金黄色葡萄球菌异质性耐药机制及实验室检测技术

 异质性耐药是一种特殊的细菌耐药类型，常表现为同一克隆来源的不同细菌亚群对某种抗菌药物表现出不一致的耐药特征，大多数亚群对某种抗菌药物敏感，而少部分亚群对其耐药或高度耐药。异质性耐药分离株常会导致特定抗菌药物抗感染治疗失败。针对异质性耐药菌较为深入的研究主要集中于革兰阴性菌，革兰阳性球菌的相关报道较少。近年有研究报道万古霉素、利奈唑胺、苯唑西林等多种类型抗菌药物异质性耐药金黄色葡萄球菌分离株出现，但其实际临床意义尚待进一步评估。此文对金黄色葡萄球菌异质性耐药机制和检测技术最新进展进行综述，为细菌异质性耐药机制研究和新型检测技术研发提供新的思路。     

Go-Ichi-Ni-San 2: A potential biomarker and therapeutic target in human cancers

Cancer incidence and mortality are increasing globally, leading to its rising status as a leading cause of death. The Go-Ichi-Ni-San (GINS) complex plays a crucial role in DNA replication and the cell cycle. The GINS complex consists of four subunits encoded by the GINS1, GINS2, GINS3, and GINS4 genes. Recent findings have shown that GINS2 expression is upregulated in many diseases, particularly tumors. For example, increased GINS2 expression has been found in cervical cancer, gastric adenocarcinoma, glioma, non-small cell lung cancer, and pancreatic cancer. It correlates with the clinicopathological characteristics of the tumors. In addition, high GINS2 expression plays a pro-carcinogenic role in tumor development by promoting tumor cell proliferation and migration, inhibiting tumor cell apoptosis, and blocking the cell cycle. This review describes the upregulation of GINS2 expression in most human tumors and the pathway of GINS2 in tumor development. GINS2 may serve as a new marker for tumor diagnosis and a new biological target for therapy.     

Disengagement of tibial insert locking pin in total knee arthroplasty - A rare failure case report

Total Knee Arthroplasty (TKA) has seen many advancements over the years. One such advancement is development of locking mechanism for polyethylene insert in modular implants. It aims to reduce micro motion and wear problems. Disengagement of locking pin from insert after primary TKA without trauma is rare complication. The author describes a rare case of disengagement of the polyethylene insert locking pin in primary total knee arthroplasty. Disengagement of the locking clip was observed 8 months after index operation without any trauma.     

Mechanisms of repigmentation induced by photobiomodulation therapy in vitiligo

Photobiomodulation (PBM) therapy is based on the exposure of biological tissues to low‐level laser light (coherent light) or light‐emitting diodes (LEDs; noncoherent light), leading to the modulation of cellular functions, such as proliferation and migration, which result in tissue regeneration. PBM therapy has important clinical applications in regenerative medicine. Vitiligo is an acquired depigmentary disorder resulting from disappearance of functional melanocytes in the involved skin. Vitiligo repigmentation depends on available melanocytes derived from (a) melanocyte stem cells located in the bulge area of hair follicles and (b) the epidermis at the lesional borders, which contains a pool of functional melanocytes. Since follicular melanoblasts (MBs) are derived from the melanocyte stem cells residing at the bulge area of hair follicle, the process of vitiligo repigmentation presents a research model for studying the regenerative effect of PBM therapy. Previous reports have shown favourable response for treatment of vitiligo with a low‐energy helium‐neon (He‐Ne) laser. This review focuses on the molecular events that took place during the repigmentation process of vitiligo triggered by He‐Ne laser (632.8 nm, red light). Monochromatic radiation in the visible and infrared A (IRA) range sustains matrix metalloproteinase (MMP), improves mitochondrial function, and increases adenosine triphosphate (ATP) synthesis and O₂ consumption, which lead to cellular regenerative pathways. Cytochrome c oxidase in the mitochondria was reported to be the photoacceptor upon which He‐Ne laser exerts its effects. Mitochondrial retrograde signalling is responsible for the cellular events by red light. This review shows that He‐Ne laser initiated mitochondrial retrograde signalling via a Ca²⁺‐dependent cascade. The impact on cytochrome c oxidase within the mitochondria, an event that results in activation of CREB (cyclic‐AMP response element binding protein)‐related cascade, is responsible for the He‐Ne laser promoting functional development at different stages of MBs and boosting functional melanocytes. He‐Ne laser irradiation induced (a) melanocyte stem cell differentiation; (b) immature outer root sheath MB migration; (c) differentiated outer root sheath MB melanogenesis and migration; and (d) perilesional melanocyte migration and proliferation. These photobiomodulation effects result in perifollocular and marginal repigmentation in vitiligo.     

白藜芦醇治疗结直肠癌的机制研究进展

【摘要】白藜芦醇是一种天然的多酚化合物，有预防心血管疾病，预防衰老，抗炎，抗癌等作用。该文总结了近年来白藜芦醇作用于结直肠癌的机制的研究进展，为白藜芦醇的进一步研究提供依据。     

不同针灸疗法干预关节炎炎症反应的机制研究进展

关节炎是一系列以关节及关节周围组织，因炎症、感染、创伤、退化或其他因素引起的炎性疾病。近年来关节炎的患病率显著增加，临床上代表性关节炎有类风湿关节炎、脊柱关节炎（以强直性脊柱炎为典型）、痛风、骨关节炎等。近年来的研究逐渐重视这些疾病中炎性细胞因子的研究，包括白介素（IL）家族系列中多种炎性因子及肿瘤坏死因子-α（TNF-α）。最新研究发现针灸在此类疾病的治疗中，可能参与相关炎性因子的致病途径，并通过调控此类细胞因子水平，从而改善炎症反应，为临床运用针灸治疗关节炎提供了理论及实验依据。     

基于网络药理学探讨黄精-百合药对抗癌作用的机制

目的:通过网络药理学的方法筛选黄精-百合药对中的有效成分,预测治疗癌症的作用靶点及信号通路,进一步探讨潜在作用机制。方法:使用全称为中药系统药理学分析平台筛选黄精-百合药对中的活性成分和靶点,通过基因疾病关联数据库(Dis Ge NET)与人类孟德尔遗传数据库(OMIM)预测与筛选药对中有效的中药成分作用的疾病靶点。选择生物信息分析学习平台(Omicshare)匹配药物和疾病的靶点,借助复杂网络可视化平台(Cytoscape3. 7. 0)软件构建"药物-成分-疾病"网络。采用蛋白质相互作用网络数据库(String)构建黄精-百合药对治疗癌症的靶点相互作用的网络。最后通过功能注释生物信息学分析平台(DAVID)对黄精-百合药对中关键作用的节点进行生物功能及代谢通路分析。结果:筛选出19个黄精-百合药对的活性成分,根据靶点预测技术预测出相关靶点234个,与疾病靶点有关的活性成分为6个,主要通过调控丝氨酸(Akt)/苏氨酸激酶1(Akt1),Jun原癌基因,AP-1转录因子亚基(JUN),血管内皮生长因子A(VEGFA),基质金属蛋白酶-9(MMP-9),半胱氨酸蛋白酶-3(Caspase-3)等靶蛋白,以及癌症中的蛋白多糖,雌激素信号转导通路,人免疫缺陷病毒1感染,缺氧诱导因子-1(HIF-1)信号通路,肿瘤坏死因子(TNF)信号通路,癌症中的微型核糖核酸(MicroRNAs)等通路发挥抗癌作用。结论:黄精-百合药对治疗癌症的作用体现了中药多成分-多靶点-多途径的特点,为阐释其抗癌治疗的作用机制与物质基础提供了科学依据。