340例咽异感症与食道疾病的相关性探讨

目的对咽异感症和食道疾病的相关性进行研究。方法选取本院于2010年1月-2014年1月收治的340例因咽部伴有异物感而就诊的患者,明确排除口腔、鼻腔、咽喉和颈部疾病,并对患者进行食道X线钡餐检查。结果所有患者中,172例（50．59％）的患者确诊患有食道疾病。其中包括食道返流性疾病患者55例（16．18％）,食道癌13例（3．80％）,食道炎75例（22．00％）,食道憩室29例（8．53％）,所有患者经对症给药后,102例（59．30％）患者咽异感症症状消失,51（29．65％）例患者咽异感症症状有显著缓解,19（11．04％）例患者咽异感症症状无明显改善。结论食道疾病会诱发咽异感症,且与咽异感症的发生有密切联系。     

乐商对教师主观幸福感的影响:品味的中介作用

目的:探索品味在乐商与幸福感间的作用。方法:采用乐商量表、牛津幸福感量表、品味信念量表对1295名中小学教师进行问卷调查。结果:(1)东部地区教师的乐商和品味显著高于中西部地区(F=6.100,9.983;P0.001);(2)在乐商、品味指标上,女教师显著高于男教师(t=-3.373,P0.01;t=-4.984,P0.001),城市教师显著高于农村教师(t=-4.869,P0.001;t=-3.335,P0.01);此外,城市教师的幸福感高于农村教师(t=-3.389,P0.01);(3)教师的乐商、主观幸福感、品味两两之间存在显著正相关(r=0.158~0.919,P0.001);(4)品味在乐商与主观幸福感之间存在中介效应[95%CI为(0.0760,0.1377)]。结论:乐商和品味是影响主观幸福感的重要因素,且品味起到中介作用,故应培养教师积极体验的能力。     

泛影葡胺治疗突发性聋的疗效观察

目的 :探讨应用泛影葡胺治疗突发性聋的疗效 ;方法 :应用前瞻性的随机分组方法进行临床试验 ,分为泛影葡胺组及常规药物组 ,两组病人均常规给予扩张血管、改善微循环、营养神经治疗 ,泛影葡胺组在此基础上 ,应用泛影葡胺治疗 ;结果 :共收治突聋患者 72例 81耳 ,泛影葡胺组和常规药物组各 3 6例 ,泛影葡胺组总有效率为 85.4% ( 3 5 41 ) ,常规药物组为 67.5% ( 2 7 40 ) ,泛影葡胺组疗效明显高于常规药物组 (P <0 .0 5) ;结论 :突发性聋应用泛影葡胺治疗可明显提高疗效     

ICU护士职业价值观和角色认知水平及其相关性研究

[目的]了解ICU护士职业价值观与其角色认知的相关性,为培养和引导积极的职业价值观提供依据。[方法]采用角色认知问卷和护士职业价值观量表对成都市两家三级甲等医院223名ICU护士进行调查。[结果]ICU护士职业价值观的信任维度与角色认知的两个维度均无明显相关性;职业价值观的照顾提供、责任自由安全、行动主义3个维度与角色认知的负向维度无相关性,而与角色认知的正向维度存在相关性。[结论]角色认知水平能部分预测职业价值观,可根据影响护士角色认知的因素进行合理干预,以提高护士角色认知水平,提升对职业价值观的认同。     

microRNA-466在宫颈癌及宫颈上皮内瘤变中的表达及其意义

目的:分析微RNA-466(microRNA-466,miR-466)在宫颈癌、宫颈上皮内瘤变(CIN)及正常宫颈的表达情况及其与临床病理之间的关系.方法:采用茎环RT-qPCR分析23例宫颈癌、47例CIN,以及13例正常宫颈组织中miR-466的表达,并分析其表达与宫颈癌常见的临床病理特征间的关系.结果:茎环RT-PCR方法能特异检测miR-466;荧光定量PCR分析示miR-466在宫颈癌中的表达低于CIN及正常宫颈组织(P＜0.05);正常宫颈与CIN之间比较差异无统计学意义(P＞0.05);miR-466的表达与年龄、肿块大小、大体类型及组织分化程度差异无统计学意义(P＞0.05);miRNA-466与预测的HPV特异性miRNA同源性分析提示,miR-466与HPV16、18的长控制区(LCR)序列高度同源;生物信息学分析提示,miR-466可调控多种靶基因.结论:miR-466在宫颈癌、CIN及正常宫颈中表达存在明显差异,其在正常宫颈及CIN中相对表达量明显高于宫颈癌;miR-466的异常表达,可能与HPV的LCR区高度同源性相关;miR-466可能调控多种靶分子,参与宫颈癌发生发展过程.     

Efficacy and safety of non-vitamin K antagonist oral anticoagulants in patients (≥80 years of age) with atrial fibrillation: systematic review and meta-analysis

Findings of prior studies about the efficacy and safety of non-vitamin K antagonist oral anticoagulants (NOACs) in patients (≥80 years of age) with atrial fibrillation (AF) are controversial. So we performed a meta-analysis to evaluate the efficacy and safety of NOACs versus vitamin K antagonists (VKAs) in patients (≥80 years of age) with AF. A systematic review of PubMed, Cochrane, Embase, Web of Science and Chinese BioMedical databases was conducted until 1 October 2022. Studies reporting the effects and safety of NOACs versus warfarin in patients (≥80 years of age) with AF were included. Two authors independently performed study selection and data extraction. Discrepancies were resolved by consensus or through an independent third reviewer. Data were synthesised according to the Preferred Reporting Items for Systematic Reviews guidelines. We identified 15 studies providing data of 70 446 participants (≥80 years of age) suffering from AF. According to the meta-analysis (odds ratio (OR) (95% confidence interval, CI)), NOACs conferred better efficacy profile than VKAs in stroke and systemic embolism (0.8 (0.73–0.88)) and all-cause mortality (0.61 (0.57–0.65)). Otherwise, NOACs conferred a better safety profile than VKAs in major bleeding (0.76 (0.70–0.83)) and intracranial haemorrhage (ICH; 0.57 (0.47–0.68)). In conclusion, for patients (≥80 years of age) with AF, the risks of stroke and systemic embolism, all-cause mortality, were lower in NOACs compared to warfarin. The risks of major bleeding and ICH were also lower in NOACs compared to warfarin. NOACs showed better efficacy and safety than warfarin.     

A proteolytic pathway that controls glucose uptake in fat and muscle

Insulin regulates glucose uptake by controlling the subcellular location of GLUT4 glucose transporters. GLUT4 is sequestered within fat and muscle cells during low-insulin states, and is translocated to the cell surface upon insulin stimulation. The TUG protein is a functional tether that sequesters GLUT4 at the Golgi matrix. To stimulate glucose uptake, insulin triggers TUG endoproteolytic cleavage. Cleavage accounts for a large proportion of the acute effect of insulin to mobilize GLUT4 to the cell surface. During ongoing insulin exposure, endocytosed GLUT4 recycles to the plasma membrane directly from endosomes, and bypasses a TUG-regulated trafficking step. Insulin acts through the TC10α GTPase and its effector protein, PIST, to stimulate TUG cleavage. This action is coordinated with insulin signals through AS160/Tbc1D4 and Tbc1D1 to modulate Rab GTPases, and with other signals to direct overall GLUT4 targeting. Data support the idea that the N-terminal TUG cleavage product, TUGUL, functions as a novel ubiquitin-like protein modifier to facilitate GLUT4 movement to the cell surface. The C-terminal TUG cleavage product is extracted from the Golgi matrix, which vacates an “anchoring” site to permit subsequent cycles of GLUT4 retention and release. Together, GLUT4 vesicle translocation and TUG cleavage may coordinate glucose uptake with physiologic effects of other proteins present in the GLUT4-containing vesicles, and with potential additional effects of the TUG C-terminal product. Understanding this TUG pathway for GLUT4 retention and release will shed light on the regulation of glucose uptake and the pathogenesis of type 2 diabetes.     

The anti-tumoral drug enzastaurin inhibits natural killer cell cytotoxicity via activation of glycogen synthase kinase-3β

Enzastaurin is a selective protein kinase Cβ inhibitor which is shown to have direct antitumor effect as well as suppress glycogen synthase kinase-3β (GSK-3β) phosphorylation (resulting in its activation) in both tumor tissues and peripheral blood mononuclear cells (PBMC). It is currently used in phase II trials for the treatment of colon cancer, refractory glioblastoma and diffuse large B cell lymphoma. In this study, the direct effect of enzastaurin on effector function of human natural killer (NK) cells was investigated. The results obtained showed that enzastaurin suppressed both natural and antibody-dependent cellular cytotoxicity (ADCC) of NK cells against different tumor targets. This inhibition was associated with a specific down-regulation of surface expression of NK cell activating receptor NKG2D and CD16 involved in natural cytotoxicity and ADCC respectively, as well as the inhibition of perforin release. Analysis of signal transduction revealed that enzastaurin activated GSK-3β by inhibition of GSK-3β phosphorylation. Treatment of NK cells with GSK-3β-specific inhibitor TDZD-8 prevented enzastaurin-induced inhibition of NK cell cytotoxicity. Apart from the known antitumor and antiangiogenic effects, these results demonstrate that enzastaurin suppresses NK cell activity and may therefore interfere with NK cell-mediated tumor control in enzastaurin-treated cancer patients.     

Diminished tyrosine hydroxylase immunoreactivity in the cardiac conduction system and myocardium in Parkinson’s disease: an anatomical study

Clinical and autopsy studies have consistently reported cardiac sympathetic dysfunction in the left ventricular wall in patients with Parkinson’s disease (PD). Whether the nerve fibers of the cardiac conduction system or the atrial walls are equally affected in this disease process has not yet been well documented. Therefore, the aim of this study was to investigate sympathetic nerves in the cardiac conduction system as well as in the walls of all four heart chambers in patients with PD, in incidental Lewy body disease (iLBD), and in controls. Heart tissue from five PD patients, two iLBD cases, and seven controls were investigated immunohistochemically using antibodies directed against tyrosine hydroxylase (TH) and α-synuclein (syn-1). A marked diminution of TH immunoreactivity (IR) within nerve fibers was observed in four PD patients and in both individuals with iLBD. In contrast, all control subjects displayed dense TH-IR nerve structures. The depletion in TH-IR involved not only the ventricles, but also the conduction system and the atrium showing a global change within cardiac TH-IR nerve fibers in the course of PD. In conclusion, the alterations in cardiac sympathetic nerves of patients with PD or in individuals with iLBD are homogeneous and global within the heart. The clinical implications related to this complete cardiac sympathetic dysfunction, including clinical correlates, diagnostic implications, and treatment, however, remain to be determined in a larger autopsy-controlled cohort of prospectively followed individuals.     

Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia

BACKGROUND AND PURPOSE: Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. METHODS: We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. RESULTS: CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. CONCLUSIONS: Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA.