Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide. Despite advances in diagnosis and treatment, the lack of effective therapeutic targets continues to limit improvements in patient outcomes. ASAP3 has been implicated in tumor progression; however, its role and underlying mechanisms in ESCC remain unclear. Paraffin-embedded ESCC tissues were analyzed by immunohistochemistry to evaluate the expression of ASAP3, NEMO, p65, phosphorylated p65 (p-p65), and MMP9 and their associations with clinicopathological parameters. In vitro, ASAP3 was silenced to assess its effects on ESCC cell proliferation, migration, and invasion and to explore the underlying mechanisms. In vivo, the role of ASAP3 in ESCC growth was validated using a mouse xenograft model, with tumor size and volume measured and changes in ASAP3, NEMO, p65, and p-p65 expression further analyzed. Clinicopathological analysis showed that elevated ASAP3, NEMO, p65, p-p65, and MMP9 expression in ESCC tissues was associated with poor prognosis. In vitro, ASAP3 knockdown inhibited the proliferation, migration, and invasion of KYSE450 cells. In vivo, ASAP3 silencing suppressed xenograft tumor growth and reduced tumor proliferative activity. Mechanistically, ASAP3 downregulation decreased NEMO expression and p65 phosphorylation, thereby suppressing ESCC cell proliferation, migration, and invasion. Collectively, ASAP3 may promote ESCC progression by interacting with NEMO and activating NF-κB signaling. These findings suggest that ASAP3 functions as an oncogenic driver and may serve as a potential biomarker in ESCC.

ABSTRACT Background Esophageal squamous cell carcinoma (ESCC) remains a lethal malignancy with limited effective therapies. Although hexokinase 2 (HK2) is upregulated in multiple cancers, its role in ESCC progression and underlying mechanisms, particularly its interaction with the mitochondrial damage pathway, remains incompletely understood. Methods Bioinformatic analyses and clinical specimens were used to evaluate HK2 expression in ESCC and its association with prognosis. Functional assays, including CCK‐8, wound healing, Transwell, flow cytometry, ROS detection, JC‐1 staining, and mitochondrial protein analyses, were performed in ESCC cells with HK2 overexpression or knockdown. Co‐immunoprecipitation (CO‐IP) was conducted to validate the physical interaction between HK2 and VDAC1. A subcutaneous xenograft model was used to assess the pro‐tumorigenic role of HK2 in vivo. Results HK2 was markedly overexpressed in ESCC and was associated with poor prognosis. Mechanistically, HK2 interacted with VDAC1 on the outer mitochondrial membrane, suppressed mitochondrial depolarization and ROS accumulation, protected mitochondrial function, and thereby promoted ESCC cell proliferation, migration, and invasion. Conversely, HK2 knockdown disrupted HK2–VDAC1‐associated mitochondrial regulation, induced mitochondrial dysfunction and apoptosis, and attenuated malignant phenotypes. In vivo, HK2 overexpression promoted tumor growth, whereas HK2 knockdown significantly suppressed tumor progression. Conclusion These findings suggest that HK2 promotes ESCC progression at least partly by interacting with VDAC1, protecting mitochondrial function and reducing cell apoptosis. The HK2–VDAC1 axis may represent a potential therapeutic vulnerability in ESCC.

Background: Esophageal cancer is becoming increasingly common worldwide, and esophageal squamous cell carcinoma is the most predominant type, for which there is no very effective treatment. Hexokinase 2 (HK2) has carcinogenic effects in a variety of tumours, and it has been found that HK2 is highly expressed in esophageal squamous cell carcinoma through bioinformatics methods and clinical sample observations, but whether HK2 promotes the development of esophageal squamous cell carcinoma and its mechanism of action is still unclear. Results: In this study, we verified that HK2 promoted the proliferation, migration and invasion of esophageal cancer by CCK8, wound healing assay, Transwell; flow cytometry detected ROS and apoptosis to explore the level of apoptosis, as well as the mitochondrial function detected by JC-1 and UCP2 protein expression. The role of HK2 was verified in an in vivo subcutaneous xenograft tumour model, and changes in tumour size and immunohistochemical indices were observed.Highly expressed HK2 inhibited the expression of type 1 voltage-dependent anion channel (VDAC1) to resist apoptosis, which in turn promoted the proliferation, migration and invasion of esophageal squamous cell carcinoma, whereas knockdown of HK2 attenuated the malignant features of ESCC. Conclusions: Overall, HK2 plays an important role as an oncogene in ESCC and accelerates cancer progression by affecting the mitochondrial apoptotic pathway, and it may serve as a potential target for ESCC therapy.

Sulfatase, traditionally known for its role in sulfate ester hydrolysis, has recently emerged as a potential player in tumor biology through its involvement in oxidative stress pathways. Here, we demonstrate for the first time that sulfatase exhibits peroxidase-like activity, catalyzing the generation of singlet oxygen (1O2) in the presence of oxygen. Based on the sulfatase-dependent 1O2 generation, the developed adamantly-enolether chemiluminescence probe QM-CF for imaging tumors of high sulfatase expression further verified the theory that sulfatase can be involved in tumor development. High-throughput screening (HTS) of natural compounds and clinical drugs identified scutellarin and sinomenine as potent sulfatase inhibitors that suppress tumor growth in mice. Mechanistic investigations revealed that these inhibitors modulate oxidative stress by downregulating MAPK and NF-κB pathways. Our findings unveil a previously unappreciated role of sulfatase in tumor-related oxidative stress and provide a promising platform for the discovery of novel sulfatase inhibitors, and advancing cancer therapeutics.

Introduction:Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor outcomes and limited targeted therapeutic options. While protein phosphatase 1γ (PP1γ) is overexpressed in various cancers, its role and mechanism in ESCC remains unclear. This study investigated the involvement of PP1γ in ESCC progression, particularly concerning YAP1 dephosphorylation and its regulation on stem cell markers. Methods:The expression levels of PP1γ, YAP1, SOX2, and NANOG in ESCC tissues and adjacent non-cancerous tissue samples were analyzed using bioinformatics and immunohistochemistry. Their association with clinical features and prognosis were also analyzed. Functional assays were performed in KYSE150 cells to assess the effects of PPP1CC silencing on cell proliferation, migration, and invasion. Western blotting and qRT-PCR were used to measure the expression of YAP1, phosphorylated YAP1 (p-YAP1), SOX2, and NANOG. Results and discussion:We found that PP1γ was highly expressed in ESCC and was significantly associated with poor prognosis, lymph node metastasis, and advanced pathological stages. Patients with high PP1γ levels had significantly shorter overall survival and progression-free survival (P < 0.05). In functional assays, silencing of PPP1CC in KYSE150 cells resulted in a marked decrease in cell proliferation, as measured by CCK-8 assays (P < 0.01). Colony formation assays confirmed the reduced colony-forming ability in PPP1CC-silenced cells (P < 0.01). Furthermore, Transwell invasion and migration assays demonstrated a significant reduction in both cell migration and invasion (P < 0.01). Western blot analysis revealed that silencing PPP1CC led to an increase in p-YAP1 and the ratio of p-YAP1 to YAP1, indicating inhibited YAP1 activity, alongside significant reductions in YAP1 and SOX2 protein levels (P < 0.05), while NANOG expression remained unchanged. This change was further confirmed by the qRT-PCR. Conclusively, PP1γ may promote ESCC progression by regulating YAP1 dephosphorylation and enhancing the expression of SOX2. The PP1γ/YAP1/SOX2 axis may provide potential therapeutic targets for ESCC treatment.

Diacetylmorphine abuse is a major social problem that jeopardizes the world, and abuse can cause serious neurological disorders. Apoptosis plays an important role in neurological diseases. A previous study by our group found that the brain tissue of diacetylmorphine-addicted rats showed severe vacuole-like degeneration and increased apoptosis, but the exact mechanism has not yet been reported. We used TMT technology to sequence the diseased brain tissue of rats, and selected neurofilament light chain (NEFL) and neuritin (NRN1) as the focus of our research. We explore the possible roles and mechanisms played by both. Based on the construction of apoptotic cell model, we used overexpression/silencing lentiviral vectors to interfere with the expression of NEFL in PC12 cells, and the results suggested that NEFL could regulate NRN1 to affect the apoptosis level. To further understand the specific mechanism, we used transmission electron microscopy to observe the ultrastructure of apoptotic cells, and the results showed that compared with the control group, mitochondria in the model group showed obvious vacuolation as well as expansion, a significant increase in the accumulation of ROS, and a significant decrease in the mitochondrial membrane potential; after overexpression/silencing of NEFL, these changes were found to occur along with the alteration of NEFL expression. In summary, we conclude that diacetylmorphine induces neuronal apoptosis, and the specific mechanism is that NEFL regulates the NRN1-mediated mitochondrial pathway to promote apoptosis.

Diacetylmorphine (DA) is widely implicated in neuronal injury; however, the underlying mechanisms remain unclear. We investigated the role of iron metamorphosis in DA-induced neurotoxicity using Sprague-Dawley rats and PC12 and SH-SY5Y cells. Tandem mass tag proteomics analysis showed that the upregulation of protein kinase C delta (PKCδ) and iron metabolism-related protein transferrin receptor (TFRC) significantly the enriched iron metabolism pathway. Subsequent experiments showed that DA exposure significantly upregulated PKCδ in PC12 cells, which increased the nuclear translocation of specificity protein 1 (SP1), and the intracellular free iron and lipid peroxide levels. In addition, silencing of PKCδ in rats improved behaviour and restored the expression level of glutathione peroxidase 4 (GPX4). In addition, DA exposure activated mitochondrial autophagy in PC12 cells, leading to a decrease in the mitochondrial membrane potential, accumulation of reactive oxygen species (ROS), elevation of LC3 (which plays a key role in autophagy), and a decrease in p62 expression. Following the inhibition of autophagy, the mitochondrial membrane potential and ROS were restored, as was the expression of voltage-dependent anion channel 1 (VDAC1) and GPX4. In conclusion, the present study suggests that PKCδ regulates SP1, further exacerbating DA-induced neuronal ferroptosis. Therefore, inhibition of PKCδ and mitochondrial autophagy or ferroptosis may be a key therapeutic target to ameliorate neurotoxicity following DA exposure.

Although opioids are necessary for the treatment of acute pain, cancer pain, and palliative care, opioid abuse is a serious threat to society. Heroin (Diacetylmorphine) is the most commonly abused opioid, and it can have a variety of effects on the body's tissues and organs, including the well-known gastrointestinal depression and respiratory depression; however, there is little known about the effects of diacetylmorphine on cardiac damage. Here, we demonstrate that diacetylmorphine induces abnormal electrocardiographic changes in rats and causes damage to cardiomyocytes in vitro by an underlying mechanism of increased autophosphorylation of CaMKII and concomitant regulation of myocardial contractile protein TPM1 and MYOM2 protein expression. The CaMKII inhibitor KN-93 was first tested to rescue the toxic effects of heroin on cardiomyocytes in vitro and the abnormal ECG changes caused by heroin in SD rats, followed by the TMT relative quantitative protein technique to analyze the proteome changes. Diacetylmorphine causes increased phosphorylation at the CaMKII Thr287 site in myocardium, resulting in increased autophosphorylation of CaMKII and subsequent alterations in myocardial contractile proteins, leading to myocardial rhythm abnormalities. These findings provide a theoretical basis for the treatment and prevention of patients with arrhythmias caused by diacetylmorphine inhalation and injection.

目的 探讨EZRIN(EZRIN-radixin-moesin)与ASAP3(Arf-GAP containing SH3)在食管鳞癌中的表达情况及其与临床病理参数间的相关性.方法 收集2008年1月-2018年12月在新疆医科大学第一附属医院样本库中经手术切除的175例食管鳞癌组织芯片样本及60例食管鳞癌癌旁组织芯片样本,利用免疫组织化学技术检测食管鳞癌组织芯片中EZRIN与ASAP3的表达情况,临床病理参数及其预后相关性.结果 EZRIN、ASAP3在食管鳞癌组织中阳性表达率分别为82.3％(144/175)、70.9％(124/175);临床病理参数研究结果显示,EZRIN与分化程度、浸润深度、TNM分期、淋巴结转移具有相关性,其中低分化、全层浸润、TNMⅢA+B+C期及有淋巴结转移阳性率更高,差异具有统计学意义(P<0.05);ASAP3与性别、肿瘤大小、分化程度、浸润深度、TNM分期及淋巴结转移具有相关性.预后因素分析结果显示,EZRIN与总生存期之间的差异无统计学意义(P>0.05);与ASAP3低表达患者相比,ASAP3高表达患者的总生存时间更短(P<0.05);ASAP3高表达和TNMⅢA+B+C期是影响食管鳞癌预后不良的独立危险因素(P<0.05).结论 EZRIN与ASAP3的表达可能与食管鳞癌的发生、进展有关,且二者表达呈正相关.

The aim of this study was to analyze the role of Ezrin in esophageal squamous cell carcinoma (ESCC) and investigate potential therapeutic targets for ESCC by interfering with Ezrin expression. Bioinformatics analysis revealed that Ezrin expression differed significantly among patients with different clinical stage ESCC. Moreover, there was a significant correlation between Ezrin and yes-associated protein/connective tissue growth factor (YAP(1)/CTGF) levels in esophageal cancer. Sixty paraffin-embedded ESCC tissue samples were examined and Ezrin and YAP(1)/CTGF levels were determined using immunohistochemistry. The positive expression rates of Ezrin and YAP(1)/CTGF were significantly lower in adjacent tissues than in ESCC tissues. Furthermore, knockdown of Ezrin expression inhibited colony formation and reduced cell migration and invasion. Compared with control ESCC cells, protein expression levels of YAP(1) and CTGF were significantly downregulated in cells with Ezrin knocked down. We conclude that Ezrin may be involved in ESCC progression through the Hippo signaling pathway.

背景与目的 小细胞肺癌(small cell lung cancer,SCLC)是一种高度侵袭性的恶性肿瘤,易于早期复发和转移.临床前研究发现,发状分裂相关增强子1(hairy and enhancer of split 1,Hes1)作为碱性螺旋–环–螺旋(basic helix-loop-helix,BHLH)家族的转录抑制因子,不仅可阻止SCLC肿瘤细胞的增殖和迁移,还可抑制神经内分泌转录因子ASCL1的功能.然而,Hes1蛋白表达在SCLC预后中的意义仍不清楚.本研究旨在分析Hes1蛋白在SCLC中的表达模式和预后意义.方法 回顾分析247例手术切除的单纯型SCLC样本,构建组织微阵列(tissue microarray,TMA),采用全自动罗氏免疫组织化学仪检测Hes1蛋白的表达水平.通过Fisher精确检验分析蛋白表达与患者年龄、淋巴结转移、主要细胞形态和肿瘤浸润淋巴细胞(tumor infiltrating lymphocytes,TILs)等临床病理特征的相关性,并通过Kaplan-Meier曲线及COX回归模型检验其对生存的影响.结果 在247例手术切除的单纯型SCLC患者中,男性有175(70.8％)例;65岁及以下患者有202(81.8％)例;根据美国癌症联合会(american joint committee on cancer,AJCC)癌症分期系统第7版分期,I期有78(31.6％)例,II期有68(27.5％)例,III期有101(40.9％)例.Hes1蛋白表达定位于肿瘤细胞核,Hes1高表达患者占52.2％(129/247),与较低年龄(≤65岁,P=0.014)、无淋巴结转移(P=0.003)、圆形细胞为主的病理形态(P=0.002)及TILs≤30％(P=0.010)呈正相关.Kaplan-Meier分析显示Hes1蛋白高表达患者无病生存期[风险比(hazard ratio,HR)=1.477;95％置信区间(confidence interval,CI):1.025–2.129;P=0.036)显著延长,总生存期(HR=1.181;95％CI:0.778–1.792;P=0.435)也有延长趋势.结论 在局限期单纯型小细胞肺癌中,Hes1蛋白高表达与年龄、淋巴结转移、主要细胞形态和TILs相关,并可能作为SCLC患者预后的潜在生物标志物.

Heroin can cause damage to many human organs, possibly leading to different types of arrhythmias and abnormal electrophysiological function of the heart muscle and the steady state of calcium-ion channels. We explored cardiomyocytes treated with heroin and the effect on calcium-ion channels. Transcriptomics and metabolomics were used to screen for differential genes and metabolite alterations after heroin administration to jointly analyze the effect of heroin on calcium channels in cardiomyocytes. Cardiomyocytes from primary neonatal rats were cultured in vitro and were treated with different concentrations of heroin to observe the changes in morphology and spontaneous beat frequency and rhythm by a patch clamp technique. Transcriptomic studies selected a total of 1,432 differentially expressed genes, 941 upregulated and 491 downregulated genes in rat cardiomyocytes from the control and drug intervention groups. Gene Ontology functional enrichment showed that 1,432 differential genes selected by the two groups were mainly involved in the regulation of the multicellular organismal process, response to external stimulus, myofibril, inflammatory response, muscle system process, cardiac muscle contraction, etc. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that these genes were mainly concentrated in cardiac muscle contraction, osteoclast differentiation, adrenergic signaling in cardiomyocytes, dilated cardiomyopathy, hypertrophic cardiomyopathy, and other important pathways. Metabolomic testing further suggested that cardiomyocyte metabolism was severely affected after heroin intervention. After the treatment with heroin, the L-type calcium channel current I-V curve was up-shifted, the peak value was significantly lower than that of the control group, action potential duration 90 was significantly increased in the action potential, resting potential negative value was lowered, and action potential amplitude was significantly decreased in cardiomyocytes. In this study, heroin could cause morphological changes in primary cardiomyocytes of neonatal rats and electrophysiological function. Heroin can cause myocardial contraction and calcium channel abnormalities, damage the myocardium, and change the action potential and L-type calcium channel.

BACKGROUND:Managing hypertension in frail older patients is challenging. Several institutions and organizations have published up-to-date hypertension guidelines suggesting frailty screening among older hypertensive patients, with new recommendations for blood pressure-lowering treatment among the frail population. However, the quality of current hypertension guidelines and the consistency of antihypertension treatment recommendations for frail older patients and their supporting evidence remain unknown.OBJECTIVE:In this review, we aimed to systematically collect guidelines with antihypertension treatment recommendations for frail older patients, examine and compare these recommendations, and critically assess reporting and methodology quality of these guidelines.METHODS:A literature search was conducted on two databases and three major websites of guideline development organizations. The AGREE instrument and RIGHT checklist were used to evaluate the methodology and reporting quality of the guidelines, respectively. The consistency of recommendations within the guidelines were compared using descriptive analysis.RESULTS:We identified 13 hypertension guidelines. The overall methodology quality scores (range 23.35-79.07%) and reporting rates (range 10/35-29/35) varied among these guidelines. Four guidelines provided an explicit definition of frailty. Considering treatment tolerability or increased likelihood of adverse effects while using pharmacotherapy in frail older patients was mentioned in all guidelines. Ten guidelines recommended adjusting blood pressure targets or specific pharmacotherapy programs. Four guidelines recommended using clinical judgment when prescribing. However, the specific recommendations lacked clarity and unity without sufficient evidence.CONCLUSIONS:There were considerable variations in methodology and reporting quality across the 13 included hypertension guidelines. Furthermore, the depth and breadth of antihypertension treatment recommendations for frail older patients were varied and inconsistent. Further trials exploring optimal treatment are urgently required to promote the development of specific guidelines for managing frail older hypertensive patients.

ASAP3 is involved in a variety of biological activities, including cancer progression in humans. In adult glioma, we explore the effects of ASAP3 and NOTCH3 and their relationships on prognosis. The Oncomine, TIMER, and Gene Expression Profiling Interactive Analysis databases were used to investigate ASAP3 expression. Immunohistochemistry was used to assess the levels of ASAP3 and NOTCH3 expressions. The effects of ASAP3 and NOTCH3 on prognosis were assessed using survival analysis. The results revealed that the amount of ASAP3 mRNA in gliomas was much higher than in normal tissue (P < 0.01). Glioma patients with high ASAP3 mRNA expression had a worse overall survival and progression-free survival. ASAP3 overexpression is directly associated with the NOTCH signaling system. Immunohistochemistry revealed that ASAP3 and NOTCH3 were overexpressed in glioblastomas (GBMs). ASAP3 expression was associated with age, recurrence, tumor resection, postoperative chemoradiotherapy, World Health Organization (WHO) grade, and Ki-67 expression. ASAP3 expression was related to the isocitrate dehydrogenase-1 mutation in low-grade glioma. Gender, local recurrence, tumor resection, postoperative radio-chemotherapy, WHO grade, recurrence, and ATRX expression were all associated with NOTCH3 expression. ASAP3 was shown to be positively associated with NOTCH3 (r = 0.337, P = 0.000). Therefore, ASAP3 and NOTCH3 as oncogene factors have the potential to be prognostic biomarkers and therapeutic targets in adult glioma.

Objective The effects of Otubain-2 (OTUB2) on the proliferation, invasion, and migration of esophageal squamous cell carcinoma (ESCC) were investigated by interfering with OTUB2 expression. Methods Bioinformatics analysis was used to analyze OTUB2 expression in esophageal carcinoma and interactions between OTUB2 and YAP1/TAZ. Paraffin-embedded ESCC tissues ( n = 183) were selected for immunohistochemical staining to detect OTUB2, YAP1, TAZ, CTGF and their relationship with clinicopathological parameters, then the survival prognosis of ESCC patients was analyzed. Immunofluorescence, western blotting, and qRT-PCR were used to evaluate OTUB2 in ESCC cell lines. Cell lines with the highest expression of OTUB2 were transfected with lentivirus to knockdown OTUB2 levels. Changes in KYSE150 cell proliferation, migration, and invasion were measured using CCK-8, wound healing, and clone formation assays. The Transwell test and flow cytometry identified OTUB2 targets and explored roles and mechanisms involved in ESCC. Effects of OTUB2 on YAP1/TAZ signaling were also observed. Results Bioinformatics analysis revealed OTUB2 was highly expressed in esophageal cancer and was associated with YAP1/TAZ. Immunohistochemistry showed that OTUB2 expression was increased in ESCC samples compared to parcancerous tissue. YAP1 and TAZ were higher expression in ESCC tissues, mainly localized in the nucleus. Compared with controls, the proliferation, migration, and invasion ability of KYSE150 cells after OTUB2 knockdown were significantly reduced ( P < 0.05). The protein expression levels of YAP1, TAZ and CTGF decreased after knocking down the expression of OTUB2 ( P < 0.05). OTUB2 knockdown in ESCC cell lines suppressed YAP1/TAZ signaling. Conclusions OTUB2 regulated the protein expression of YAP1/TAZ to promote cell proliferation, migration, invasion, and tumor development. Therefore, OTUB2 may represent a biomarker for ESCC and a potential target for ESCC treatment.

ObjectiveTo investigate the expression of AJUBA in esophageal squamous cell carcinoma (ESCC) and whether AJUBA affects the proliferation, invasion, and migration of ESCC by regulating MST1, YAP1 and TAZ factors. Methods Western blot was used to detect the expression levels of the AJUBA protein in the esophageal cancer cell lines KYSE30, KYSE150 and KYSE450. A ShRNA interference vector for AJUBA was constructed and transfected into the KYSE150 esophageal cancer cell lines. The effects of AJUBA on the proliferation, cycle, migration and invasion of KYSE150 cells were investigated by in vitro cloning and formation assay, flow cytometry, scratch assay, and Transwell migration assay. The mRNA and protein expressions of MST1, YAP1 and TAZ were detected by RT-PCR and Western blot. The expression of the AJUBA, YAP1 and TAZ proteins were detected by nucleo-cytoplasmic separation assay. ResultsThe stable knockdown of AJUBA gene in KYSE150 cell line was established. The results of plate cloning experiment showed that the number of cell clones formed in shAJUBA group was significantly lower than that in the negative control group (P< 0.0001). Flow cytometry results showed that KYSE150 cells in shAJUBA group were mainly blocked in G0/G1 phase, and and the number of cells were significantly reduced in G2/M and S phases (P<0.05). The results of scratch test and Transwell invasion test showed that the migration ability and invasion ability of shAJUBA group were significantly decreased compared with control group c(P< 0.001). RT-PCR and Western blot results showed that the mRNA and protein expression levels of MST1, YAP1 and TAZ in shAJUBA group were significantly decreased, the differences were statistically significant (P<0.05). The results of nucleo-cytoplasmic separation indicated that AJUBA was expressed in SHEE(Human esophagus epithelial cell) nucleus, and AJUBA protein was expressed in KYSE150 cells cytoplasm and nucleus. The proteins of YAP1and TAZ were not expressed in SHEE, but proteins of YAP1 and TAZ were expressed in cytoplasm and nucleus in KYSE150 cells. The above results showed statistically significant differences (P<0.05).ConclusionsThe AJUBA protein can promote the proliferation, invasion, and migration of esophageal carcinoma cells. This may be related to the activation of MST1, YAP1, and TAZ which may consequently affect the progression of ESCC.

目的 研究AJUBA对食管鳞状细胞癌(ESCC)细胞迁移与增殖的作用.方法 用慢病毒转染AJUBA的短发夹RNA(short hairpin RNA,shRNA)至KYSE150细胞系,实验分为对照组与敲降组,其中对照组包括KYSE150组(未转染的KYSE150细胞)和KYSE150shnon组(转染随机序列),敲降组为KYSE150shAJUBA组(分别转染KYSE150shAJUBA-1、KYSE150shAJUBA-2、KYSE150shAJU-BA-3),并用实时荧光定量法(qRT-PCR)与Western blotting实验共同筛选出敲降效率最高的细胞株进行后续实验.采用细胞计数(Cell Counting Kit-8,CCK-8)增殖实验、Transwell迁移实验检测AJUBA不同表达水平对食管鳞状细胞癌细胞增殖及迁移能力的影响.结果 慢病毒转染敲降AJUBA在食管鳞癌细胞中表达,通过qRT-PCR与Western blotting实验表明,对照组与敲降组相比,敲降组中AJUBA在食管鳞癌细胞中表达水平降低,且敲降组中KYSE150shAJUBA-3的AJUBA表达水平最低(P<0.0001);CCK-8实验结果表明,对照组与敲降组相比,敲降组细胞的增殖能力受抑制(P<0.001);Transwell迁移实验结果表明,对照组与敲降组相比,敲降组的迁移能力明显受抑制,差异有统计学意义(P<0.0001).结论 AJUBA在食管鳞状细胞癌中对肿瘤细胞的增殖与迁移能力有促进作用,这有望为食管癌的临床分子靶向治疗提供新的研究方向.

目的 明确急诊腹腔镜下胃肠手术使用的无菌手套细菌污染与穿孔情况,为减少医患交叉感染提供依据.方法 选取于我院手术室行急诊腹腔镜下胃肠手术使用的无菌手套1280只为研究对象,统计手套的细菌污染与穿孔情况,并进行统计学比较.结果 急诊腹腔镜下胃肠手术参与者使用的1280只无菌手套中,有117只(9.14％)手套发生了穿孔,检出了126株病原菌,最常见的3种依次为:大肠埃希菌32株(25.40％)、金黄色葡萄球菌23株(18.25％)及铜绿假单胞菌19株(15.08％).左手使用的无菌手套穿孔率显著高于右手,差异有统计学意义(P<0.05);手术主刀及手术器械护士使用的无菌手套穿孔率显著高于主刀助手使用的无菌手套,差异有统计学意义(P<0.01).手术时间1～3 h及>3 h的手术使用的无菌手套穿孔率显著高于手术时间<1 h的手术使用的无菌手套,差异有统计学意义(P<0.01).结论 急诊腹腔镜下胃肠手术使用的无菌手套穿孔率较高,术中常被大肠埃希菌、金黄色葡萄球菌及铜绿假单胞菌等细菌污染,手术主刀及器械护士的无菌手套更容易穿孔,建议手术时间超过1h即更换无菌手套.

目的:探讨ICU机械通气心脏术后患者实施标准化早期活动对谵妄发生率影响.方法:将2021年1至2022年1月期间于本院接受治疗的讨ICU机械通气心脏术后患者共计150例作为研究对象,使用随机数字分配表法将其分为2组.对照组(75例)接受常规的早期活动指导,观察组(75例)采用标准化早期活动指导,比较2组术后发生谵妄情况、首次出现的时间、谵妄持续时间、机体通气时间、治疗依从性以及并发症发生情况.结果:术后8小时内、术后8～48小时、术后48小时以上较谵妄发生率与对照组比较,观察组显著较低(P<0.05).首次谵妄出现时间、持续时间、机体通气时间与对照组比较,观察组均相对较短(P<0.05).对照组治疗依从性为89.33％,观察组治疗依从性为97.33％,观察组高于对照组(P<0.05).气管导管意外拔管、引流管意外拔管、血压血氧异常等并发症发生率观察组低于对照组(P<0.05).结论:ICU机械通气心脏术后患者实施标准化早期活动可降低术后谵妄发生率,缩短谵妄首次出现时间、谵妄持续时间、机体通气时间,可提升患者治疗依从性和护理满意度,利于减少气管导管意外拔管、引流管意外拔管、血压血氧异常等并发症,得到了患者的满意认可,建议临床推广应用.

目的 探讨荧光标记法用于静脉用药调配中心(PIVAS)物表清洁消毒监控的应用效果.方法 应用荧光标记法在PIVAS 3个区域25类重点物体表面进行布点标记,监测荧光清除情况并计算清除率.结果 PIVAS洁净区、非洁净控制区和辅助工作区物体表面干预后的清除率分别为95.05％,88.57％,92.92％,显著高于干预前的57.79％,63.46％,39.20％(P<0.01).结论 荧光标记法用于PI-VAS物表清洁消毒监控有一定成效,且方法简便.