骨科围手术期患者静脉血栓栓塞症物理预防的最佳证据总结

目的总结骨科围手术期患者静脉血栓栓塞症（VTE）物理预防的证据，提高护理人员VTE物理预防措施实施依从性。方法根据澳大利亚JBI循证卫生保健中心证据总结方法学，检索骨科围手术期患者VTE物理预防相关文献，根据纳入文献类型，由研究人员独立进行质量评价，并提取、汇总最佳证据。结果共纳入文献17篇，包含10篇指南、1篇证据总结、2篇专家共识、4篇系统评价。经过分析，总结出7类共30条骨科围手术期患者VTE物理预防最佳证据。结论最佳证据可为护士提供循证依据。但在应用时，还需评估具体临床情境，结合专业判断和患者意愿，针对性选择证据，以促进护理质量的持续改进。     

对分课堂在《中医诊断学》教学中的应用及探索

探讨对分课堂在《中医诊断学》教学中的应用。将对分课堂授课模式引入《中医诊断学》教学过程中，通过学生的课堂表现及课后对学生的问卷调查，评价对分课堂教学模式对《中医诊断学》教学效果的影响。学生普遍认可对分课堂教学模式，学生课堂活跃程度提高、主观能动性增加，自主学习能力增加，学习效率提高。通过对分课堂教学，有助于提高学生对《中医诊断学》的学习热情，提高学习成绩，提升教学质量。具有一定的推广意义。     

Renal cell carcinoma staging: pitfalls,challenges, and updates

Renal cell carcinoma (RCC) is unusual among cancers in that it often grows as a spherical, well‐circumscribed mass. Increasing tumour size influences the pathological pT stage category within pT1 and pT2, with cutoffs of 40, 70 and 100 mm; however, with increasing size also comes a sharp increase in the likelihood of renal sinus or renal vein tributary invasion, such that clear cell RCC rarely reaches 70 mm without invading one of these. To clarify some previous challenges in assigning tumour stage, the American Joint Committee on Cancer 2016 tumor–node–metastasis classification has removed the requirements than vein invasion be recognised grossly and that vein walls contain muscle for the diagnosis of vein invasion. Renal pelvis invasion has also been added as an additional route to pT3a. Multinodularity or finger‐like extensions from a renal mass should be viewed with great suspicion for the possibility of vein or renal sinus invasion, and, as tumour size increases to over 40–50 mm, thorough sampling of the renal sinus interface should always be undertaken. With increasing interest in adjuvant therapy in renal cancer, the pathologist's role in RCC staging will continue to be an important prognostic parameter and a tool for selection of patients for enrolment in clinical trials.     

Chemical isotope labeling liquid chromatography mass spectrometry for investigating acute dietary effects of cow milk consumption on human urine metabolome

Biomarker discovery has been increasingly important in the field of metabolomics for the detection and understanding of diseases. Of the many biofluids available for metabolomics, urine is a preferred option as it is non-invasive to collect and contains a wide range of metabolites reflective of the health status of the testing individual. However, urine also contains many exogenous metabolites which are introduced through various sources such as diet. This complicates the data interpretation when searching the metabolome for disease-related endogenous metabolites. Since diet is difficult to control, this work aims to study the acute effects of diet (particularly cow milk) consumption on the human urine amine/phenol submetabolome by utilizing differential chemical isotope labeling (CIL) liquid chromatography mass spectrometry (LC-MS). LC-MS analysis of 62 urine samples collected before and after (1 hour and 2 hours) milk intake resulted in the detection of 4985 metabolites with an average of 3815 ± 206 (n = 62) detected per sample. The work aims to differentiate the exogenous “food” metabolites from the endogenous metabolite pool and to determine any dietary effects from milk intake on the human urine metabolome.     

Coinheritance of generalized pustular psoriasis and familial Behçet‐like autoinflammatory syndrome with variants in IL36RN and TNFAIP3 in the heterozygous state

Generalized pustular psoriasis (GPP) is now known to be caused by biallelic variants in IL36RN and monoallelic variants in CARD14 and AP1S3. The presence of a modifier locus or oligogenic inheritance have been hypothesized. We report on a patient with a unique coinheritance of pathogenic variants in IL36RN (c.115+6T>C) and TNFAIP3 (c.547C>T, p.R183 * ) causing the genetic entities GPP and familial Behçet‐like autoinflammatory syndrome (AISBL). The heterozygous variant in IL36RN identified by Sanger sequencing was inherited from his unaffected father, while the heterozygous variant in TNFAIP3 was detected by whole‐exome sequencing and was also identified in the patient's AISBL‐affected maternal relatives. Further functional studies are required to research whether the variant of TNFAIP3 plays a part in the development of GPP or simply causes the Behçet's disease phenotype. However, our data suggest that whole‐exome sequencing for the heterozygous carrier of the IL36RN gene in GPP be used to find the potential second genetic locus.