Conclusions HAS is often complicated with higher serum AFP and prone to vascular invasion,lymph node metastasis and distant metastasis,hence a poorer prognosis.

Objective To study the changes of serum myeloperoxidase(MPO)in patients with acute ischemic stroke ,and to probe into the relationship of serum MPO with types of carotid atherosclerotic plaques ,the degree of neural function defect and the activi‐ties of daily living (Barthel Index) .Methods Totally 78 cases of patients with acute ischemic stroke was selected as observation ob‐jects .The patients with acute ischemic stroke were divided into good ,medium and poor three groups according to Barthel index . Based on the scoring of neurologic impairment degree from standards of CSS :mild impairment group(0 to 15 points) ,moderate im‐pairment group(16 to 30 points) ,and severe impairment group(31 to 45 points) .Based on the type of atherosclerotic plaques all pa‐tients were divided into soft plaque group ,mixed plaque and hard plaque group .The 1evels of serum MPO was compared between different group .Results The heavier nerve function defect degree ,the levels of serum MPO in patients with ischemic stroke were higher ,and it had significant difference between groups (P<0 .05) .The Barthel index was the better ,the levels of serum MPO was lower .The levels of serum MPO was different among the soft plaque group ,mixed plaque and hard plaque group ,and its were sig‐nificantly different between the three groups ,and the type of atherosclerotic plaque was related to the neural function defect and Barthel index level .Conclusion Ischemic stroke is associated with serum MPO levels ,neurological deficits ,Barthel index and stabil‐ity of atherosclerotic plaque ,and the levels of serum M PO is helpful for judging state of the disease and guiding in clinical diagnosis and treatment .

Objective To investigate the short and long term effects of Sunmax injection for the rhytidoplasty on different parts of the fa-cial wrinkles. Methods 1 028 face lift patients were collected from January 2007 to December 2011 who admitted to our plastic surgery de-partment,236 cases of male,792 cases of female,with an average age of 48. 7 (21~72)years old. According to different drug injection sites, all the patients were divided into 5 groups:wrinkles between eyebrows,the forehead wrinkles,nasolabial fold wrinkles, crow's feet,nose wrin-kles. The rhytidoplasty effects of 5 groups a day,1 month,3 months,6 months,9 months after injection were observed and compared. Further-more,the short and long term effects of the Sunmax injections were integrated to analyze. Results After Sunmax injection,a variety of skin wrinkles and sags disappeared;1 month after injection,wrinkles did not appear;3~6 months after injection,the effects was still as the same as the day after injection. 9 months after injection,the effects for the forehead wrinkles and crow's feet was slightly diminished. Conclusion Sunmax injection is an emerging technology to remove facial wrinkles,which has been widelymused inmour department for severalmyears and got patients' postoperative satisfaction. It is worth spreading for rhytidoplasty.

ObjectiveTo investigate the treatment and prevention of auricle reconstruction complications by Medpor framework and autoallergic rib cartilage framework implantation.Methods A total of 158 microtia were performed ear reconstructive operation,in which postoperative complications happened in 18 cases during January 2003 to June 2011,and studied retrospectively.Results There were three cases of dilator haematoma (incidence rate was 1.90 ％),and they were cured after treatment.There were two dilator infection cases (incidence rate was 1.27 ％).One case was cured after treatment,and another one revealed no effect after treatment and dilator implantation operation was done half a year later.There were thirteen cases of framework plantation exposure and infection after Ⅱ stage operation,in which there were seven rib cartilage framework cases (incidence rate was 5.79 ％),and they were cured after change dressings and operation; there were six Medpor framework cases (incidence rate was 16.22 ％),and the three cases were cured after change dressings and operation,and other three cases revealed no effects after change dressings and so the operation failed.ConclusionsPreoperative percise plan and fine manipulation can decrease the incidence of haematoma.The main reasons of framework exposure include the skin tension,thin skin flap or the effect of external force.On account of the high incidence of framework exposure and difficult treatemnt,it is better to use rib cartilage framework for uricle reconstruction.

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.