BACKGROUND:This study aimed to evaluate the safety and efficacy of TACE combined with durvalumab for treating advanced and metastatic BTC. Research design and methods: Data were collected retrospectively from a single center. The TACE procedures were performed 1 to 19 times, with repetitions occurring every 4 to 12 weeks based on the patient's liver function and tumor shrinkage. Durvalumab was given as an intravenous injection every three weeks at a dose of 1000 to 1500 mg. RESULTS:The estimated median progression-free survival (PFS) was 9.0 months (95% CI: 6.8 to 11.2), with a 1-year PFS rate of 23.8%. The estimated median overall survival (OS) was 16.0 months (95% CI: 7.5 to 24.5), with a 1-year OS rate of 58.7%. The investigator-confirmed objective response rate (ORR) was 35.9%. Elevated baseline carcinoembryonic antigen (CEA) levels and neutrophil-to-lymphocyte ratio (NLR) ≥ 3 showed negative correlations with PFS (p = 0.035, CEA; p = 0.038, NLR) and OS (p = 0.040, NLR). Adverse events occurred in 36 patients (92.3%). Additionally, 7 patients (17.9%) experienced immune-mediated AEs (imAEs). CONCLUSIONS:These results indicate promising efficacy and acceptable safety for the combination of TACE and durvalumab as a first-line treatment for advanced and metastatic BTC.

Background:There is relatively scant evidence concerning the effects of Lenvatinib and Pembrolizumab together with TACE for advanced HCC Lenvatinib and pembrolizumab have been widely applied in clinical settings. PIVKA-II serving as the sensitive biomarker for evaluating liver cancer was employed by us to further assess the therapeutic effectiveness of TACE combined with Lenvatinib in the treatment of BCLC C. Methods:In this retrospective study, 260 patients with HCC BCLC C stage were included in the present study. TACE (TL group) included 126 patients, TACE-Lenvatinib-Pembrolizumab (TPB group) consisted of 134 patients. OS and PFS were compared between the two groups. Alternatively, the impact of PIVKA-II in TPB on the PFS of BCLC C stage was also assessed. Results:The median overall survival (OS) in the TL group was significantly prolonged compared to that in the TPB group (13.7 months versus 9.6 months). Conversely, the median progression - free survival (PFS) was extended in the TPB group as opposed to the TL group (9.3 months versus 6.2 months). The adverse events in the TPB group were controllable and tolerable. After six months of combined treatment, the change in PIVKA - II became less significant. This suggests that PIVKA-II is negatively correlated with PFS, meaning that the greater the decrease in PIVKA-II after 6 months of combined therapy, the longer the PFS time for the patient. Conclusion:TACE combined with Lenvatinib and Pembrolizumab exhibited remarkable survival benefits for HCC BCLC C patients. Given the extremely dismal prognosis of advanced HCC, the safety and efficacy of TACE in combination with Lenvatinib and Pembrolizumab justify its clinical application.

Background: Non-small cell lung cancer (NSCLC) represents 85% of all lung cancer (LC) cases that are malignant tumors, while lung adenocarcinoma (LUAD) is the commonest type of NSCLC. Family with sequence similarity 107 member A (FAM107A) is a suppressor gene in many cancers, but its mechanism in LUAD has been less studied. The objective of the experiment is to explore the role and potential mechanism of FAM107A in the progression of LUAD. Methods: Expression levels of histone deacetylase 2 (HDAC2) and FAM107A in LUAD tissues/cells were determined using StarBase and quantitative reverse transcription polymerase chain reaction. In the first part, FAM107A specific short hairpin RNA (shFAM107A) was transfected into H1299 cells and FAM107A overexpression plasmid was transfected into PC9 cells. In the second part, shHDAC2 and shFAM107A were co-transfected into H1299 cells, and HDAC2 and FAM107A overexpression plasmids were co-transfected into PC9 cells. Then, chromatin immunoprecipitation assays were employed to determine HDAC2 enrichment in FAM107A promoter region. Loss- and gain-of-function experiments (3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT), colony formation assay, and flow cytometry) were conducted to verify the regulation of FAM107A on malignant phenotype of LUAD cells. The influence of HDAC2/FAM107A axis on LUAD cell biological behaviors was verified through rescue experiments. Results: FAM107A mRNA exhibited a low expression in LUAD tissues/cells (p < 0.001). Its overexpression suppressed the viability, proliferation, and B-cell lymphoma-2 (Bcl-2) level in LUAD cells, and promoted the apoptosis as well as Bcl-2-Associated X (Bax) and Cleaved Caspase-3 protein levels (p < 0.01), while its silencing produced the opposite results. HDAC2 mRNA expression was highly expressed in LUAD tissues (p < 0.001). Its overexpression negated the aforementioned effects of FAM107A overexpression (p < 0.01), while its inhibition neutralized the effects of FAM107A silencing (p < 0.01). HDAC2 protein expression was enriched in FAM107A promoter region (p < 0.001), and FAM107A protein expression was inhibited by HDAC2 through its histone deacetylation. Conclusions: Repression of FAM107A induced by HDAC2 promotes colony formation, while inhibiting the apoptosis of LUAD cells.

Purpose For patients with advanced or unresectable hepatocellular carcinoma (HCC), safe and effective therapies are urgently needed to improve their long-term prognosis. Although the guidelines recommend first-line treatments such as sorafenib, lenvatinib, and atezolizumab in combination with bevacizumab (T+A) and second-line treatments such as regorafenib, the efficacy comparison between drugs is lacking, that is, a treatment is not recommended as the optimal or alternative choice for a specific patient population. Therefore, we will conduct a high-quality network meta-analysis based on Phase III randomized controlled trials (RCTs) to systematically evaluate and compare overall survival (OS), progression-free survival (PFS), objective response rate (ORR), and serious adverse events (SAE) of different treatment protocols in the context of first-line and second-line therapies, which are critical for clinical decision making and prognostic improvement in advanced HCC patients. Methods The studies of interest were Phase III RCTs evaluating the efficacy or safety of first- or second-line therapies in patients with unresectable or advanced HCC. Literature published in English from the four databases of PubMed, Embase, Cochrane Library, and Web of Science was comprehensively searched from the inception to May 23, 2022. Outcomes of interest included OS, PFS, ORR, and SAE. A league table was developed to show the results of the comparison between different treatments. A histogram of cumulative probability was drawn to discuss the ranking probability of treatments based on different outcomes. The effectiveness and safety of various treatments were comprehensively considered and the two-dimensional diagram was plotted to guide clinical practice. The Gemtc package in R Studio was used for network meta-analysis in a Bayesian framework. Results The results showed that HAIC-FO was superior to T+A regimen, regardless of OS, PFS or ORR. TACE combined with lenvatinib performed better than T+A in PFS, and ORR. In addition to the T+A regimen, Sintilimab combined with IBI305 and camrelizumab combined with apatinib were also associated with longer OS, PFS, and ORR, and their SAE incidence was not higher than that of T+A, especially for camrelizumab combined with apatinib, its safety was better than that of T+A regimen. There were no new treatments or combinations that were more effective than regorafenib. It was important to note that for PFS, the efficacy of apatinib and cabozantinib was not statistically different from that of regorafenib, so these two treatments could be used as alternative treatment options in cases where regorafenib was not tolerated or treatment failed. Conclusions We conducted a network meta-analysis to evaluate the efficacy and safety of multiple treatment modalities by integrating the results of direct and indirect comparisons. This study included high-quality multicenter Phase III RCTs, collated and summarized all treatments involved in advanced or unresectable HCC in first-line and second-line settings, and compared with T+A and regorafenib, respectively, and ranked based on efficacy and safety to support clinical decision making.

PURPOSE:Acute rejection is a frequent complication among lung transplant recipients and poses substantial therapeutic challenges. 15-hydroxyprostaglandin dehydrogenase (15-PGDH), an enzyme responsible for the inactivation of prostaglandin E2 (PGE2), has recently been implicated in inflammatory lung diseases. However, the role of 15-PGDH in lung transplantation rejection remains elusive. The present study was undertaken to examine the expression of 15-PGDH in rejected lung allografts and whether inhibition of 15-PGDH ameliorates acute lung allograft rejection.METHODS:Orthotopic mouse lung transplantations were performed between donor and recipient mice of the same strain or allogeneic mismatched pairs. The expression of 15-PGDH in mouse lung grafts was measured. The efficacy of a selective 15-PGDH inhibitor (SW033291) in ameliorating acute rejection was assessed through histopathological examination, micro-CT imaging, and pulmonary function tests. Additionally, the mechanism underlying the effects of SW033291 treatment was explored using CD8+ T cells isolated from mouse lung allografts.RESULTS:Increased 15-PGDH expression was observed in rejected allografts and allogeneic CD8+ T cells. Treatment with SW033291 led to an accumulation of PGE2, modulation of CD8+ T-cell responses and mitochondrial activity, and improved allograft function and survival.CONCLUSION:Our study provides new insights into the role of 15-PGDH in acute lung rejection and highlights the therapeutic potential of inhibiting 15-PGDH for enhancing graft survival. The accumulation of PGE2 and modulation of CD8+ T-cell responses represent potential mechanisms underlying the benefits of 15-PGDH inhibition in this model. Our findings provide impetus for further exploring 15-PGDH as a target for improving lung transplantation outcomes.

Lung fibrosis is a devastating outcome of various diffuse parenchymal lung diseases. Despite rigorous research efforts, the mechanisms that propagate its progressive and nonresolving nature remain enigmatic. Oxidative stress has been implicated in the pathogenesis of lung fibrosis. However, the role of extracellular redox state in disease progression and resolution remains largely unexplored. Here, we show that compartmentalized control over extracellular reactive oxygen species (ROS) by aerosolized delivery of recombinant extracellular superoxide dismutase (ECSOD) suppresses an established bleomycin-induced fibrotic process in mice. Further analysis of publicly available microarray, RNA-seq and single-cell RNAseq datasets reveals a significant decrease in ECSOD expression in fibrotic lung tissues that can be spontaneously restored during fibrosis resolution. Therefore, we investigate the effect of siRNA-mediated ECSOD depletion during the established fibrotic phase on the self-limiting nature of the bleomycin mouse model. Our results demonstrate that in vivo knockdown of ECSOD in mouse fibrotic lungs impairs fibrosis resolution. Mechanistically, we demonstrate that transforming growth factor (TGF)-β1 downregulates endogenous ECSOD expression, leading to the accumulation of extracellular superoxide via Smad-mediated signaling and the activation of additional stores of latent TGF-β1. In addition, depletion of endogenous ECSOD during the fibrotic phase in the bleomycin model induces an apoptosis-resistant phenotype in lung fibroblasts through unrestricted Akt signaling. Taken together, our data strongly support the critical role of extracellular redox state in fibrosis persistence and resolution. Based on these findings, we propose that compartment-specific control over extracellular ROS may be a potential therapeutic strategy for managing fibrotic lung disorders.

Hepatocellular carcinoma (HCC) is widespread cancer with a high degree of morbidity and mortality in individuals worldwide and a serious concern for its resistance to present chemotherapy drugs. In this investigation, the combination of cisplatin (CPT) and metformin (MET) to kill the HepG2 and caco-2 cells was developed into a new pH-responding magnetic nanocomposite based on reduced graphene oxide. Polyhydroxyethyl methacrylic (PHEA) was then linked employing grafting from approach to the reduced graphene oxide by ATRP polymerization (Fe3O4@rGO-G-PSEA). FT-IR, SEM, XRD, DLS, and TGA analyses evaluated physicochemical characteristics of the nanocomposite. In addition, the cellular uptake property of the nanocomposites was examined by the HepG2 cells. The outcomes of cell viability results indicate that the nanoparticles loaded with MET&CPT showed the lowest concentration rate of HepG2 and Caco-2 cells compared to the drug-loaded single nanocomposite groups and free drugs. The histological analysis has demonstrated relatively safe and does not produce different stress such as swelling and inflammation of the mice organs. Our results show the enhancement in cytotoxicity in HepG2 and Cocoa-2 cells by MET and CPT graphene oxide-based nanocomposite by promoting apoptotic response. Moreover, Fe3O4@rGO-G-PSEA showed potent in vivo antitumor efficacy but showed no adverse toxicity to normal tissues. Together, this study can provide insight into how surface embellishment may tune these nanocomposites' tumor specificity and provide the basis for developing anticancer efficacy.

Exposure to airborne fine particulate matter (PM2.5) is associated with a variety of respiratory health effects and contributes to premature mortality. Lymphatic vessels are instrumental in facilitating the transport of toxic materials away from the lung to maintain alveolar clearance and have been shown to play important roles in lung injury and repair. Despite intense research efforts in delineating the effects of PM2.5 on blood vascular endothelial cells, the impacts of PM2.5 on lymphatic endothelial cells (LECs), a specialized subset of endothelial cells that comprise lymphatic vessels, remain enigmatic. Here, we conducted MTT assay and show that treatment of human pulmonary LECs with PM2.5 suppresses cell viability in a time- and dose-dependent manner. We subsequently performed Annexin V/propidium iodide labeling and demonstrate that PM2.5 induces LECs apoptosis and necrosis. Furthermore, we found that manganese superoxide dismutase (SOD2) expression and mitochondrial SOD activity were profoundly reduced following PM2.5 exposure. Mechanistically, we provide compelling evidence that PM2.5 reduces SOD2 expression through activation of Akt pathway, which leads to a disruption of mitochondrial redox homeostasis characterized by increased accumulation of mitochondrial superoxide. Conversely, mitochondria-targeted SOD mimetic (MitoTEMPO) corrects the disturbed oxidative milieu in PM2.5-treated LECs. Additionally, MitoTEMPO ameliorates the deleterious impacts of PM2.5 on mitochondrial DNA integrity and preserves the viability of LECs. Taken together, these novel data support a critical role for mitochondrial superoxide in the pathogenesis of PM2.5-induced LECs injury and identity mitochondrial-targeted antioxidants as promising therapeutic options to treat environmental lung diseases. Our findings are limited to experimental studies with primary LECs, and future investigations in animal models are warranted to shed light on the precise pathophysiology of lymphatic system in response to PM exposure.

目的 探讨支架孔率对模拟乙状窦憩室内血流动力学的影响.方法 基于计算流体力学(CFD)方法构建理想化乙状窦憩室血流动力学模型(S0模型,无支架),观察支架孔率75％、50％、25％模型(分别对应S1、S2、S3模型)的血流动力学变化.结果 S0、S1、S2、S3模型乙状窦憩室内血流速度分别为12.65、4.68、2.20及0.41 mm/s.相对于S0模型,S1、S2、S3模型血流速度分别降低了63.00％(7.97/12.65)、82.61％(10.45/12.65)和96.76％(12.24/12.65).乙状窦憩室远侧壁的高压力区及高壁面切应力(WSS)区随支架孔率降低而逐渐减小,整个憩室内压力及WSS分布趋于均匀.S0、S1、S2、S3模型乙状窦憩室内压力分别为64.04、63.86、62.54及60.95 Pa,各模型压力值差异不明显.结论 低孔率支架可明显改善模拟乙状窦憩室内血液流动和血流动力学应力条件.

目的 描述搏动性耳鸣(PT)患者的血管造影表现,并评估与PT相关的静脉窦狭窄的压力梯度.方法 回顾性分析37例临床诊断为PT患者的脑血管造影资料.除常规动脉图像外,所有血管造影均包括侧重于相关静脉窦的间接二维和三维静脉造影.在筛选已知与PT相关的原因后,分析横窦、乙状窦狭窄的亚组中间接静脉造影结果,再对该亚组病例进行直接静脉造影和静脉压力梯度的测量.结果 本组造影显示4例硬脑膜动静脉瘘,2例病例动脉和静脉模式完全正常,其余31例均存在复杂或孤立的静脉异常.其中,9例同时合并了乙状窦憩室(SSD)、同侧上游静脉窦狭窄(SS)、同侧优势回流静脉窦(DVS)的三种静脉异常.SSD在合并或孤立静脉异常中共计15例(15/31,48.4％).在25例出现横窦、乙状窦SS(25/31,80.6％)的病例中,静脉窦狭窄的平均压力梯度为6.8±2.9(1.0～16.3)mmHg.此外,耳鸣侧的DVS(21/31,67.7％)可能与PT也有一定关系.结论 除了动脉性原因外,在PT患者中观察到高比例的横窦和乙状窦异常;伴有压力梯度的相关静脉窦狭窄或额外的同侧优势回流静脉窦可能与PT有关.

As a novel vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor (VEGFR2-TKI), apatinib has a certain anti-tumor effect for a variety of solid tumors. The present study evaluates its efficacy and safety in advanced hepatocellular carcinoma (HCC). In this study, 47 patients with advanced HCC were included. TACE monotherapy group included 22 patients that responded to TACE, while the group that received TACE and apatinib included 25 patients that progressed on TACE and were able to receive apatinib off label. Median overall survival (OS) was significantly improved in the apatinib plus TACE group compared with the TACE group. Similarly, apatinib in combination with TACE significantly prolonged median progression-free survival (PFS) compared with TACE monotherapy. Furthermore, there was a significant difference between combination therapy and monotherapy in both Barcelona clinic liver cancer (BCLC) B and BCLC C group. The combination therapy had a dramatic effect on OS and PFS for patients at both BCLC B and BCLC C level. The most common clinically adverse events of apatinib plus TACE group were fatigue, weight loss, hypertension, hand-foot syndrome and anorexia, which were manageable and tolerable. The efficacy analysis showed that there was no significant association of survival benefit with age, gender, Eastern Cooperative Oncology Group (ECOG) performance status, hypertension and hand-foot syndrome. Patients with macrovascular invasion and extrahepatic invasion showed worse survival benefits. In conclusion, apatinib combined with TACE revealed certain survival benefits for HCC patients who experienced progression following TACE, which can provide a promising strategy for HCC treatment.

Bone metastases are the most common sites for malignant tumors. Patients who failed to respond to initial first-line treatment with bisphosphonates usually suffer from extreme pain. The aim of this study was to observe the efficacy of arterial chemoembolization combined with Iodine-125 seed implantation in the treatment of bone metastatic cancer pain. All 14 patients with metastatic bone tumor wo failed first-line treatment underwent arterial chemoembolization the day before the implantation of the particles. A computer stereoscopic TPS was used to design the treatment plans, the number and dose of particles required for implantation. Pain relief was evaluated using several parameters such as Visual Analog Scale (VAS) and Verbal Rating Scales (VRS). Pain intensity was measured pre-operation and 1-week, 1-month, 3-month after the treatment. Meanwhile, we also assessed tumor size using computer tomography (CT). Pain palliation was observed in 35.7% (5/14), 57.1% (8/14), and 78.6% (11/14) of all patients at 1-week, 1-month and 3-month post treatment. Likewise, our analysis showed that the combination therapy resulted in a significant decrease of VAS score (6.71 ± 0.49 before treatment vs 3.36 ± 0.40 at 3 month post treatment) and overall responding rate of 92.0% using VRS pain assessment. Consistently, tumor size was reduced from 42.16 ± 10.32 before treatment to 29.11 ± 8.73 at 3 months post treatment. No serious complications were detected. Our study demonstrate that the combination of arterial chemoembolization and 125I particles resulted in evident pain relief and reduction of tumor burden, suggesting that the combination treatment could be a feasible and promising therapy for bone tumor management.

目的 探讨NR5A2对大鼠胰腺腺泡细胞系AR42J炎性反应的影响.方法 用雨蛙素刺激AR42J细胞,建立胰腺炎细胞模型.分别用慢病毒和sh-RNA感染AR42J细胞,上调和下调细胞内的NR5A2,用Western blot检测NR5A2的含量.在此基础上,用流式细胞计量术检测细胞凋亡率,用ELISA检测细胞培养上清中炎性因子IL-1、TNF-α的水平.结果 用100 nmol/L雨蛙素刺激AR42J细胞,成功诱导炎性反应和细胞凋亡,刺激6 h凋亡率达到峰值;刺激24 h NR5A2含量降到最低点,刺激48 h基本恢复至正常水平.用慢病毒载体过表达NR5A2,再用雨蛙素刺激,过表达组的细胞凋亡率显著高于对照组(P<0.05);IL-1和TNF-α在过表达组均显著降低(P<0.01,P<0.05).用shRNA沉默NR5A2,雨蛙素刺激后沉默组的细胞凋亡率显著低于对照组(P<0.05);IL-1和TNF-α 在沉默组均显著升高(P<0.05,P<0.01).在过表达NR5A2基础上沉默β-catenin,与对照组相比,凋亡率降低(P<0.05),IL-1和TNF-α显著增高(P<0.05,P<0.01).结论 NR5A2能够促进炎性反应条件下胰腺腺泡细胞的凋亡,抑制炎性反应.β-catenin参与NR5A2在腺泡细胞炎性反应应激条件下的调节作用.

Objective: To evaluate the therapeutic effect of transarterial chemoembolization (TACE) combined with apatinib on pa-tients with advanced hepatocellular carcinoma (HCC). Methods:Twenty-one patients were treated with TACE combined with 250 mg of apatinib once a day. Disease classification was assessed by investigators using the modified Response Evaluation Criteria in Solid Tu-mors (mRECIST). The evaluation period was 28 days. Results:The therapeutic effects were classified as follows:3 patients (14.3%) had complete response, 6 patients (28.6%) had partial response, 5 patients (23.8%) had stable disease, and 2 patients (9.5%) had progres-sive disease. The disease control rate was 61.9%, and the objective response rate was 38.1%. In patients, the most frequent adverse events were fatigue (94.4%), anorexia (23.8%), diarrhea (19.0%), hypertension (19.0%), and hand-foot syndrome (19.0%). Conclusion:The short-term therapeutic effect revealed that the combination of TACE and apatinib could be a promising treatment for patients with advanced HCC. Adverse events should be closely monitored and provided with active management.

OBJECTIVE: To investigate the relationships between upstream venous sinus stenosis and pulsatile tinnitus (PT), and to assess the correlation with diverticulum growth and the effectiveness of stent implantation. METHODS: Patient-specific geometric models were constructed using computed tomography venography images from a patient with PT, with sigmoid sinus diverticulum, and with upstream transverse sinus stenosis, in whom stenting of the upstream sinus stenosis alone achieved complete remission of PT. Computational fluid dynamics simulation based on this patient-specific geometry was performed using commercially available finite element software (ANSYS-14) to qualitatively and quantitatively compare the flow velocity, flow rate, velocity vector, pressure, vorticity, and wall shear stress on the affected side transverse and sigmoid sinuses, before and after stent implantation. RESULTS: Stenting improved the flow direction and magnitude. After stenting, the flow pattern became smoother and more regular. High-speed blood flow at the level of the diverticulum neck was confined to a smaller area, and its direction changed from approximately perpendicular to the diverticular dome to the distal side of the diverticular neck. The diverticulum showed obvious flow reduction, with decreases of 80.7%, 68.7%, 96.1%, and 91.3% in peak velocity, inflow rate, pressure gradient, and peak vorticity, respectively. The abnormally low wall shear stress at the dome of diverticulum was eliminated. CONCLUSIONS: Our findings strongly support a major role of diverticulum stenosis before in PT development and suggest that such stenosis is a causative factor of diverticulum growth. They also confirm the effectiveness of stent implantation for the treatment of PT.

Nonalcoholic steatohepatitis (NASH) is characterized by fat accumulation in the hepatocyte, inflammation, liver cell injury, and varying degrees of fibrosis, and can lead to oxidative stress in liver. Here, we investigated whether Salidroside, a natural phenolic antioxidant product, can protect rat from liver injury during NASH.

肠道正常菌群参与机体的物质代谢，营养物质的吸收合成，并能够促进生长发育，维持人体正常生理活动，其对胃肠道消化和免疫作用的发挥与肠杆菌、肠球菌、类杆菌和乳杆菌的关系密不可分。肠道黏膜免疫反应主要依靠肠腔内黏膜表面的免疫球蛋白（ sIgA为主）和淋巴细胞为主体的免疫活性细胞，共同完成肠道局部免疫。抗生素的使用可诱导肠道菌群失调，脑－肠轴参与了肠道菌群失调，其不仅可引起全身免疫疾病，还能导致肥胖、2型糖尿病及肠癌。

目的 探讨主动脉瓣狭窄患者行主动脉瓣置换术后相关危险因素对消化道出血的影响.方法 回顾性分析8877例主动脉瓣狭窄患者行主动脉瓣置换术患者的临床资料,将术后出现消化道出血的35例列为实验组,并据性别、年龄、主动脉瓣狭窄程度、左室平均射血分数、EuroSCORE风险评分随机选取50例作为对照组.分析两组患者术前伴发疾病、术后血液指标、口服药物及并发症等相关因素对术后消化道出血的影响.结果 术前伴有脑卒中、慢性阻塞性肺疾病(COPD)、肾损害者,术后消化道出血率增加,与对照组比较,差异有显著性(P＜0.05).实验组术前红细胞、白细胞数、血红蛋白含量低于对照组(P＜0.05).术后凝血酶原时间、国际标准化比值较对照组明显升高(P＜0.05).曾有口服非甾体类抗炎药者较对照组术后消化道出血率增高(P＜0.05).术后并发症中有胸腔积液、心包积血、呼吸机依赖、脑血管疾病者较对照组消化道出血率增加(P＜0.05).结论 术前伴有脑卒中、COPD,曾有口服非甾体类抗炎药物史,术后呼吸机依赖、国际标准化比值升高、伴发胸腔积液、心包积血等因素是主动脉瓣狭窄患者行主动脉瓣置换术后消化道出血的相关危险因素.

Objective To analyze the status and influence factors of helicobacter pylori (Hp) infection in patients taking non-steroidal antiinflammatory drugs (NSAID) in Beijing.Methods One hundred and ninety outpatients with long term usage of NSAID in Beijing were enrolled and underwent 13C-urea breath test (13 C-UBT).The proportion of Hp infection was calculated; the correlations of age,sex,smoking history,drinking history,education degree,working condition,family history of gastritis and peptic ulcer,dietary habits with Hp infection were analyzed.Results Among these 190 patients,there were 102 Hp positive patients (53.7％) and 88 Hp negative patients (46.3％).The infection rate of Hp was significantly different among patients with different ages,working conditions,family history of gastritis and peptic ulcer disease,dietary habits [＜ 40 years old:60.0％ (30/50),40-65 years old:59.1％ (52/88),＞65 years old:38.5％ (20/52) ; working:80.0％ (80/100),not working:24.4％ (22/90) ; positive family history:86.0％ (74/86),negative family history:27.0％ (28/104); regular diet:25.5％ (28/110),irregular diet:92.5％ (74/80)] (P ＜ 0.05).Conclusion The Hp infection in patients taking NSAID drugs for long time in Beijing is significantly related to age,working conditions,family history of gastritis and peptic ulcer and diet habits.