胆总管结石内镜逆行胰胆管造影术后行胆道支架置入和鼻胆管引流并发症的比较

目的探讨胆总管结石患者采用内镜逆行胰胆管造影术（ERCP）取石后同期开展胆道支架置入术或开展经内镜鼻胆管引流术（ENBD），对于防范并发症的价值。 方法按照前瞻性研究原则，选择2017年4月至2019年1月新疆医科大学第一附属医院收治的338例胆总管结石患者，随机分为支架组（170例）与引流组（168例）。两组患者均行ERCP治疗，其中引流组术后同期开展ENBD，支架组患者术后开展胆道支架置入术，对比两组患者腹痛评分、并发症发生情况及预后。 结果两组患者术后均未合并严重出血、穿孔或病死，结石完全清除率差异无统计学意义。与支架组相比，引流组术中胰腺管插管次数，术后4 h血淀粉酶水平、高淀粉酶血症、急性胰腺炎以及并发症总发生率更高，差异有统计学意义（P<0.05），术后24、48、72 h不同时点腹痛测评分值居更高水平（P<0.05）。 结论对于胆总管结石行ERCP治疗的患者，术后予以ENBD、胆道支架置入术的结石完全清除效果对比无明显差异，但胆道支架置入术更能降低术后并发症风险、缓解腹痛症状，患者获益更多。     

Pruritus secondary to primary biliary cholangitis: a review of the pathophysiology and management with phototherapy

Primary biliary cholangitis (PBC) is a long-term disease affecting 35 in every 100,000 people in the United Kingdom (UK) and United States. It is driven by the immune system and causes inflammation of bile ducts (tubes carrying bile from the liver to the gut), leading to bile duct destruction and eventual scarring of the liver. For unclear reasons, PBC causes persistent itch (cholestatic itch) that is difficult to suppress with conventional treatments. Several case studies have shown that phototherapy (treatment of the skin with UV light) can be used to reduce cholestatic itch, although the processes behind this treatment remain poorly understood. This review article, written by researchers in the UK, summarises the evidence behind the use of phototherapy to treat cholestatic itch and explores potential reasons (mechanisms) for how it works. Fifty articles were included in this review, alongside the authors’ own expertise. Key theories about potential mechanisms include the effect of phototherapy on bile salt components, enzyme activity and the expression of receptors involved in cholestatic itch pathways. This paper has developed several testable hypotheses (theories) that can be trialled to increase knowledge on this important subject and to aid the development of effective treatments.     

Protein Kinase CK2, a Potential Therapeutic Target in Carcinoma Management

The Protein kinase CK2 (formerly known as casein kinase 2) is a highly conserved serine/ threonine kinaseoverexpressed in various human carcinomas and its high expression often correlates with poor prognosis. CK2 proteinis localized in the nucleus of many tumor cells and correlates with clinical features in many cases. Increased expressionof CK2 in mice results in the development of various types of carcinomas (both solids and blood related tumors, suchas (breast carcinoma, lymphoma, etc), which reveals its carcinogenic properties. CK2 plays essential roles in many keybiological processes related to carcinoma, including cell apoptosis, DNA damage responses and cell cycle regulation.CK2 has become a potential anti-carcinoma target. Various CK2 inhibitors have been developed with anti-neoplasticproperties against a variety of carcinomas. Some CK2 inhibitors have showed good results in in vitro and pre-clinicalmodels, and have even entered in clinical trials. This article will review effects of CK2 and its inhibitors on commoncarcinomas in in vitro and pre-clinical studies.     

Omega‐3 fatty acids regulate plasticity in distinct hippocampal glutamatergic synapses

Dietary omega‐3 fatty acids accumulate and are actively retained in central nervous system membranes, mainly in synapses, dendrites and photoreceptors. Despite this selective enrichment, their impact on synaptic function and plasticity has not been fully determined at the molecular level. In this study, we explored the impact of omega‐3 fatty acid deficiency on synaptic function in the hippocampus. Dietary omega‐3 fatty acid deficiency for 5 months after weaning led to a 65% reduction in the concentration of docosahexaenoic acid in whole brain synaptosomal phospholipids with no impact on global dopaminergic or serotonergic turnover. We observed reduced concentrations of glutamate receptor subunits, including GluA1, GluA2 and NR2B, and synaptic vesicle proteins synaptophysin and synaptotagmin 1 in hippocampal synaptosomes of omega‐3 fatty acid‐deficient mice as compared to the omega‐3 fatty acid rich group. In contrast, an increased concentration of neuronal inositol 1,4,5‐trisphosphate‐receptor (IP₃‐R) was observed in the deficient group. Furthermore, omega‐3 fatty acid deficiency reduced the long‐term potentiation (LTP) in stratum oriens of the hippocampal CA1 area, but not in stratum radiatum. Thus, omega‐3 fatty acids seem to have specific effects in distinct subsets of glutamatergic synapses, suggesting specific molecular interactions in addition to altering plasma membrane properties on a more global scale.