Objective To compare the efficacy and safety of transurethral blue laser vaporization of the prostate, transurethral resection of the prostate (TURP) or plasmakinetic resection of the prostate in the treatment of benign prostatic hyperplasia (BPH). Methods The domestic and foreign clinical studies on transurethral blue laser vaporization of the prostate (observation group), TURP or plasmakinetic resection of the prostate (control group) in the treatment of BPH during Jan. 2015 and Mar. 2025 were retrieved. The data were extracted with Cochrane systematic review method. The operation time, decrease in hemoglobin, bladder irrigation time, catheter indwelling time, total complication rate, retrograde ejaculation rate and urinary incontinence rate of the two groups were compared with RevMan 5.3.0 statistical software. Results A total of 5 Chinese studies involving 491 patients (248 in the observation group and 243 in the control group) were included in the Meta-analysis. Compared with the control group, the observation group had shorter operation time [MD=-20.80, 95%CI:-26.88—-14.72, P＜0.00001], less decrease in hemoglobin [MD=-10.61, 95%CI: -20.21—-1.01, P=0.03], shorter bladder irrigation time [MD=-17.85, 95%CI: -32.62—-3.09, P=0.002], shorter catheter indwelling time [MD=-1.71, 95%CI: -2.81—- 0.62, P=0.002], lower total complication rate [OR=0.11, 95%CI: 0.06—0.21, P＜0.00001], lower retrograde ejaculation rate [OR=0.05, 95%CI: 0.02—0.16, P＜0.00001] and lower urinary incontinence rate [OR=0.24, 95%CI: 0.07—0.79, P=0.02]. There were no significant differences in other complications between the two groups (P＞0.05). The international erectile function score (IIEF-5) of the observation group was significantly higher than that of the control group [MD=1.87, 95%CI:1.16—2.57, P＜0.00001]. There were no significant differences in international prostate symptom score (IPSS), maximum urinary flow rate (Qmax) and post-voiding residual (PVR) between the two groups (P＞0.05). Conclusion All three surgical procedures can effectively improve the lower urinary tract symptoms of BPH patients. Compared with TURP or plasmakinetic resection of the prostate, transurethral blue laser vaporization of the prostate has obvious advantages in terms of perioperative recovery, reduction of total complications, urinary incontinence and retrograde ejaculation rates, and preservation of sexual function.

Objective To explore the efficacy and safety of blue laser vaporization in the treatment of large-volume (＞80 mL) benign prostatic hyperplasia (BPH). Methods A retrospective analysis was conducted on the clinical data of 149 BPH patients with prostate volume＞80 mL who underwent blue laser vaporization at our hospital during Aug. 2023 and Aug. 2025. The 1-month postoperative maximum urinary flow rate (Qmax) and international prostate symptom score (IPSS), operation time, postoperative hemoglobin drop, bladder irrigation volume, catheter indwelling time, and incidence of postoperative complications were recorded and analyzed. Results All operations were successfully completed, without conversion to other approaches. The operation time was (41.47±11.05) minutes, postoperative hemoglobin drop (2.78±1.19) g/L, bladder irrigation volume (9.97±1.49) bags, and catheter indwelling time (3.30±1.85) days. One month after surgery, the Qmax was significantly higher than the preoperative value [(20.19±3.39) mL/s vs. (2.39±2.17) mL/s], while the IPSS was significantly lower [(4.46±0.87) vs. (27.69±2.06)], with statistically significant differences (P＜0.001). Postoperative complications included 1 case of incontinence (0.67%), 2 cases of urethral stricture/bladder neck contracture (1.34%), and 1 case of secondary bleeding (0.67%), all of which improved with symptomatic treatment. Conclusion Blue laser vaporization is effective for treating large-volume BPH, with advantages such as minimal bleeding risk, short operation time, fast recovery and safety.

ObjectiveTo investigate the potential mechanism of heat-sensitive moxibustion on chronic atrophic gastritis （CAG） through the phosphoinositide 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsFifty-eight SD rats were randomly divided into blank group （n=14） and modeling group （n=44）. Rats in the blank group were fed routinely， while the rats in the modeling group received drinking water containing 1-methyl-3-nitro-1-nitrosoguanidine （MNNG） at a concentration of 140 μg/ml， combined with irregular fasting and feeding for 12 weeks to establish CAG model. After successful modeling， the rats were randomly divided into model group （n=10）， inhibitor group （n=10） and moxibustion group （n=20）. After 40 minutes of suspended moxibustion at "Zhongwan" （CV 12） daily， the rats in the moxibustion group were divided into heat-sensitive moxibustion group （n=10） and non-heat-sensitive moxibustion group （n=9） according to the change of tail temperature during moxibustion. The inhibitor group was bound for 40 minutes daily， and then administered with PI3K/Akt signaling pathway inhibitor， rapamycin solution， by gavage at a dose of 1 mg/kg. The model group received intragastric administration of 1 ml/kg normal saline after 40 minutes of restraint stress each day. All interventions were administered once daily for 28 consecutive days， while the blank group received no intervention. After the intervention finished， the body weight of rats in each group was compared. HE staining was used to observe the histopathological changes of gastric mucosa. The apoptosis-positive rate of gastric mucosal cells was detected by TUNEL assay. Immunohistochemistry was performed to determine the protein levels of matric metalloproteinase-7 （MMP7）， vascular endothelial growth factor A （VEGFA） and epidermal growth factor receptor （EGFR） in gastric mucosa. The mRNA expression levels of PI3K， Akt and mammalian target of rapamycin （mTOR） in gastric mucosal tissues were detected by qPCR. The protein levels of phosphorylated Akt （p-Akt） and phosphorylated mTOR （p-mTOR） in rat gastric mucosal tissues were measured by Western Blotting. ResultsCompared to the blank group， rats in all other groups exhibited decreased body weight， significantly increased gastric mucosal cell apoptosis-positive rates， elevated protein levels of MMP7， VEGFA and EGFR in gastric mucosa， increased mRNA expression levels of PI3K， Akt and mTOR， and enhanced protein expression levels of p-Akt and p-mTOR （P＜0.05 or P＜0.01）. Histopathological examination revealed thinning of the gastric mucosa， glandular disorganization and atrophy， accompanied by intestinal metaplasia.Compared to the model group， the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group all showed significant improvements in the above-mentioned indicators （P＜0.05 or P＜0.01）. Compared to the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group exhibited increased positive rates of gastric mucosal cell apoptosis； the non-heat-sensitive moxibustion group showed increased protein levels of MMP7， VEGFA and EGFR， as well as mRNA expression levels of PI3K， Akt and mTOR， and protein expressions of p-Akt and p-mTOR； the inhibitor group exhibited elevated protein expression level of EGFR （P＜0.05 or P＜0.01）. Histopathological examination showed that the gastric mucosal glands in the heat-sensitive moxibustion group were arranged more regularly， with an approximately normal structural appearance. ConclusionHeat-sensitive moxibustion can improve the body weight of CAG rats and repair gastric mucosal injury. Its therapeutic effects may be mediated by inhibiting excessive activation of gastric mucosal PI3K/Akt signaling pathway， thereby reducing gastric mucosal cell apoptosis.

ObjectiveTo investigate the potential mechanism of heat-sensitive moxibustion on chronic atrophic gastritis （CAG） through the phosphoinositide 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsFifty-eight SD rats were randomly divided into blank group （n=14） and modeling group （n=44）. Rats in the blank group were fed routinely， while the rats in the modeling group received drinking water containing 1-methyl-3-nitro-1-nitrosoguanidine （MNNG） at a concentration of 140 μg/ml， combined with irregular fasting and feeding for 12 weeks to establish CAG model. After successful modeling， the rats were randomly divided into model group （n=10）， inhibitor group （n=10） and moxibustion group （n=20）. After 40 minutes of suspended moxibustion at "Zhongwan" （CV 12） daily， the rats in the moxibustion group were divided into heat-sensitive moxibustion group （n=10） and non-heat-sensitive moxibustion group （n=9） according to the change of tail temperature during moxibustion. The inhibitor group was bound for 40 minutes daily， and then administered with PI3K/Akt signaling pathway inhibitor， rapamycin solution， by gavage at a dose of 1 mg/kg. The model group received intragastric administration of 1 ml/kg normal saline after 40 minutes of restraint stress each day. All interventions were administered once daily for 28 consecutive days， while the blank group received no intervention. After the intervention finished， the body weight of rats in each group was compared. HE staining was used to observe the histopathological changes of gastric mucosa. The apoptosis-positive rate of gastric mucosal cells was detected by TUNEL assay. Immunohistochemistry was performed to determine the protein levels of matric metalloproteinase-7 （MMP7）， vascular endothelial growth factor A （VEGFA） and epidermal growth factor receptor （EGFR） in gastric mucosa. The mRNA expression levels of PI3K， Akt and mammalian target of rapamycin （mTOR） in gastric mucosal tissues were detected by qPCR. The protein levels of phosphorylated Akt （p-Akt） and phosphorylated mTOR （p-mTOR） in rat gastric mucosal tissues were measured by Western Blotting. ResultsCompared to the blank group， rats in all other groups exhibited decreased body weight， significantly increased gastric mucosal cell apoptosis-positive rates， elevated protein levels of MMP7， VEGFA and EGFR in gastric mucosa， increased mRNA expression levels of PI3K， Akt and mTOR， and enhanced protein expression levels of p-Akt and p-mTOR （P＜0.05 or P＜0.01）. Histopathological examination revealed thinning of the gastric mucosa， glandular disorganization and atrophy， accompanied by intestinal metaplasia.Compared to the model group， the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group all showed significant improvements in the above-mentioned indicators （P＜0.05 or P＜0.01）. Compared to the heat-sensitive moxibustion group， the non-heat-sensitive moxibustion group and the inhibitor group exhibited increased positive rates of gastric mucosal cell apoptosis； the non-heat-sensitive moxibustion group showed increased protein levels of MMP7， VEGFA and EGFR， as well as mRNA expression levels of PI3K， Akt and mTOR， and protein expressions of p-Akt and p-mTOR； the inhibitor group exhibited elevated protein expression level of EGFR （P＜0.05 or P＜0.01）. Histopathological examination showed that the gastric mucosal glands in the heat-sensitive moxibustion group were arranged more regularly， with an approximately normal structural appearance. ConclusionHeat-sensitive moxibustion can improve the body weight of CAG rats and repair gastric mucosal injury. Its therapeutic effects may be mediated by inhibiting excessive activation of gastric mucosal PI3K/Akt signaling pathway， thereby reducing gastric mucosal cell apoptosis.

Background: Whether there is a causal relationship between childhood obesity and increased risk of chronic kidney disease (CKD) remains controversial. This study sought to explore how body size in childhood and adulthood independently affects CKD risk in later life using a Mendelian randomization (MR) approach. Methods: Univariate and multivariate MR was used to estimate total and independent effects of body size exposures. Genetic associations with early-life and adult body size were obtained from a genome-wide association study of 453,169 participants in the U.K. Biobank, and genetic associations with CKD were obtained from the CKDGen and FinnGen consortia. Results: A larger genetically predicted early-life body size was associated with an increased risk of CKD (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.14 to 1.41; P= 1.70E-05) and increased blood urea nitrogen (BUN) levels (β=0.010; 95% CI, 0.005 to 0.021; P=0.001). However, the association between the impact of early-life body size on CKD (OR, 1.12; 95% CI, 0.95 to 1.31; P=0.173) and BUN level (β=0.001; 95% CI, –0.010 to 0.012;P= 0.853) did not remain statistically significant after adjustment for adult body size. Larger genetically predicted adult body size was associated with an increased risk of CKD (OR, 1.37; 95% CI, 1.21 to 1.54; P= 4.60E-07), decreased estimated glomerular filtration rate (β=–0.011; 95% CI, –0.017 to –0.006; P=5.79E-05), and increased BUN level (β= 0.010; 95% CI, 0.002 to 0.019; P= 0.018). Conclusion Our research indicates that the significant correlation between early-life body size and CKD risk is likely due to maintaining a large body size into adulthood.

Background: Whether there is a causal relationship between childhood obesity and increased risk of chronic kidney disease (CKD) remains controversial. This study sought to explore how body size in childhood and adulthood independently affects CKD risk in later life using a Mendelian randomization (MR) approach. Methods: Univariate and multivariate MR was used to estimate total and independent effects of body size exposures. Genetic associations with early-life and adult body size were obtained from a genome-wide association study of 453,169 participants in the U.K. Biobank, and genetic associations with CKD were obtained from the CKDGen and FinnGen consortia. Results: A larger genetically predicted early-life body size was associated with an increased risk of CKD (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.14 to 1.41; P= 1.70E-05) and increased blood urea nitrogen (BUN) levels (β=0.010; 95% CI, 0.005 to 0.021; P=0.001). However, the association between the impact of early-life body size on CKD (OR, 1.12; 95% CI, 0.95 to 1.31; P=0.173) and BUN level (β=0.001; 95% CI, –0.010 to 0.012;P= 0.853) did not remain statistically significant after adjustment for adult body size. Larger genetically predicted adult body size was associated with an increased risk of CKD (OR, 1.37; 95% CI, 1.21 to 1.54; P= 4.60E-07), decreased estimated glomerular filtration rate (β=–0.011; 95% CI, –0.017 to –0.006; P=5.79E-05), and increased BUN level (β= 0.010; 95% CI, 0.002 to 0.019; P= 0.018). Conclusion Our research indicates that the significant correlation between early-life body size and CKD risk is likely due to maintaining a large body size into adulthood.

BACKGROUND:The absence of blood vessels in tendon tissue makes tendon repair challenging.Therefore,improving tendon healing and raising the efficacy of stem cell and other therapeutic cell transplantation after tendon damage have become hotspots for research in both clinical and scientific contexts. OBJECTIVE:The stem cells and gelatin microcarrier scaffold were joined to form tissue engineered stem cells.Human umbilical cord mesenchymal stem cells cultured in gelatin microcarriers were used to investigate the therapeutic impact and mode of action on tendinopathy healing in rats in vitro and In vivo. METHODS:(1)In vitro cell experiments:After seeding human umbilical cord mesenchymal stem cells with three-dimensional gelatin microcarriers,the cell vitality and survival were assessed.Human umbilical cord mesenchymal stem cells conventionally cultured were cultured as controls.(2)In vivo experiment:Adult SD rats were randomly assigned to normal group,tendinopathy group,2D group(tendinopathy+conventional culture of human umbilical cord mesenchymal stem cells),and 3D group(tendinopathy+gelatin microcarrier three-dimensional culture of human umbilical cord mesenchymal stem cells),with 6 rats in each group.Four weeks after therapy,animal behavior tests and histopathologic morphology of the Achilles tendon was examined. RESULTS AND CONCLUSION:(1)In vitro cell experiments:the seeded human umbilical cord mesenchymal stem cells on gelatin microcarriers showed high viability and as time went on,the stem cell proliferation level grew.Compared with the control group,3D stem cell culture preserved cell viability.(2)In vivo experiment:Following a 4-week treatment,the 3D stem cell culture group showed a significant improvement in both functional recovery of the lower limbs and histopathological scores when compared to the tendinopathy group.The 2D stem cell culture group also showed improvement in tendinopathy injury,but its effect is not as much as the 3D stem cell culture group.(3)The outcomes demonstrate that human umbilical cord mesenchymal stem cells cultured with three-dimensional gelatin microcarrier can promote the repair and regeneration of tendon injury tissue,and the repair effect is better than that of conventional human umbilical cord mesenchymal stem cells.

Background: Whether there is a causal relationship between childhood obesity and increased risk of chronic kidney disease (CKD) remains controversial. This study sought to explore how body size in childhood and adulthood independently affects CKD risk in later life using a Mendelian randomization (MR) approach. Methods: Univariate and multivariate MR was used to estimate total and independent effects of body size exposures. Genetic associations with early-life and adult body size were obtained from a genome-wide association study of 453,169 participants in the U.K. Biobank, and genetic associations with CKD were obtained from the CKDGen and FinnGen consortia. Results: A larger genetically predicted early-life body size was associated with an increased risk of CKD (odds ratio [OR], 1.27; 95% confidence interval [CI], 1.14 to 1.41; P= 1.70E-05) and increased blood urea nitrogen (BUN) levels (β=0.010; 95% CI, 0.005 to 0.021; P=0.001). However, the association between the impact of early-life body size on CKD (OR, 1.12; 95% CI, 0.95 to 1.31; P=0.173) and BUN level (β=0.001; 95% CI, –0.010 to 0.012;P= 0.853) did not remain statistically significant after adjustment for adult body size. Larger genetically predicted adult body size was associated with an increased risk of CKD (OR, 1.37; 95% CI, 1.21 to 1.54; P= 4.60E-07), decreased estimated glomerular filtration rate (β=–0.011; 95% CI, –0.017 to –0.006; P=5.79E-05), and increased BUN level (β= 0.010; 95% CI, 0.002 to 0.019; P= 0.018). Conclusion Our research indicates that the significant correlation between early-life body size and CKD risk is likely due to maintaining a large body size into adulthood.

Objective To investigate the distribution and antimicrobial resistance profiles of clinical isolates in Xi'an No.3 Hospital from 2019 to 2023.Methods Clinical isolates were collected from January 1,2019 to December 31,2023.Antimicrobial susceptibility testing was carried out according to a unified protocol of China Antimicrobial Resistance Surveillance Network using Kirby-Bauer method or automated systems.The data were interpreted according to the breakpoints released by the Clinical and Laboratory Standards Institute(CLSI)in 2023.Results A total of 6 621 clinical isolates were collected from 2019 to 2023,including 1 569(23.7％)strains of Gram-positive bacteria and 5 052(76.3％)strains of Gram-negative bacteria.The prevalence of methicillin-resistant S.aureus,S.epidermidis and other Staphylococcus species(except SS.pseudintermedius and S.schleiferi)was 39.0％,62.3％,and 74.4％,respectively.Methicillin-resistant strains showed much higher resistance rates to most of other antimicrobial agents than methicillin-sensitive strains.No Staphylococcus strains were found resistant to vancomycin or linezolid.E.faecium strains demonstrated much higher resistance rates to most antimicrobial agents tested than E.faecalis.The prevalence of linezolid-resistant E.faecalis and vancomycin-resistant E.faecium was 0.9％and 0.4％,respectively.The prevalence of penicillin-nonsusceptible strains(PISP+PRSP)was 5.8％in nonmeningitis S.pneumoniae isolates.The prevalence of ESBL-producing E.coli,K.pneumoniae,and P.mirabilis in Enterobacterales was 48.5％,37.8％,and 47.2％,respectively.Among Enterobacterales strains,K.pneumoniae had the highest resistance rate to imipenem(18.2％)and meropenem(17.9％).Other Enterobacterales were highly sensitive to carbapenems.The resistance rates of P.aeruginosa to imipenem and meropenem were 22.5％and 19.5％,respectively.The resistance rates of A.baumannii to imipenem and meropenem were 65.0％and 71.6％,respectively.Conclusions Antibiotic resistance is still serious in this hospital.Nearly half of the strains of E.coli,K.pneumoniae and P.mirabilis produced ESBLs.K.pneumoniae and A.baumannii showed high resistance rates to carbapenems.Antimicrobial resistance surveillance should be performed appropriately.Relevant departments need to strengthen cooperation to curb the spread of drug-resistant bacteria.

Objective:To investigate the effects of KH-type splicing regulatory protein(KHSRP)targeting and regulating JAK1/STAT3 signaling axis on the proliferation,migration and invasion of the adenocarcinoma of esophagogastric junction(AEG)cells,as well as the growth of transplanted tumors and lung metastasis.Methods:A total of 64 pairs of AEG tissue and adjacent normal tissue samples,along with clinical data from patients diagnosed at Huaihe Hospital from January 2017 to December 2018 were collected.The expression level of KHSRP in AEG tissues and adjacent normal tissues was observed using immunohistochemical staining.The differential expression of KHSRP in AEG cells(OE-19,TE-7,BIC-1,FLO-1,SK-GT-4,BE-3)and normal esophageal epithelial cells(Het-1A)was detected by qPCR.Lentiviral vectors were used to knockdown and overexpress KHSRP in OE-19,TE-7,FLO-1,and SK-GT-4 cells.The experiment was divided into the following groups:sh-NC group,sh-KHSRP group,Vector group,and KHSRP overexpression group(KHSRP group).The knockdown or overexpression efficiency was detected by qPCR,and the effects of KHSRP knockdown or overexpression on AEG cell proliferation,migration and invasion were evaluated using CCK-8 and Transwell assays,respectively.A mouse xenograft and lung metastasis model was established to observe the effects of KHSRP on tumor growth and metastasis in vivo.The targeted regulation of JAK/STAT signaling pathway by KHSRP was verified by Western blotting.A rescue experiment was conducted to verify whether KHSRP promoted malignant progression of AEG cells through the JAK1/STAT3 signaling pathway.Results:Compared with adjacent normal tissues,the expression level of KHSRP in AEG tissues was significantly increased(P<0.05 or P<0.01).Cell function experiments showed that KHSRP overexpression significantly promoted AEG cell proliferation,migration,and invasion in vitro(P<0.05 or P<0.01).In vivo animal experiments showed that KHSRP promoted AEG cell xenograft tumor growth and lung metastasis in nude mice(P<0.05 or P<0.01).After KHSRP knockdown,the phosphorylation levels of JAK1 and STAT3 in the JAK/STAT signaling pathway were significantly reduced,while overexpression of KHSRP led to the opposite results(P<0.05 or P<0.01).Rescue experiment showed that KHSRP could reverse the inhibition of cell proliferation,migration,and invasion caused by JAK1/STAT3 knockdown(P<0.05 or P<0.01).Conclusion:KHSRP regulates the malignant progression of AEG cells by activating JAK1/STAT3 signaling axis.KHSRP may become a potential target for the clinical treatment of AEG.