滋肾续骨汤联合鲑鱼降钙素对老年椎体压缩性骨折术后血清骨形态发生蛋白9及血管内皮生长因子水平的影响

目的观察滋肾续骨汤联合鲑鱼降钙素对老年椎体压缩性骨折术后血清骨形态发生蛋白9(BMP9)及血管内皮生长因子(VEGF)水平的影响。方法将80例老年椎体压缩性骨折术后患者按照随机数字表法分为2组。对照组39例予鲑鱼降钙素治疗;治疗组41例在对照组治疗基础上加用滋肾续骨汤治疗。2组均治疗24周后统计临床疗效,并观察2组治疗前后血清BMP9、VEGF水平及疼痛视觉模拟评分(VAS)、胸腰椎损伤分类及损伤程度评分系统(TLICS)、Oswestry功能障碍指数(ODI)评分、日本骨科协会(JOA)腰痛评分,以及椎体前缘丢失高度、伤椎Cobb角、伤椎骨密度水平及并发症发生情况。结果治疗组总有效率95.12%(39/41),对照组总有效率76.92%(30/39),治疗组临床疗效优于对照组(P<0.05)。2组治疗后血清BMP9、VEGF水平均升高(P<0.05),且治疗组高于对照组(P<0.05)。2组治疗后疼痛VAS、TLICS评分均降低(P<0.05),且治疗组低于对照组(P<0.05)。治疗后2组ODI评分均降低(P<0.05),且治疗组低于对照组(P<0.05);治疗后2组JOA腰痛评分均升高(P<0.05),且治疗组高于对照组(P<0.05)。治疗后2组椎体前缘丢失高度、伤椎Cobb角均降低(P<0.05),伤椎骨密度均升高(P<0.05),且治疗组改善均优于对照组(P<0.05)。治疗组并发症总发生率4.88%(2/41),对照组并发症总发生率20.51%(8/39),治疗组并发症总发生率低于对照组(P<0.05)。结论滋肾续骨汤治疗老年椎体压缩性骨折术后患者疗效显著,可有效改善临床症状及血清BMP9、VEGF水平。     

B cell and B cell-related pathways for novel cancer treatments

B cells are recognized as the main effector cells of humoral immunity which suppress tumor progression by secreting immunoglobulins, promoting T cell response, and killing cancer cells directly. Given these properties, their anti-tumor immune response in the tumor micro-environment (TME) is of great interest. Although T cell-related immune responses have become a therapeutic target with the introduction of immune checkpoint inhibitors, not all patients benefit from these treatments. B cell and B cell-related pathways (CCL19, −21/CCR7 axis and CXCL13/CXCR5 axis) play key roles in activating immune response through humoral immunity and local immune activation via tertiary lymphoid structure (TLS) formation. However they have some protumorigenic works in the TME. Thus, a better understanding of B cell and B cell-related pathways is necessary to develop effective cancer control. In this review, we summarize recent evidences regarding the roles of B cell and B cell-related pathways in the TME and immune response and discuss their potential roles for novel cancer treatment strategies.     

口服硝酸盐对大鼠背部随意皮瓣的保护作用及机制探讨

目的 探讨口服硝酸盐对大鼠背部随意皮瓣的影响,以硝酸盐-亚硝酸盐-NO通路为切入点,探讨其可能的机制。方法 将24只雄性Wistar大鼠随机分为硝酸盐组、氯化钠组和对照组,每组8只。采用改良大鼠背部随意皮瓣制作方法造模。硝酸盐干预组在术前7 d及术后每天口服0.5 mmol/L硝酸钠,氯化钠组每天口服等量氯化钠,对照组每天口服蒸馏水。术后第7天,检测各组皮瓣的存活情况,大鼠血清中硝酸盐、亚硝酸盐、肿瘤坏死因子（tumor necrosis factor alpha,TNF-a）和白介素6（interleukin-6,IL-6）水平,以及皮瓣组织中超氧化物歧化酶（superoxide dismutase,SOD）和丙二醛（malondialdehyde,MDA）水平。采用SPSS 20.0软件包对数据进行t检验。结果 硝酸盐组皮瓣的存活面积显著高于对照组（P<0.05）。H-E染色显示,硝酸盐明显减轻了皮瓣的组织学损伤。硝酸钠显著增加了血清中硝酸盐和亚硝酸盐水平（P<0.05）,并显著下调血清中TNF-a和IL-6水平（P<0.05）。此外,硝酸盐组皮瓣组织内MDA表达显著减少（P<0.05）,SOD表达显著增加（P<0.05）。结论 口服硝酸盐可通过调控皮瓣的氧化应激和炎症反应保护皮瓣。     

糖尿病视网膜病变中视网膜内皮细胞功能障碍的研究进展北大核心

视网膜内皮细胞(REC)是参与糖尿病视网膜病变和许多眼部疾病的主要细胞类型之一。视网膜微血管系统有助于血-视网膜屏障的维持,这对正常的视功能至关重要。REC的改变在视网膜疾病的发生发展中起着关键作用。高血糖是糖尿病微血管损伤的重要原因,通过不同的机制导致REC功能障碍,包括向衰老表型改变、迁移和增殖能力增强、炎性凋亡等,最终导致无细胞毛细血管及病理性新生血管形成。本文对糖尿病视网膜病变中REC的功能障碍作一综述。     

Hiperplasia endotelial papilar intravascular (tumor Masson) de localización ginecológica

Intravascular papillary endothelial hyperplasia or Masson's tumour is a non-neoplastic vascular lesion of reactive character. It is a rare diagnosis, clinically non-specific and with diverse locations. It is essential to take it into consideration and make a differential diagnosis with malignant vascular tumours such as angiosarcoma. Pathological study is fundamental for diagnosis. Treatment consists of complete resection of the tumour, including sufficiently wide margins to avoid recurrence.The case reported is an exceptional event, because of the pelvic location of the Masson's tumour that was diagnosed as part of the surgical staging of an ovarian cancer.     

Single-dose combination nanovaccine induces both rapid and durable humoral immunity and toxin neutralizing antibody responses against Bacillus anthracis

Bacillus anthracis, the causative agent of anthrax, continues to be a prominent biological warfare and bioterrorism threat. Vaccination is likely to remain the most effective and user-friendly public health measure to counter this threat in the foreseeable future. The commercially available AVA BioThrax vaccine has a number of shortcomings where improvement would lead to a more practical and effective vaccine for use in the case of an exposure event. Identification of more effective adjuvants and novel delivery platforms is necessary to improve not only the effectiveness of the anthrax vaccine, but also enhance its shelf stability and ease-of-use. Polyanhydride particles have proven to be an effective platform at adjuvanting the vaccine-associated adaptive immune response as well as enhancing stability of encapsulated antigens. Another class of adjuvants, the STING pathway-targeting cyclic dinucleotides, have proven to be uniquely effective at inducing a beneficial inflammatory response that leads to the rapid induction of high titer antibodies post-vaccination capable of providing protection against bacterial pathogens. In this work, we evaluate the individual contributions of cyclic di-GMP (CDG), polyanhydride nanoparticles, and a combination thereof towards inducing neutralizing antibody (nAb) against the secreted protective antigen (PA) from B. anthracis. Our results show that the combination nanovaccine elicited rapid, high titer, and neutralizing IgG anti-PA antibody following single dose immunization that persisted for at least 108 DPI.     

Metabotropic glutamate receptors and nitric oxide in dopaminergic neurotoxicity

Dopaminergic neurotoxicity is characterized by damage and death of dopaminergic neurons. Parkinson's disease (PD) is a neurodegenerative disorder that primarily involves the loss of dopaminergic neurons in the substantia nigra. Therefore, the study of the mechanisms, as well as the search for new targets for the prevention and treatment of neurodegenerative diseases, is an important focus of modern neuroscience. PD is primarily caused by dysfunction of dopaminergic neurons; however, other neurotransmitter systems are also involved. Research reports have indicated that the glutamatergic system is involved in different pathological conditions, including dopaminergic neurotoxicity. Over the last two decades, the important functional interplay between dopaminergic and glutamatergic systems has stimulated interest in the possible role of metabotropic glutamate receptors (mGluRs) in the development of extrapyramidal disorders. However, the specific mechanisms driving these processes are presently unclear. The participation of the universal neuronal messenger nitric oxide (NO) in the mechanisms of dopaminergic neurotoxicity has attracted increased attention. The current paper aims to review the involvement of mGluRs and the contribution of NO to dopaminergic neurotoxicity. More precisely, we focused on studies conducted on the rotenone-induced PD model. This review is also an outline of our own results obtained using the method of electron paramagnetic resonance, which allows quantitation of NO radicals in brain structures.