PBL结合绘图教学模式在胰腺癌患者肝素钠皮下注射临床教学中的作用

[摘要]目的探讨问题导向学习(PBL)结合绘图教学模式在临床护理带教中的应用效果。方法纳入2016年6月~2017年6月在我院实习的本科护生78名,按等比例随机分为观察组和対照组,观察组采取PBL结合绘图学模式法,对照组采用单纯PBL教学模式,利用统计学方法按照参考指标对两组实习生的考核数据进行对比分。结果观察组理论知识得分明显大于对照组[(90.31±4.55)分vs.(81.30±5.69)分],观察组临床实践技能得分明显大于对照组[(92.21±4.18)分vs.(80.31±5.39)分],差异均有统计学意义(P0.05)。结论PBL结合绘图教学模式临床护理带教中效果显著,比单纯PBL教学模式更具有优势,更有利于培养学生的循证思维与创新能力,提高临护理教学质量,在临床护理带教中值得推广。     

Four cases of sodium nitrite suicidal ingestion: A new trend and a relevant Forensic Pathology and Toxicology challenge

Sodium nitrite (NaNO₂) is an inorganic compound commonly used as a food additive, antifreeze admixture, and fertilizer. Its toxicity mechanism is mainly represented by the oxidation of ferrous iron to ferric iron of one of the four heme structures in haemoglobin with the onset of methaemoglobin. The mechanism of death by sodium nitrite toxicity is severe hypoxia. We present four cases of suicidal sodium nitrite ingestion that closely occurred within a two months-period. Self-poisoning with sodium nitrite actually represents an increasing trend in nitrates’ related deaths. In order to reach a precise diagnosis of NaNO₂ intoxication, a complete toxicological analysis should be carried out including not only MetHb blood levels but also nitrites and nitrites in standard or alternative matrices as a routine procedure. Autopsy should be carefully performed to detect common indicators of hypoxia or more rarely evident typical by themselves-non specific signs of sodium nitrite toxicity. Suicidal manner of death should be carefully considered when circumstantial data support that ingestion of large amounts of NaNO₂ occurred as a consequence of a self-injurious behaviour. Relevant informations include victim’s previous Internet or book researches about paths to follow to commit suicide with sodium nitrate, employment and past medical history, with strong regard to psychiatric diseases as well as eventual taking psycotropic drugs.Finally, an accurate integration of autoptic and toxicological results with circumstantial data is necessary to make correct diagnosis of death due to acute respiratory failure secondary to suicidal sodium nitrite ingestion.     

关节镜清理术联合透明质酸钠治疗膝骨性关节炎的效果

目的探讨关节镜清理术联合透明质酸钠治疗膝骨性关节炎患者的效果。方法100例膝骨性关节炎患者随机分为两组各50例,对照组采用关节镜清理术治疗,实验组采用关节镜清理术联合透明质酸钠治疗,比较两组的关节液炎性因子水平、膝关节功能以及疼痛情况。结果治疗后,实验组的TNF-α、IL-6、IL-8水平均显著低于对照组(P<0.05)。治疗1个月、3个月、6个月后,实验组的Lysholm评分均显著高于对照组,VAS评分均显著低于对照组(P<0.05)。结论关节镜清理术联合透明质酸钠治疗膝骨性关节炎可降低患者关节液炎性因子水平,改善膝关节功能,减轻疼痛。     

A 16q22.2-q23.1 deletion identified in a male infant with West syndrome

In partial monosomy of the distal part of chromosome 16q, abnormal facial features, intellectual disability (ID), and feeding dysfunction are often reported. However, seizures are not typical and the majority of them were seizure-free. Here we present the case of a 16q22.2-q23.1 interstitial deletion identified in a male patient with severe ID, facial anomalies including forehead protrusions and flat nose bridge, patent ductus arteriosus, bilateral vocal cord atresia treated by tracheotomy, and West syndrome, which were developed 10 months after birth. Although phenobarbital, sodium valproate (VPA), and zonisamide were not effective as monotherapies or combination therapies, the patient's epileptic seizures and electroencephalogram anomalies disappeared following combined therapy with lamotrigine and VPA. Although WW Domain Containing Oxidoreductase (WWOX), which is known as a cause of autosomal recessive epileptic encephalopathy, was included within the 6.8-Mb deleted region which identified by targeted panel sequencing and validated by chromosomal microarray analysis, no pathogenic variants were detected in the other allele of WWOX. Therefore, it is possible that other genes within or outside of the long deleted region or their interactions may cause West syndrome in this patient.     

玻璃酸钠注射结合乙哌立松治疗膝骨关节炎的效果观察

目的 探讨玻璃酸钠注射结合乙哌立松治疗膝骨关节炎的临床效果。方法 94例膝骨关节炎患者,按照随机数字法将其分为对照组与实验组,每组47例。对照组患者使用玻璃酸钠进行治疗,实验组患者使用玻璃酸钠注射结合乙哌立松进行治疗。比较两组患者治疗前后尿液中CTX-Ⅱ含量、疼痛评分、膝关节功能评分、生活质量评分。结果 治疗后,实验组尿液中CTX-Ⅱ含量(236.78±26.59)ng/mmol低于对照组的(364.45±41.23)ng/mmol,差异具有统计学意义(P<0.05)。实验组疼痛评分(3.01±0.89)分低于对照组的(4.46±1.68)分,差异具有统计学意义(P<0.05)。实验组膝关节功能评分(84.45±11.68)分高于对照组的(75.89±11.84)分,差异具有统计学意义(P<0.05)。实验组物质生活、社会角色、心理健康、躯体健康评分分别为(86.23±1.89)、(87.43±2.13)、(87.52±3.01)、(88.23±4.13)分,均高于对照组的(76.02±4.31)、(79.23±4.56)、(79.01±4.89)、(77.25±4.89)分,差异具有统计学意义(P<0.05)。结论 玻璃酸钠注射结合乙哌立松治疗膝骨关节炎的临床效果显著。     

发作性睡病的药物治疗进展

发作性睡病是致残性白天睡眠增多的最常见原因之一，其治疗旨在减少白天睡眠增多和猝倒，改善夜间睡眠紊乱、睡眠瘫痪及与睡眠有关的幻觉。2019年，组胺H3受体拮抗剂替洛利生（Pitolisant）和多巴胺及去甲肾上腺素再摄取抑制剂索利氨酯（Solriamfetol）分别在欧盟和美国上市，前者具有促醒和抗猝倒作用，后者也有促醒作用，且戒断症状和滥用的发生率更低。目前，控释型羟丁酸钠（FT218）、低钠型羟丁酸盐（JZP-258）、选择性去甲肾上腺素再摄取抑制剂（瑞波西汀，又称AXS-12）以及莫达非尼联合氟卡尼制剂（THN102）等药物仍在开发和测试中，均可作为治疗发作性睡病相关白天睡眠增多和猝倒的潜在药物。本文重点介绍这些最近研发的发作性睡病治疗药物。     

Investigating the inotropic effect of pyruvic acid on the isolated rat heart and its underlying mechanism

Pyruvic acid is important organic chemical intermediates that plays a role in cardiomyocyte pathophysiology and therapy. This study sought to explore the inotropic effects of pyruvic acid on the function of the isolated rat hearts and investigate its underlying mechanism. Pyruvic acid produced a greater negative inotropic effect compared to HCl and sodium pyruvate in a concentration-dependent pattern in the hearts. The role of low dose of pyruvic acid on heart function was regulated by pyruvic acid molecules and high dose pyruvic acid may be influenced by pyruvic acid molecules and pH. K_v channels may be involved in the pyruvic acid-induced negative inotropic effect. Finally, pyruvic acid markedly increased the level of LDH and CK and reduced the level of Ca²⁺Mg²⁺-ATPase and Na⁺K⁺-ATPase. These results suggest that pyruvic acid may modulate cardiac function at physiological or low doses but can cause damage to cardiomyocytes at high doses.     

Nitric oxide donors offer protection to RBC from storage lesion

BackgroundRed blood cell (RBC), which is the most commonly transfused blood component, due to its ability to save a life in absence of any other blood components, can be stored up to maximum 6 weeks by following standard preservation procedure. During storage, RBC undergoes various biophysical and biochemical changes (commonly known as storage lesion) for which blood transfusion with “old RBC” shows a lot of clinical problems especially relevant to critically ill patients. Recent research on S-nitrosylation of haemoglobin to improve oxygen delivery of banked blood revealed the important role of nitric oxide (NO) in protecting storage lesion.Materials and methodsIn the present study, we used various “NO donating” chemicals with different NO release dynamics and chemistries in RBC storage cocktails to test the effects of NO on storage lesion. Changes in different storage markers were evaluated after 7 days storage of pre-treated RBC.ResultsAll the NO donors have shown protection against hemolysis. However, S-nitroso glutathione (GSNO) ranks first in shielding RBCs from storage lesion and additionally, it helps in elevating the value of 2, 3-di phosphoglycerate (2, 3-DPG), improving the RBC membrane fluidity and decreasing the adhesion towards endothelial monolayer.DiscussionPresent study reveals that NO released from NO donors confers protection against storage lesions of the RBC. Further, the study confirms that pre-treatment with GSNO, a NO donor and a nitrosylating agent, ensures the best protection to RBC during low temperature storage, when compared to other NO donor treatments.     

Challenges in the acute management of profound hyponatremia presenting with severe symptoms

Currently available guidelines in the acute management of severely symptomatic hypotonic hyponatremia vary in their approach to the use of hypertonic saline. In the acute setting, deciding on when to implement available treatment algorithm using hypertonic saline may be difficult, given that the duration of hyponatremia and potential alternative diagnoses presenting with similar symptoms may be hard to establish promptly. We present the case of a young female with symptomatic profound hyponatremia who subsequently developed osmotic demyelination syndrome due to rapid overcorrection of serum sodium concentration. We discuss the interplay between the dynamic pathophysiological processes responsible for hypotonic hyponatremia in adrenal insufficiency and conduct a detailed analysis of currently available guidelines to highlight the challenges in acute and reactive treatment in clinical practice.