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1.
2.
目的:通过对某医院2017-2020年医疗不良事件数据分析,结合运用专业人员访谈法,发现存在问题,针对性地提出对策与建议。方法:采用回顾性分析法,对某医院2017 年1月1日—2020年12月31日医疗安全不良事件管理系统收集的1 117例事件进行分析,并对临床科室负责人、医护人员及行政人员12名进行专家访谈。结果:医疗不良事件中Ⅲ、Ⅳ级上报比例高,普外科、骨科、妇科、产科等手术科室上报例数多。医疗不良事件漏报瞒报的主要原因是担心职能部门追责、引发纠纷及影响科室质量考核评分。管理中存在问题主要是上报意识不足、追踪整改不到位。结论:提高医护风险意识,完善闭环管理流程体系,强化院科两级督查,构建和谐安全文化氛围,以提高医疗不良事件上报率。  相似文献   
3.
This study assessed the indirect effect of 38% silver diamine fluoride (SDF) on demineralization of adjacent untreated sound and pre‐demineralized enamel and dentine using a single‐section model for digital transverse microradiography (TMR‐D). Forty‐eight bovine dentine single sections were demineralized, stratified (n = 12) according to integrated mineral loss (ΔZ), and treated with SDF or deionized water (DIW). Each “treated dentine” section was attached between untreated sound and pre‐demineralized enamel or dentine and then subjected to demineralization. ΔZ and lesion depths (LD) of all specimens at baseline, 24 and 48 h demineralization, and after treatment of “treated dentine” were quantified using TMR‐D. Fluoride in the demineralization solution of SDF clusters was determined using an ion‐selective electrode. ΔZ and LD of sound and ΔZ of pre‐demineralized enamel adjacent to SDF‐treated dentine did not increase over time. All untreated dentine demineralized significantly; however, ΔZ of sound dentine adjacent to SDF‐treated specimen was still significantly lower than control. SDF‐treated dentine remineralized and released fluoride even after 48 h. Consistent with clinical findings, when applied only to demineralized teeth in this chemical model, 38% SDF completely inhibited demineralization in adjacent untreated sound enamel. Demineralization prevention was observed to a lesser extent in adjacent pre‐demineralized enamel but not in dentine.  相似文献   
4.
The neuropathological hallmarks of Parkinson's disease (PD) are the degeneration and death of dopamine‐producing neurons in the ventral midbrain, the widespread intraneuronal aggregation of alpha‐synuclein (α) in Lewy bodies and neurites, neuroinflammation, and gliosis. Signs of microglia activation in the PD brain postmortem as well as during disease development revealed by neuroimaging, implicate immune responses in the pathophysiology of the disease. Intensive research during the last two decades has advanced our understanding of the role of these responses in the disease process, yet many questions remain unanswered. A transformative finding in the field has been the confirmation that in vivo microglia are able to respond directly to pathological a‐syn aggregates but also to neuronal dysfunction due to intraneuronal a‐syn toxicity well in advance of neuronal death. In addition, clinical research and disease models have revealed the involvement of both the innate and adaptive immune systems. Indeed, the data suggest that PD leads not only to a microglia response, but also to a cellular and humoral peripheral immune response. Together, these findings compel us to consider a more holistic view of the immunological processes associated with the disease. Central and peripheral immune responses aimed at maintaining neuronal health will ultimately have consequences on neuronal survival. We will review here the most significant findings that have contributed to the current understanding of the immune response in PD, which is proposed to occur early, involve peripheral and brain immune cells, evolve as neuronal dysfunction progresses, and is likely to influence disease progression.  相似文献   
5.
目的探讨长链非编码RNA SNHG7 (LncRNA SNHG7)在乳腺癌细胞系中的功能及其机制。方法 RT-qPCR检测LncRNA SNHG7在乳腺癌组织和乳腺癌细胞系的表达水平,核浆分离实验检测LncRNA SNHG7在乳腺癌细胞系MDA-MB-231中的定位。在MDA-MB-231细胞系中,siRNA沉默LncRNA SNHG7后,利用MTS和平板克隆形成实验研究LncRNA SNHG7对细胞增殖的影响;利用划痕和transwell实验研究LncRNA SNHG7对细胞侵袭迁移的影响。通过Western blot(WB)实验研究LncRNA SNHG7在乳腺癌细胞系中可能参与的分子机制。结果 qPCR结果显示,与癌旁组织相比,LncRNA SNHG7在乳腺癌组织中高表达(P0.05);与乳腺正常上皮MCF-10A相比,LncRNA SNHG7在乳腺癌细胞系中高表达。siRNA沉默LncRNA SNHG7后,细胞增殖能力和平板克隆形成能力被抑制(P0.05),划痕实验显示细胞的愈合能力降低(P0.05),trans well实验显示细胞的迁移和侵袭能力均被抑制(P0.05)。WB结果显示β-catenin、 C-Myc和CyclinD1蛋白的表达下调,磷酸化的β-catenin(p-β-catenin)蛋白降解增加。结论 LncRNA SNHG7在乳腺癌组织和乳腺癌细胞系中高表达。沉默LncRNA SNHG7后,细胞的增殖和侵袭迁移能力均降低。WB结果表明LncRNA SN HG7调控乳腺癌细胞的增殖和侵袭迁移可能与β-catenin蛋白的表达下调和p-β-catenin蛋白降解增加有关。  相似文献   
6.

Background

Obesity is a risk factor for acetabular component malposition when total hip arthroplasty is performed with manual techniques. The utility of imageless navigation in obese patients remains unknown. This study compared the accuracy and precision of imageless navigation for component orientation between obese and nonobese patients.

Methods

A total of 459 total hip arthroplasties performed for osteoarthritis using imageless navigation were reviewed from a single surgeon’s institutional review board–approved database. Einzel-Bild-Roentgen Analyse determined component orientation on 6-week postoperative anteroposterior radiographs. Mean orientation error (accuracy) and precision were compared between obese (body mass index ≥ 30 kg/m2) and nonobese patients. Regression analysis evaluated the influence of obesity on component position.

Results

The difference in mean inclination and anteversion between obese and nonobese groups was 1.1° (43.0° ± 3.5°; range, 35.8°-57.8° vs 41.9° ± 4.4°; range, 33.0°-57.1° and 24.9° ± 6.3°; range, 14.2°-44.3° vs 23.8° ± 6.6°; range, 7.0°-38.6°, respectively). Inclination precision was better for nonobese patients. No difference in inclination accuracy or anteversion accuracy or precision was detected between groups. And 83% of components were placed within the target range. There was no relationship between obesity (dichotomized) and component placement outside the target ranges for inclination, anteversion, or both. As a continuous variable, increased body mass index correlated with higher odds of inclination outside the target zone (odds ratio, 1.06; P = .001).

Conclusion

Using imageless navigation, inclination orientation was less precise for obese patients, but the observed difference is likely not clinically relevant. Accurate superficial registration of landmarks in obese patients is achievable, and the use of imageless navigation similarly improves acetabular component positioning in obese and nonobese patients.

Level of Evidence

Therapeutic Level IV.  相似文献   
7.
8.
The study of myxoma virus (MYXV) infections in the European rabbit (Oryctolagus cuniculus) has produced one of the most accepted host–pathogen evolutionary models. To date, myxomatosis has been limited to the European rabbit with sporadic reports in hares. However, reports of widespread mortalities in the Iberian hare (Lepus granatensis) with myxomatosis‐like clinical signs indicate a potential species jump has occurred. The presence of MYXV DNA was confirmed by PCR in 244 samples received from regional veterinary services, animal health laboratories, hunters or rangers over a 5‐month period. PCR analysis of 4 MYXV positive hare samples revealed a 2.8 kb insertion located within the M009 gene with respect to MYXV. The presence of this insertion was subsequently confirmed in 20 samples from 18 Spanish provinces. Sanger sequencing and subsequent analysis show that the insert contained 4 ORFs which are phylogenetically related to MYXV genes M060, M061, M064 and M065. The complete MYXV genome from hare tissue was sequenced using Ion torrent next‐generation technology and a summary of the data presented here. With the exception of the inserted region, the virus genome had no large scale modifications and 110 mutations with respect to the MYXV reference strain Lausanne were observed. The next phase in the evolution of MYXV has taken place as a host species jump from the European rabbit to the Iberian hare an occurrence which could have important effects on this naïve population.  相似文献   
9.
Background: Corneal Dystrophy and Perceptive Deafness (CDPD) or Harboyan syndrome is an autosomal recessive rare disorder, characterized by congenital corneal opacities and progressive sensorineural hearing loss, which usually begins after the second decades of life. This study reports the ophthalmic, audiological and genetic features, in five CDPD affected patients from three Chilean families.

Materials and Methods: Five individuals affected with CDPD from three unrelated Chilean families were clinically and genetically examined. To evaluate a putative founder mutation 7 SNPs were analyzed in the three families, an Argentinian patient (carrier of the same mutation previously reported) and 87 Chilean controls.

Results: The ophthalmic symptoms in the five patients were bilateral and symmetric, starting before one year of age, and visual acuity varied from 0.1 to 0.3. In all cases, hearing loss began over 8 years old. The sequence of the 19 exons of SLC4A11 gene of all the affected patients exhibited homozygous eight nucleotide sequence duplication (c.2233_2240dup TATGACAC, p.(Ile748Metfs*5)) at the end of exon 16. All the affected patients of the three families were homozygous for a haplotype composed of five SNPs and covering 4,1 Mb. The same haplotype was present in one allele of the heterozygous Argentinean patient and has a frequency of 2.76% in Chilean population.

Conclusions: The five CDPD patients were homozygous for the same mutation in the SLC4A11 gene. Haplotype analysis of all the affected, including the case reported from Argentina was in accordance with a founder mutation.  相似文献   

10.
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