基于奥马哈理论的护理模式 对慢性阻塞性肺疾病患者肺功能及细菌感染率的影响

目的探讨基于奥马哈理论的护理模式对慢性阻塞性肺疾病(COPD)患者肺功能、症状控制、细菌感染率及生活质量的影响。方法选取2018年1月至2019年1月我院收治的134例COPD患者,采用随机数字表法将研究对象分为观察组(n=69)与对照组(n=65),对两组患者住院期间肺功能、症状控制情况、细菌感染率、睡眠情况以及生活质量进行评估和分析。结果观察组患者肺功能情况优于入院时(P0.05)。两组患者泌尿系统感染发生率最高,其次为褥疮创面感染和口腔感染。观察组患者泌尿系感染的发生率低于对照组(P0.05)。两组患者干预后PSQI量表评分和CAT评分均低于入院前,且观察组患者总分低于对照组(均P0.05)。干预后观察组患者SF-36评分均高于对照组(均P0.05)。结论在基于奥马哈理论的护理模式下,COPD患者的肺功能得到加强,继发感染的发生减少,生活质量得到提高。     

宝乐安联合金酸萍颗粒对新生儿黄疸的治疗

目的 观察宝乐安联合金酸萍颗粒对新生儿黄疸的临床疗效。方法 选择我院和酒泉市人民医院2016年10月至2018年9月间诊治的86例新生儿黄疸患儿为研究对象。入选患儿随机分成对照组与试验组各43例。其中对照组患儿给予金酸萍颗粒治疗,试验组患儿给予金酸萍颗粒联合宝乐安治疗。对两组患儿的临床治疗效果进行评价比较。结果 试验组与对照组患儿的临床治疗总有效率分别为95.3%和81.4%,差异有统计学意义(χ~2=9.385,P0.05)。试验组患儿胆红素恢复正常时间以及黄疸消失时间均显著短于对照组,差异有统计学意义(均P0.05)。结论 宝乐安与金酸萍颗粒联合用药对新生儿黄疸的临床疗效优于单用金酸萍颗粒,值得推广。     

Cellular aspects of pathogenesis of hypertrophic cardiomyopathy: Role of cardiomyocyte polyploidy and activation of nuclear antigen of the proliferating cell in myocardium

For a comparative analysis of cytomorphological characteristics of hypertrophied interventricular septum (IVS), both patients different ages with severe courses of obstructive hypertrophic cardiomyopathy (OHCMP) were examined, including children, and patients with essential arterial hypertension (EAH). The course of OHCMP in children as compared with adults was found to be characterized by considerable IVS hypertrophy that was accompanied by an acceleration of cardiomyocyte polyploidization. The mean ploidy level of cardiomyocytes in children with OHCMP was higher than in adult patients. The mean ploidy level of nuclei, the number of prolipherative cell nuclear antigen (PCNA)-positive nuclei, and the number of polyploid cardiomyocyte nuclei in adult patients with OHCMP were significantly higher statistically than in patients with EAH. The PCNA-positive labels in stromal cells were revealed only in patients with OHCMP. The obtained data indicate an important role of cardiomyocyte polyploidy and of activation of the proliferating cell nuclear antigen in development of myocardial hypertrophy in patients with OHCMP.     

急性加重期慢性阻塞性肺疾病患者痰色评分与肺部微生物和病情严重程度的相关性CSCD

目的 探讨急性加重期慢性阻塞性肺疾病患者痰色评分与肺部微生物、病情严重程度的相关性。方法 选择2018年3月至2019年9月我院收治的122例急性加重期慢性阻塞性肺疾病患者,根据其痰色评分分为1~2分组(n=30)与3~4分组(n=92),比较两组患者肺部微生物分布、病情严重程度分布、慢性阻塞性肺疾病评估测试(CAT)评分、白细胞(WBC)水平、C反应蛋白(CRP)水平,分析急性加重期慢性阻塞性肺疾病患者痰色评分与肺部微生物、病情严重程度的相关性。结果 3~4分组患者肺部肺炎克雷伯菌、铜绿假单胞菌、金黄色葡萄球菌、肺炎链球菌、草绿色链球菌、白假丝酵母、酵母样真菌、丝状真菌检出率与1~2分组比较差异无统计学意义(均P>0.05)。3~4分组患者鲍曼不动杆菌检出率显著高于1~2分组(P<0.05)。3~4分组患者病情严重程度分布与1~2分组比较差异有统计学意义(P<0.05)。3~4分组患者CAT评分、WBC水平、CRP水平均显著高于1~2分组(均P<0.05)。急性加重期慢性阻塞性肺疾病患者痰色评分与肺炎克雷伯菌、铜绿假单胞菌、金黄色葡萄球菌、肺炎链球菌、草绿色链球菌、白假丝酵母、酵母样真菌、丝状真菌检出率无显著相关性(均P>0.05),而与鲍曼不动杆菌检出率、CAT评分、WBC水平、CRP水平、病情严重程度呈显著相关性(均P<0.05)。结论 痰色评分与急性加重期慢性阻塞性肺疾病患者肺部微生物和病情严重程度关系密切,有望成为临床评价该类患者肺部微生物分布及病情严重程度的方法之一。     

Pravastatin sodium attenuated TREM-1-mediated inflammation in human peripheral blood mononuclear cells

Pravastatin sodium on triggering receptor expressed on myeloid cell-1 (TREM-1)-mediated inflammation in human peripheral blood mononuclear cells (PBMCs) has been poorly investigated. In this study, we isolated PBMCs from the peripheral blood samples of patients with chronic obstructive pulmonary disease, treated the cells with pravastatin sodium, and determined a concentration at which more than 90% cells could survive. Then we treated cells with 10?ng/ml of lipopolysaccharide, added with 10, 50, 100?μM of pravastatin sodium combined with or without LR-12, a known TREM-1 inhibitor. The expression of TREM-1 was determined by quantitative RT-PCR. The levels of TREM-1, IL-6, and TNF-α in cell culture supernatant were measured with ELISA. Simultaneously, NF-κB signaling pathway-related protein p-p65 and p-IκBα were detected by Western blot assay. Results demonstrated that pravastatin sodium significantly mitigated lipopolysaccharide-stimulated TREM-1 over-expression at mRNA and protein levels dose-dependently. Elevated IL-6 and TNF-α levels changed synchronously. LR-12 inhibited the TREM-1 over-expression and inflammatory factor production but did not show extra synergistic effect to pravastatin. Lipopolysaccharide induced phospho-p65 and -IκBα over-expression was weakened significantly when cells were treated with pravastatin sodium. In conclusion, pravastatin could inhibit TREM-1-medieted inflammation and NF-κB signaling pathway was involved.     

Recent advancement in the discovery and development of COX-2 inhibitors: Insight into biological activities and SAR studies (2008–2019)

Cyclooxygenase-2 is a very important physiological enzyme playing key roles in various biological functions especially in the mechanism of pain and inflammation, among other roles, making it a molecule of high interest to the pharmaceutical community as a target. COX 2 enzyme is induced only during inflammatory processes or cancer and reflects no role in the guarding stomach lining. Thus, selective COX-2 inhibition can significantly reduce the adverse effects including GI tract damage and hepatotoxic effects of traditional NSAIDs like aspirin, ibuprofen, etc. Recent developments on COX-2 inhibitors is primarily focused on improving the selectivity index of the drug towards COX-2 along with enhancing the potency of the drug by modifying the scaffolds of Coxibs currently in the market like Celecoxib, Indomethacin, Oxaprozin, etc. We have reported the progress on new COX-2 inhibitors in the last decade (2008–2019) focussing on five heterocyclic rings- Pyrazole, Indole, Oxazole, Pyridine and Pyrrole. The addition of various moieties to these core rings and their structure-activity relationship along with their molecular modelling data have been explored in the article. This review aims to aid medicinal chemists in the design and discovery of better COX-2 inhibitors constructed on these five heterocyclic pharmacophores.     

Potential roles and targeted therapy of the CXCLs/CXCR2 axis in cancer and inflammatory diseases

The chemokine receptor CXCR2 and its ligands are implicated in the progression of tumours and various inflammatory diseases. Activation of the CXCLs/CXCR2 axis activates multiple signalling pathways, including the PI3K, p38/ERK, and JAK pathways, and regulates cell survival and migration. The CXCLs/CXCR2 axis plays a vital role in the tumour microenvironment and in recruiting neutrophils to inflammatory sites. Extensive infiltration of neutrophils during chronic inflammation is one of the most important pathogenic factors in various inflammatory diseases. Chronic inflammation is considered to be closely correlated with initiation of cancer. In addition, immunosuppressive effects of myeloid-derived suppressor cells (MDSCs) against T cells attenuate the anti-tumour effects of T cells and promote tumour invasion and metastasis. Over the last several decades, many therapeutic strategies targeting CXCR2 have shown promising results and entered clinical trials. In this review, we focus on the features and functions of the CXCLs/CXCR2 axis and highlight its role in cancer and inflammatory diseases. We also discuss its potential use in targeted therapies.     

Endothelial cell autophagy in chronic intermittent hypoxia is impaired by miRNA-30a-mediated translational control of Beclin-1

Chronic intermittent hypoxia (CIH) in obstructive sleep apnea causes damage of aortic endothelial cells, which predisposes the development of many cardiovascular diseases. Recently, both altered expression of microRNAs (miRNAs) and impaired autophagy were found to be associated with endothelial cell dysfunction in CIH. However, the exact molecular regulatory pathway has not been determined. Here, we address this question. In a mouse model of CIH, we detected significant upregulation of miR-30a, a miRNA that targets 3′-untranslated region of autophagy-associated protein 6 (Beclin-1) messenger RNA (mRNA) for suppressing the protein translation, which subsequently attenuated the endothelial cell autophagy against cell death. Indeed, unlike Beclin-1 mRNA, the Beclin-1 protein in endothelial cells did not increase after CIH. Suppression of miR-30a by expression of antisense of miR-30a significantly increased Beclin-1 levels to enhance endothelial cell autophagy in vitro and in vivo, which improved endothelial cell survival against CIH. Together, these data suggest that endothelial cell autophagy in CIH may be attenuated by miR-30a-mediated translational control of Beclin-1 as an important cause of endothelial cell dysfunction and damage.     

Proteomic analysis of CA1 and CA3 regions of rat hippocampus and differential susceptibility to intermittent hypoxia

The CA1 and CA3 regions of the hippocampus markedly differ in their susceptibility to hypoxia in general, and more particularly to the intermittent hypoxia that characterizes sleep apnea. Proteomic approaches were used to identify proteins differentially expressed in the CA1 and CA3 regions of the rat hippocampus and to assess changes in protein expression following a 6-h exposure to intermittent hypoxia (IH). Ninety-nine proteins were identified, and 15 were differentially expressed in the CA1 and the CA3 regions. Following IH, 32 proteins in the CA1 region and only 7 proteins in the more resistant CA3 area were up-regulated. Hypoxia-regulated proteins in the CA1 region included structural proteins, proteins related to apoptosis, primarily chaperone proteins, and proteins involved in cellular metabolic pathways. We conclude that IH-mediated CA1 injury results from complex interactions between pathways involving increased metabolism, induction of stress-induced proteins and apoptosis, and, ultimately, disruption of structural proteins and cell integrity. These findings provide initial insights into mechanisms underlying differences in susceptibility to hypoxia in neural tissue, and may allow for future delineation of interventional strategies aiming to enhance neuronal adaptation to IH.