On the Modern Interpretation of Zen Calligraphy Thoughts

中国佛教禅宗书法艺术,风采独特,其书学著述,丰富多彩.综观禅宗书学著述,可以清楚地看到,“写经”是禅家所从事的书法艺术创作活动,是禅家特别关注和讨论的重要话题之一.僧人通过写经,宏扬教义、传播佛法、善行佛事、参禅悟道,乃是“栖身大乘”,“游戏翰墨,作大佛事”.禅宗书学著述从一个特殊的视角,论述了写经的重要意义、巨大功德、书写宗旨、价值取向、艺术特点、特殊形态.     

采用结构-过程-结果三维质量评价模式实施CABG延续护理实践

  目的  探讨基于结构-过程-结果的三维质量评价模式的延续性护理在冠状动脉旁路移植术（coronary artery bypass grafting，CABG）患者中的应用效果。  方法  选取2018年8月至2019年12月收治昆明市延安医院心脏大血管外科行CABG围术期的168例患者为研究对象，采用随机数字表法分成两组，每组各84例，对照组实施常规延续护理，干预组实施基于结构-过程-结果三维质量评估模式构建的延续性护理方案，干预后比较两组患者《中国心血管病人生活质量评定问卷》（CCQQ）评分、服药依从性评分、主要心脑血管事件（MACCE）发生率。  结果  干预组《中国心血管病人生活质量评定问卷》（CCQQ）评分、服药依从性评分、主要心脑血管事件（MACCE）发生率均高于对照组，差异有统计学意义（P < 0.05）。  结论  Donabedian的结构-过程-结果延续性护理三维质量评价模式构建有助于提高CABG术后患者自我管理效能感及生活质量，是提升延续性护理质量的有效途径。     

滇龙胆草对肺纤维化小鼠肺组织NF-κB和CTGF表达的影响

  目的  研究滇龙胆草对肺纤维化小鼠肺组织NF-κB和CTGF表达的影响。  方法  气管滴注博莱霉素（5 mg/kg ）制备昆明小鼠肺纤维化模型，造模后灌胃给予低、中、高剂量（50、100、200 mg/kg）的滇龙胆草，每日给药1次，设比非尼酮为阳性对照。在建模后第28天，取肺组织进行检测，肉眼观察肺组织大体病理改变，Masson染色观察肺组织纤维化程度；采用Western blot检测肺组织中NF-κB和CTGF蛋白的表达。  结果  与模型组比较，不同剂量的滇龙胆草组和阳性药物比非尼酮组小鼠肺组织胶原沉积明显减少。与模型组比较，不同剂量的滇龙胆草组和阳性药物比非尼酮组小鼠肺组织NF-κB和CTGF蛋白表达明显下调，差异有统计学意义（P < 0.05）。  结论  滇龙胆草具有抗肺纤维化作用，其机制与下调NF-κB和CTGF蛋白表达，减轻肺组织炎症和胶原沉积有关。     

Multiple sclerosis: immunopathogenesis and controversies in defining the cause

PURPOSE OF REVIEW: Multiple sclerosis is a major cause of neurological disability in Western societies. The most important reason for the limited success obtained in the treatment and prevention so far is most likely related to the limited knowledge about its cause and pathogenesis. This paper discusses recent progress and controversies in the understanding of the pathogenesis and cause of multiple sclerosis. RECENT FINDINGS: Both T helper cells type 1 (Th1 cells), Th17 cells, cytotoxic T cells, B cells and regulatory T cells are involved in the inflammatory process. Axonal loss seems to be driven by inflammation during the early stages of disease but may become independent of inflammation at later stages. The target antigen of the immune response has not been identified. Weak genetic association has been established in two cytokine receptors, whereas increasing female: male ratio support the importance of environmental risk factors. A substantial proportion of intrathecal B cells are infected with Epstein-Barr virus. SUMMARY: Multiple sclerosis is a complex disease and calls for integrated efforts from immunology, epidemiology, neuroscience and genetics. In particular, the immunological implications of environmental risk factors such as vitamin D desufficiency, smoking and Epstein-Barr virus infection need to be explored.     

CYP3A4 Mediates Oxidative Metabolism of the Synthetic Cannabinoid AKB-48

Synthetic cannabinoid designer drugs have emerged as drugs of abuse during the last decade, and acute intoxication cases are documented in the scientific literature. Synthetic cannabinoids are extensively metabolized, but our knowledge of the involved enzymes is limited. Here, we investigated the metabolism of N-(1-adamantyl)-1-pentyl-1H-indazole-3-carboxamide (AKB-48), a compound identified in herbal blends from 2012 and onwards. We screened for metabolite formation using a panel of nine recombinant cytochrome P450 (CYP) enzymes (CYP1A2, 2B6, 2C8, 2C9, 2C18, 2C19, 2D6, 2E1, and 3A4) and compared the formed metabolites to human liver microsomal (HLM) incubations with specific inhibitors against CYP2D6, 2C19, and 3A4, respectively. The data reported here demonstrate CYP3A4 to be the major CYP enzyme responsible for the oxidative metabolism of AKB-48, preferentially performing the oxidation on the adamantyl moiety. Genetic polymorphisms are likely not important with regard to toxicity given the major involvement of CYP3A4. Adverse drug-drug interactions (DDIs) could potentially occur in cases with co-intake of strong CYP3A4 inhibitors, e.g., HIV antivirals and azole antifungal agents.

Electronic supplementary material

The online version of this article (doi:10.1208/s12248-015-9788-7) contains supplementary material, which is available to authorized users.KEY WORDS: adamantyl, cytochrome P450, metabolism, metabolites, synthetic cannabinoids     

Increase in gamma/delta T cell receptor bearing lymphocytes in normal small bowel mucosa in latent coeliac disease.

A jejunal biopsy specimen from an asymptomatic 35 year old man was studied because of a low serum titre of reticulin antibody and the finding of coeliac disease in his son. In this specimen villous structure was quite normal as was the total number of intraepithelial lymphocytes, but the number of gamma/delta T cell receptor bearing lymphocytes was 10 times higher than the mean in control subjects. Two years later a further biopsy specimen was obtained because of clinical symptoms and an increased titre of reticulin antibody. This specimen showed villous atrophy with crypt hyperplasia and increased infiltration of intraepithelial lymphocytes compatible with coeliac disease. A control biopsy specimen taken during gluten free diet showed normalisation of the villous architecture. Latent coeliac disease may be characterised by an increase in gamma/delta positive cells similar to that seen in established coeliac disease.     

Resistance to activated protein C due to a factor V gene mutation The most common inherited risk factor of thrombosis

The protein C anticoagulant pathway is of major importance in maintaining vascular patency. Resistance to the key enzyme of this system, activated protein C (APC), is a recently discovered congenital defect of the protein C system. This genetic defect is present in 20% to 60% of venous thrombosis patients, making it by far the most common known pathogenetic risk factor of thrombosis. APC resistance is due to a single point mutation in the factor V gene (G to A at nucleotide position 1691) that predicts the replacement of arginine(506) by glutamine. This is associated with the loss of one of three APC cleavage sites in factor Va, one of the substrates for APC, and hypercoagulability. The identification of APC resistance as an additional genetic risk factor in a large proportion of symptomatic protein C- and protein S-deficient families has provided evidence that thrombosis is a polygenetic disease. Thus, several genetic defects act in concert with environmental factors in the pathogenesis of venous thromboembolism.