Objective: To investigate the safety and feasibility of transurethral blue laser vaporization of the prostate (BVP) under intravenous anesthesia without intubation. Methods: Clinical data of 30 benign prostatic hyperplasia (BPH) (prostate volume <40 mL) patients undergoing BVP under intravenous anesthesia without intubation in our hospital during Jul.and Nov.2024 were retrospectively analyzed.Preoperative and 1-month postoperative international prostate symptom score (IPSS), quality of life score (QoL), maximum urinary flow rate (Qmax), and postvoid residual volume (PVR) were compared.The operation time, cumulative blue laser activation time, recovery time, postoperative bladder irrigation time, postoperative catheter indwelling time, postoperative 2-hour visual analog scale (VAS) score and incidence of surgical and anesthetic complications were recorded. Results: All 30 patients successfully completed BVP under intravenous anesthesia without intubation.The operation time was (12.5±5.0) min, cumulative laser activation time (9.8±4.1) min, recovery time (6.8±1.2) min, postoperative bladder irrigation time (11.0±4.6) h, postoperative catheter indwelling time (2.7±1.1) days and postoperative 2-hour VAS score was (3.0±1.3).No cases required conversion to intubated general anesthesia, and no severe perioperative surgical or anesthetic complications occurred.Significant improvements in IPSS, QoL, Qmax, and PVR were observed 1 month postoperatively (P＜0.001). Conclusion: BVP under intravenous anesthesia without intubation in the treatment of prostate volume <40 mL BPH is clinically feasible, significantly improving lower urinary tract symptoms without significant surgical or anesthetic complications.

Background: SM-like (LSM) genes a family of RNA-binding proteins, are involved in mRNA regulation and can function as oncogenes by altering mRNA stability. However, their roles in B-cell progression and tumorigenesis remain poorly understood. Methods: We analyzed gene expression profiles and overall survival data of 123 patients with mantle cell lymphoma (MCL). The LSM index was developed to assess its potential as a prognostic marker of MCL survival. Results: Five of the eight LSM genes were identified as potential prognostic markers for survival in MCL, with particular emphasis on the LSM.index. The expression levels of these LSM genes demonstrated their potential utility as classifiers of MCL. The LSM.index-high group exhibited both poorer survival rates and lower RNA levels than did the overall transcript profile. Notably, LSM1 and LSM8 were overexpressed in the LSM.index-high group, with LSM1 showing 2.5-fold increase (p < 0.001) and LSM8 depicting 1.8-fold increase (p < 0.01) than those in the LSM.index-low group.Furthermore, elevated LSM gene expression was associated with increased cell division and RNA splicing pathway activity. Conclusions The LSM.index demonstrates potential as a prognostic marker for survival in patients with MCL. Elevated expression of LSM genes, particularly LSM1 and LSM8, may be linked to poor survival outcomes through their involvement in cell division and RNA splicing pathways. These findings suggest that LSM genes may contribute to the aggressive behavior of MCL and represent potential targets for therapeutic interventions.

Background: SM-like (LSM) genes a family of RNA-binding proteins, are involved in mRNA regulation and can function as oncogenes by altering mRNA stability. However, their roles in B-cell progression and tumorigenesis remain poorly understood. Methods: We analyzed gene expression profiles and overall survival data of 123 patients with mantle cell lymphoma (MCL). The LSM index was developed to assess its potential as a prognostic marker of MCL survival. Results: Five of the eight LSM genes were identified as potential prognostic markers for survival in MCL, with particular emphasis on the LSM.index. The expression levels of these LSM genes demonstrated their potential utility as classifiers of MCL. The LSM.index-high group exhibited both poorer survival rates and lower RNA levels than did the overall transcript profile. Notably, LSM1 and LSM8 were overexpressed in the LSM.index-high group, with LSM1 showing 2.5-fold increase (p < 0.001) and LSM8 depicting 1.8-fold increase (p < 0.01) than those in the LSM.index-low group.Furthermore, elevated LSM gene expression was associated with increased cell division and RNA splicing pathway activity. Conclusions The LSM.index demonstrates potential as a prognostic marker for survival in patients with MCL. Elevated expression of LSM genes, particularly LSM1 and LSM8, may be linked to poor survival outcomes through their involvement in cell division and RNA splicing pathways. These findings suggest that LSM genes may contribute to the aggressive behavior of MCL and represent potential targets for therapeutic interventions.

Background: SM-like (LSM) genes a family of RNA-binding proteins, are involved in mRNA regulation and can function as oncogenes by altering mRNA stability. However, their roles in B-cell progression and tumorigenesis remain poorly understood. Methods: We analyzed gene expression profiles and overall survival data of 123 patients with mantle cell lymphoma (MCL). The LSM index was developed to assess its potential as a prognostic marker of MCL survival. Results: Five of the eight LSM genes were identified as potential prognostic markers for survival in MCL, with particular emphasis on the LSM.index. The expression levels of these LSM genes demonstrated their potential utility as classifiers of MCL. The LSM.index-high group exhibited both poorer survival rates and lower RNA levels than did the overall transcript profile. Notably, LSM1 and LSM8 were overexpressed in the LSM.index-high group, with LSM1 showing 2.5-fold increase (p < 0.001) and LSM8 depicting 1.8-fold increase (p < 0.01) than those in the LSM.index-low group.Furthermore, elevated LSM gene expression was associated with increased cell division and RNA splicing pathway activity. Conclusions The LSM.index demonstrates potential as a prognostic marker for survival in patients with MCL. Elevated expression of LSM genes, particularly LSM1 and LSM8, may be linked to poor survival outcomes through their involvement in cell division and RNA splicing pathways. These findings suggest that LSM genes may contribute to the aggressive behavior of MCL and represent potential targets for therapeutic interventions.

Objective:To investigate the effects of hydrogen rich-saline (HRS) on intestinal mucosal barrier in rat with intestinal ischemia/reperfusion injury (IIRI).Methods:Twenty-four healthy male Sprague-Dawley rats, aged 8 weeks, were randomly divided into 3 groups (8 in each group) by random number table method: sham group, model group and HRS group.Rats in HRS group were intraperitoneally injected with HRS (10 mL/kg) at 30 min of ischemia, and the same amount of normal saline was intraperitoneally injected in model group.After 45 min of ischemia and 6 h of reperfusion, rats were sacrificed.Serum and ileum were collected for further detection.Tumor necrosis factor alpha (TNF-α), interleukin (IL)- 1β and IL-17A expression levels in serum were detected by conducting enzyme-linked immunosorbent assay (ELISA). The localization expressions of tight junction protein Occludin was detected by immunohistochemical staining (IHC), while the localization expression of tight junction protein zonula occluden-1 (ZO-1) were detected by immunofluorescence staining (IF). The protein expression of Occludin, ZO-1, and Lysozyme were detected by performing Western blot.The mRNA expression of Lysozyme and α-defensin were detected by real-time PCR (qPCR).Results:ELISA results proved that the levels of serum TNF-α and IL-1β in HRS group rats were significantly lower than those in model group [(62.02±29.97) ng/L vs.(113.40±44.58) ng/L, (21.68±0.35) ng/L vs.(28.29±3.49) ng/L], while the level of IL-17A increased [(28.18±5.28) ng/L vs. (15.10±3.60) ng/L] (all P<0.05). IHC staining: compared with model group, the expression of Occludin in HRS group was uniform and continuous, and the staining was darker.IF results: compared with model group, the fluorescence signal intensity of ZO-1 in HRS group rats significantly increased, and the distribution was clear and continuous.Wes-tern blot results: compared with model group, the expression levels of Occludin and ZO-1 proteins in HRS group rats remarkably increased (0.79±0.06 vs. 0.54±0.04, 0.91±0.11 vs. 0.51±0.13), while Lysozyme protein decreased (1.50±0.40 vs. 2.99±0.80) (all P<0.05). qPCR results revealed that the expression level of Lysozyme mRNA in HRS group rats was lower than that in model group (1.64±0.33 vs. 2.20±0.40), while α-defensin mRNA obviously increased (0.82±0.19 vs. 0.47±0.13) (all P<0.01). Conclusions:HRS protects intestinal mucosal barrier by inhibiting the expression of tight junctions and the secretion of antimicrobial peptides in rat suffering from IIRI.

Objective To identify the pathogenesis gene mutation of a pedigree with Cockayne syndrome.Methods The peripheral blood samples of the patient and his family members were collected and the genomic DNA was then extracted.Whole exome sequencing(WES)was performed for proband′s DNA.The disease-causing mutations were identified by bioinformatics analysis and pedigree analysis. Meanwhile,the mutations were confirmed by Sanger sequencing.Results Two novel mutations in ERCC8 gene,including c.400-2A >G and c.394_398delATGTA(p.L132fs)were identified in proband.The splicing mutation originated from his father and changed the splice acceptor site AG to GG, thus possibly caused alternative splicing.The c.394_398delATGTA(p.L132fs)frameshifting mutation was inherited from his mother.The proband′s sister also carried the same compound heterozygous mutation and had the same phenotype as proband.Conclusion The pathogenesis ERCC8 gene mutation of this pedigree with Cockayne syndrome was identified by using whole exome sequencing.

Objective To explore the effect of low concentration 5-fluorouracil combined with triamcinolone acetonide on rabbit ear hypertrophic scar model.Methods White rabbits post-traumatic scars were randomly divided into A,B,C and D groups,each group contained 18 cases.Group A was given triamcinolone acetonide and low concentration 5-fluorouracil,Group B was given low concentration 5-fluorouracil,Group C was given triamcinolone acetonide and Group D was used as the control group.The dynamic changes of the scar were observed by naked eyes,hematoxylin-eosin (HE) staining and van Gieson (VG) staining through microscope.Vascular endothelial growth factor (VEGF) and CD34 were detected and compared within 4 groups by immunohistochemical staining.Results We successfully established a rabbit ear scar model.It was observed that the scars of Groups A,B and C had been shorter and flatter than Group D,close to the normal tissue.In HE and VG staining,the number of fibroblasts,inflammatory cells,blood vessels in groups A,B and C had been decreased,compared with Group D.Immunohistochemical results showed that the positive rates of VEGF and CD34 from the most to the lest were Groups D,B,C and A.The scar proliferation index from the most to the lest were Groups D,B,C and A.Conclusions The effect of low concentration 5-fluorouracil in treatment of the rabbit ear hypertrophic scar is better than that of triamcinolone acetonide.Low concentration 5-fluorouracil combined with triamcinolone acetonide has a synergistic effect in treatment of hypertrophic scar,which has better effect than that of low concentration 5-fluorouracil or triamcinolone acetonide alone.

Objective To analyze the changes in distribution of occupational radiation cases reported from 2013 to 2017 in China and learn about the occupational health risks of radiation workers.Methods Descriptive analyses were made of regional distribution,disease category distribution,occupation category distribution and exposure mode distribution of these cases,according to the reports (2013-2017) of occupational radiation sickness from " Occupational Health of Radiation Workers Management System".Results There were 54 diagnostic radiology agencies for occupational radiation sickness in China that covered all provinces,autonomous regions and municipalities except Tibet and Production and Construction Corps of Xinjiang.A total of 106 new cases were reported from 2013 to 2017.Most of the cases were radiogenic neoplasm (43.40％),and chronic radiation sickness were from external exposure (16.98％) and radiation cataract (16.04％).Most of the cases (70.75％) were engaged in medical application and a small part of the cases (13.21％) engaged in industry application.Chronic exposure (80.19％) was the most frequent form of exposure mode,but acute exposure (5.66％) was very few.A part of cases (14.15％) were reported without exposure mode.Conclusions The morbidity of occupational radiation sickness declined generally in China and occupational health management of key workers should be strengthened continuously.

Objective To examine the role of β-tubulin on the interaction between the cholecystokinin B receptor (CCKBR),dopamine D5 receptor(D5R), and water-sodium metabolism. Methods Normotensive and hypertensive renal proximal tubular cells(RPTC)were equally randomized into three separate groups: a gastrin group, fenoldopam group,and gastrin+nocodazole group. Immunofluorescence was used to determine localization of β-tubulin,CCKBR,and D5R. Western blotting was used to detect CCKBR, D5R, and Na-K-ATP expression. Results Gastrin stimulation in normotensive RPTC increased D5R expression(P < 0.05)and decreased Na-K-ATP expression(P < 0.05). These changes were blocked by a tubulin inhibitor(P < 0.05). However, interaction between CCKBR, D5R, and Na-K-ATP expression was not significantly affected in hypertensive RPTC. Immunofluorescence showed that CCKBR and D5R can induce one another,followed by transport to the plasma membrane, which can prevented by a tubulin inhibitor. Further, tubulin is disordered in hypertensive RPTC,which cannot support intracellular CCKBR and D5R transport. Conclusions tubulin plays a key role in the interaction between CCKBR, D5R, and water-sodium metabolism by improving protein transfer from the cytoplasm to cell membrane.