穴位埋线调节变应性鼻炎大鼠鼻黏膜免疫微环境的研究

目的 通过动物实验验证穴位埋线治疗变应性鼻炎(AR)的疗效,并从鼻黏膜免疫微环境方面探讨其作用机制。 方法 将70只健康SPF级SD大鼠随机分为空白组、AR模型组、AR西药组、AR穴位假埋线组、AR穴位埋线组。造模方法采用改进后的卵蛋白注射及其鼻黏膜刺激法。除空白组外各组予以不同治疗方法,治疗末日在卵白蛋白激发后,观察30 min,观察大鼠AR症状,记录并比较各组大鼠鼻部症状评分,之后立即处死动物,采集大鼠鼻中隔黏膜,采用免疫组化方法检测鼻黏膜组织 TGF-β1、IL-17的表达情况。 结果 穴位埋线能明显缓解AR大鼠鼻部症状,如喷嚏、流涕、抓搔鼻部。与模型组比较,穴位埋线能降低鼻黏膜中TGF-β1、IL-17 含量。穴位假埋线也能降低AR大鼠鼻黏膜中TGF-β1含量。 结论 穴位埋线可降低AR大鼠鼻黏膜中TGF-β1、IL-17 含量,从而调节AR大鼠鼻黏膜免疫微环境。     

Is direction selectivity of cat area 17 cells always independent of contrast and dependent on short-distance interactions?

Summary In a study of area 17 of the paralysed and anesthetized cat it was found that for a small sub-group of cells with peripherally located receptive fields (11/123), the direction selectivity was critically dependent on the use of high contrast stimulation. By covering parts of the receptive field with a mask, it was found that in some cells the suppression of responses to movement in the non-preferred direction was due to the presence of a suppressive area located just outside the discharge region. Direction selective suppression was present only when a high contrast bar (light or dark) crossed this area before entering the discharge region.     

The effects of soybean isoflavones and 17β-estradiol in uterus and mammary glands of diabetic rat models

The objective of this study was to evaluate the action of soy isoflavones and 17 beta estradiol on the extracellular matrix in the uterus and mammary gland of diabetic rats. Sixty adult female rats underwent ovariectomy, then randomized into seven groups of ten animals each: Non-diabetic: GI Sham control animals ovariectomized; and GII control ovariectomized that received propylene glycol vehicle. Diabetic: GIII Sham control diabetic animals ovariectomized; GIV ovariectomized diabetic animals receiving propylene glycol vehicle; GV diabetic ovariectomized animals treated with soy isoflavones (150?mg/kg by gavage); GVI ovariectomized diabetic rats treated with estrogen (17b-estradiol, 10?mg/kg, subcutaneously); GVII diabetic ovariectomized animals treated with soy isoflavones (150 mg/kg by gavage), and with estrogen (17b-estradiol, 10 mg/kg combination therapy). Treatments occurred during 30 consecutive days. After animals euthanasia, a portion of the uterus was immersed in liquid nitrogen for molecular biology analysis, the other portion of uterus and mammary glands were removed and processed for paraffin embedding. Soy isoflavones (GV) and 17b estradiol improved the production of compounds of extracellular matrix, such as small leucine-rich proteoglycans (SLRPs). The combination of both therapies had an additive effect in SLRPs expression. Soy isoflavones contribute to the uterine integrity of SLRPs of diabetic rats.     

Two consecutive successful live birth in woman with 17α hydroxylase deficiency by frozen–thaw embryo transfer under hormone replacement endometrium preparation

17α-Hydroxylase deficiency is rare autosomal recessive disorder that manifested by hypertension, hypokalemia, delayed sexual development, primary amenorrhea and infertility. The information regarding infertility care and conception in women with this disorder are extremely limited. We report a 24-year-old Japanese woman with primary amenorrhea who was diagnosed as partial 17α-hydroxylase deficiency caused by homozygous 3?bp deletion in exon 1 of 17α-hydroxylase gene. In vitro fertilization with controlled ovarian stimulation was carried out and all viable embryo were frozen. During ovarian stimulation, serum progesterone levels were markedly elevated, and endometrial growth was impaired. Utilizing frozen-thaw embryo transfer under hormonal replacement (glucocorticoid, estradiol and progesterone), she had successfully given two consecutive live birth. Women with 17α-hydroxylase deficiency with residual ovarian reserve can afford reproductive success by appropriate diagnosis and treatment by assisted reproductive technology.     

Th17细胞的分化调控与自身免疫性疾病

Th17细胞是最近发现的一种在分化和功能上均不同于Th1和Th2的新型CD4＋T细胞亚群.该群细胞以主要分泌细胞因子IL-17而得名.IL-6、TGF-β、IL-21及IL-23等对Th17细胞的分化调控发挥重要作用.研究表明,Th17细胞可参与多种自身免疫性疾病的发生、发展与转归.     

Anti‐Aspergillus human host defence relies on type 1 T helper (Th1), rather than type 17 T helper (Th17), cellular immunity

Both interferon‐γ‐producing type 1 T helper (Th1)‐ and interleukin‐17 (IL‐17)‐producing Th17 cells have been proposed to be involved in anti‐fungal host defence. Although invasive aspergillosis is one of the most severe human fungal infections, little is known regarding the relative importance of the Th1 versus Th17 cellular immune pathways for the human anti‐Aspergillus host defence. Using human peripheral blood mononuclear cells and a system consisting of monocyte‐derived macrophages with lymphocytes, we found that Aspergillus fumigatus is a weak inducer of human IL‐17 but induces a strong Th1 response. These data were validated by the very low IL‐17 levels in bronchoalveolar lavage fluid and serum of patients with invasive aspergillosis. Surprisingly, live A. fumigatus reduced IL‐17 production induced by mitogenic stimuli. This effect was mediated through the propensity of A. fumigatus to metabolize tryptophan and release kynurenine, which modulates the inflammatory response through inhibition of IL‐17 production. In conclusion, A. fumigatus does not stimulate production of IL‐17 and human host defence against aspergillosis may not rely on potent Th17 responses.     

Th17 cells and their associated cytokines in liver diseases

T helper 17 (Th17) cells are a newly identified subset of T helper cells that play important roles in host defense against extracellular bacteria as well as in the pathogenesis of autoimmune disease. The functions of Th17 cells are mediated via the production of several cytokines including interleukin (IL)-17 and IL-22. Recent studies show that the frequency of IL-17⁺ cells is significantly elevated in a variety of chronic liver diseases including alcoholic liver disease, viral hepatitis and hepatocellular carcinoma. IL-17 receptor is expressed virtually on all types of liver cells, while IL-22 receptor expression is restricted to epithelial cells including hepatocytes in the liver. IL-17 seems to play an important role in inducing liver inflammation via stimulating multiple types of liver nonparenchymal cells to produce proinflammatory cytokines and chemokines, while IL-22 appears to be an important factor in promoting hepatocyte survival and proliferation.     

炎症性肠病患儿血清Th17相关细胞因子表达及其意义

目的　探讨儿童IBD患者血清中Th17相关细胞因子的表达水平及其临床意义。方法　收集2017年4月至2019年5月在西安交通大学附属儿童医院消化科住院治疗的儿童IBD患者40例,以同期21例非炎症性疾病儿童作为对照组。采集受检者血清标本,通过酶联免疫吸附试验检测白细胞介素-17A（IL-17A）、 IL-17F、 IL-21、 IL-22、 IL-25的表达水平。结果　IL-17A、 IL-17F、 IL-21和IL-22在溃疡性结肠炎（UC）及克罗恩病（CD）患儿血清中表达明显升高,IL-25明显降低（P＜0.05）;IL-17A、 IL-17F及IL-21血清水平与UC患儿疾病活动度呈正相关（P＜0.05）;IL-21在UC患儿血清中的表达与IL-17A和IL-17F的表达呈正相关（P＜0.05）。结论　Th17相关细胞因子在IBD患儿血清中表达失调,为进一步研究Th17细胞在儿童IBD中的作用提供了依据;IL-17A、 IL-17F、 IL-21血清水平与UC患儿疾病活动度呈正相关,表明其可能是Th17细胞触发儿童UC的重要促炎细胞因子。     

Sister chromatid exchange in normal and Ph1-positive leukemic cells after mitomycin-C treatment in vitro

The sister chromatid exchange (SCE) frequency was investigated in normal bone marrow and Ph1-positive cells of chronic myelocytic leukemia (CML) patients with and without mitomycin-C (MMC) treatment in vitro. Even though the spontaneous SCE frequency was found to be significantly lower in CML cells, the absolute SCE values after MMC treatment did not differ between leukemic and normal cells, and this seems to indicate an equilization of SCE rates. However, the fact that leukemic cells with lower spontaneous SCE rates need a further increase of SCE to reach values equal to those of normal cells might indicate a somewhat higher susceptibility of leukemic cells to DNA damage by MMC. This interpretation appears to be confirmed by the fact that the inhibition of cellular proliferation at higher MMC doses considerably reduced the number of leukemic cells that was able to divide twice during a given culture time.     

A monoclonal antibody that blocks class II histocompatibility-related immune interactions

Previous studies using conventional hetero- or isoantisera have indicated the involvement of class II (Ia) molecules in presentation of soluble by monocytes to inducer T lymphocytes, stimulation of inducer T cells in MLR, and recognition of Ia-bearing targets cells by cytotoxic T lymphocytes (CTL). The experience in using monoclonal anti-Ia reagents capable of blocking these phenomena in the human system is limited. Recently, however, we have characterized a lytic IgG2a monoclonal antibody, 9–49, that binds to functionally significant class II molecules. This antibody blocks (in the absence of complement): (1) specific binding of peripheral blood lymphocytes (PBL) to antigen-pulsed monocyte monolayers, (2) proliferation of PBL in response to soluble antigen (tetanus toxoid or mumps) or cell surface class II antigen stimulation in allogeneic or autologus MLR, (3) proliferation of cloned T4+ (inducer) lymphocyte cell lines to class II antigens, (4) generation of cytotoxic lymphocytes during allogenic MLR, and (5) recognition (and killing) of class II-bearing target cells by T4+ CTL clones. Proliferation and CTL activity of a T8+ clone is unaffected by the 9–49 antibody. These results indicate the usefulness of this monoclonal reagent in studies evaluating the functional role of Ia molecules in immune recognition phenomena.