微创手术机器人机械臂结构设计与工作空间分析

目的现有双平行四边形机构设计的机械臂需要串联一个伸缩自由度机构,导致机械臂体积增大,运动灵活性降低,持镜臂与持器械臂发生干涉。针对这一问题,提出一种新型机械臂结构,增强运动灵活性、减小机械臂的体积。方法采用5连杆机构、滑块与滑轨的低副机构和丝传动机构设计机械臂,实现末端执行器的伸缩运动,建立机械臂的运动学模型,以MATLAB为仿真工具验证零位关节角D-H参数的正确性,求解出机械臂的运动方程;同时运用蒙特卡洛算法,得到末端执行器的三维工作空间范围,并对3条机械臂作术前动物实验规划;最后,在猪体内进行胆囊切除等操作,验证机械臂的双5连杆2自由度设计的合理性和可操作性。结果蒙特卡洛算法在MATLAB环境下得到的工作空间范围为:-650.4 mmx649 mm,163.8 mmy1 202 mm,-254.6 mmz829.8 mm,并成功完成16例猪的胆囊切除实验,平均操作时间为51 min。结论新型设计的双5连杆2自由度机械臂在猪体内成功完成胆囊切除等操作,且猪术后无其他不良症状,机械臂之间的运动无干涉,充分验证了所提出的微创手术机器人机械臂设计方案的可行性。     

腹主动脉瘤计算机仿真研究进展

腹主动脉瘤(abdominal aortic aneurysm,AAA)是腹主动脉较常见的疾病,破裂之后致死率极高,因此,及时发现和评估AAA破裂的风险就具有重要意义。近年来随着医学影像、计算机及血流动力学等理论和技术的快速发展,利用计算机模拟技术对AAA进行仿真研究已成为研究的热点,其模拟的结果趋于人体真实的动脉瘤,并在揭示AAA的发生及演变的机制方面发挥了重要作用。本文介绍了AAA仿真研究的原理及模型分类,详细地阐述了瘤体形态、瘤壁的结构及属性、血液及血流的属性、腔内血栓等相关因素在仿真研究中的作用,并对其目前的进展及局限性予以综述。     

数字病理扫描在颈动脉粥样硬化斑块组织学研究中的应用

目的颈动脉粥样硬化斑块的形成是脑血管病变的独立危险因素之一。对颈动脉内膜剥脱术(carotid endarterectomy,CEA)斑块进行充分的组织学判读和研究,将有助于全面把握CEA斑块的组织学表现,进而推进临床辅助诊断。方法本文我们将运用数字病理扫描仪对CEA斑块的切片经H&E染色后进行扫描,介绍数字病理扫描在CEA斑块组织学研究中的应用。结果经数字病理扫描所得的图片,有助于全面掌握和保存CEA斑块组织切片的全层面信息;在软件的帮助下有助于非常方便地测量斑块内各成分的大小;有助于精确评估斑块的狭窄程度。结论综上,数字病理成像应用于CEA斑块,结合MRI,有助于高效且准确地判读斑块组成和预测斑块稳定性,亦有助于人工智能的训练。     

Visible Light Controlled Polymerization of Azide‐Derived Monomers: A Facile,Metal‐Free PET‐ATRP Route to Construct Azide Polymers

Well‐defined azide polymers are successfully synthesized by visible‐light‐induced metal‐free electron transfer–atom transfer radical polymerization (PET‐ATRP) at room temperature. This technique uses Eosin Y/Et₃N as the reductive quenching photocatalyst system, which can effectively prevent the destruction of the azide group in polymerization. Four kinds of azide‐derived monomers participate well in this reaction and obtain satisfactory results. The kinetic behavior, “ON/OFF” experiment, and chain‐extension experiment confirm the living feature of this visible light controlled polymerization. Moreover, random copolymers obtained by this protocol can be used as surface modifier which further demonstrates the utility and reliability of this method.     

Adoptive transfer of IFN-γ-induced M-MDSCs promotes immune tolerance to allografts through iNOS pathway

Inflammation Research - Efficient production of monocytic myeloid-derived suppressor cells (M-MDSCs) with stable immunosuppressive function is crucial for immunomodulatory cell therapy for many...     

Novel missense mutation in VPS33B is associated with isolated low gamma‐glutamyltransferase cholestasis: Attenuated,incomplete phenotype of arthrogryposis,renal dysfunction,and cholestasis syndrome

The typical phenotype of arthrogryposis, renal dysfunction, and cholestasis (ARC) syndrome involves three cardinal symptoms as the name describes, harboring biallelic mutations on VPS33B or VIPAS39. Except for ARC syndrome, low gamma‐glutamyltransferase (GGT) cholestasis often implies hereditary hepatopathy of different severity; however, some remain undiagnosed. Several monogenic defects typically with multiorgan manifestations may only present liver dysfunction at times, such as DGUOK defect and AGL defect. Previously, four VPS33B mutated cases were reported without arthrogryposis, or with less severe symptoms and longer lifespan, indicating the possibility of incomplete ARC phenotype of isolated hepatopathy. So we retrospectively reviewed all patients with confirmed VPS33B/VIPARS39 defect in our center and identified three presenting isolated low‐GGT cholestasis with intractable pruritus. Distinguished from others with typical ARC phenotype, these patients did not suffer the other two typical characteristics, survived much longer, and shared a novel missense VPS33B variation c.1726T>C, p.Cys576Arg, causing declined protein expression and abolished interaction with VIPAS39 in‐vitro. Serum bile acid profiles of our VPS33B/VIPAS39 mutated patients revealed similar changes to primary defect of bile salt export pump, among which those with isolated cholestasis phenotype had a higher level of total secondary bile acids than that with typical ARC phenotype, indicating the partial residual function of VPS33B.     

Involvement of thromboxane A2 in interleukin-31-induced itch-associated response in mice

Background

Atopic dermatitis is a chronic and severe pruritic skin disease. Interlukin-31 (IL-31) has been recently demonstrated to be one of the key pruritogens in atopic dermatitis. However, the mechanisms underlying IL-31-induced itching remains unclear. In our previous study, we have shown that thromboxane (TX) A₂ is involved in itch-associated responses in mice with atopy-like skin diseases.

Regulation of cytochrome P450 gene expression by ketamine: a review

Introduction: Although used as an anesthetic drug for decades, ketamine appears to have garnered renewed interest due to its potential therapeutic uses in pain therapy, neurology, and psychiatry. Ketamine undergoes extensive oxidative metabolism by cytochrome P450 (CYP) enzymes. Considerable efforts have been expended to elucidate the ketamine-induced regulation of CYP gene expression. The safety profile of chronic ketamine administration is still unclear. Understanding how ketamine regulates CYP gene expression is clinically meaningful.

Areas covered: In this article, the authors provide a brief review of clinical applications of ketamine and its metabolism by CYP enzymes. We discuss the effects of ketamine on the regulation of CYP gene expression, exploring aspects of cytoskeletal remodeling, mitochondrial functions, and calcium homeostasis.

Expert opinion: Ketamine may inhibit CYP gene expression through inhibiting calcium signaling, decreasing ATP levels, producing excessive reactive oxygen species, and subsequently perturbing cytoskeletal dynamics. Further research is still needed to avoid possible ketamine–drug interactions during long-term use in the clinic.