乳腺癌中郑氏植物蛋白的表达及其与Her-2基因扩增的关系

目的检测郑氏植物蛋白片段(Zheng’s plant protein segment,ZPPS)在乳腺癌中的表达,探讨其临床病理联系及其与Her-2基因表达的相关性。方法应用免疫组化SP法检测51例乳腺癌与23例正常乳腺组织中ZPPS的表达;应用FISH技术检测Her-2基因在乳腺癌中的表达。结果正常乳腺组织中,8例ZPPS呈阳性表达,阳性率为34.78%;乳腺癌组织中,38例ZPPS呈阳性表达,阳性率为74.51%,二者表达差异有统计学意义(P<0.05)。51例乳腺癌中Her-2基因扩增率为39.22%,ZPPS阳性表达与FISH检测Her-2基因扩增呈负相关(P<0.05)。ZPPS的表达与淋巴结转移呈负相关(P<0.05)。结论标记ZPPS对乳腺癌的诊断及判定淋巴结转移具有实用价值。因在乳腺癌中ZPPS的表达与Her-2基因扩增呈负相关,所以临床病理工作中可选择ZPPS阴性病例进行FISH检测,从而减少盲目进行FISH基因扩增和Herceptin分子靶向治疗的病例。     

高脂饮食诱发胰岛素抵抗大鼠模型的建立与评价

目的建立饮食性胰岛素抵抗大鼠模型及评价方法。方法高脂饲料喂养不同年龄和体质量Wistar大鼠,4周后检测血糖、血脂、游离脂肪酸和胰岛素水平并行高胰岛素-正葡萄糖钳夹实验。结果青年高脂组较青年对照组、老年对照组较老年高脂组相比,高脂喂养大鼠体质量虽有所增加,但差异无统计学意义(P均>0.05)。青年高脂组与青年对照组、老年高脂组与老年对照组、老年对照组与青年对照组及老年高脂组与青年高脂组相比,血清总胆固醇、血清甘油三酯及空腹胰岛素升高,空腹血糖升高,葡萄糖输注率下降,有显著性差异(P<0.05或0.01)。结论高脂饲料喂养青年和老年大鼠,均可成功建立胰岛素抵抗大鼠模型,钳夹实验用于胰岛素抵抗大鼠模型的评价更准确、可靠。年龄和体质量因素与胰岛素抵抗有关。     

井穴针刺配合教育训练治疗重度智力低下儿童的临床研究

ObjectiveTo observe clinical efficacy of acupuncture at Jing-well point combined with educational training for the treatment of children with severe mental retardation.MethodsSixty children with severe mental retardation were randomly divided into jing-well point acupuncture plus simple special education and language training group (group A) and simple special education and language training group (group B) with 30 child patients in each group according to registration order. All the patients were treated once every other day, 10 times as a course of treatment. There were 20 days of interval between each course of treatment. Curative effect was analyzed after 3 courses of treatment. Gesell Developmental Scale test was conducted for all children before and after treatment. Development quotient at the functional area of social adaptability, large motor, fine motor, language skill and social behavior of individuals was recorded and compared between groups and before and after treatment to evaluate the curative effect.ResultsSocial adaptability and fine motor of children were improved in the group B after treatment. And in the group A, social adaptability, fine motor, language skill and social behavior of individuals were improved after treatment. Meanwhile, the group A was superior to the group B in curative effect of overall social adaptability and language skill (both P<0.05). The overall response rate in group B was 23.3% (7/30) and in group A was 46.6% (14/30, P<0.05).ConclusionAcupuncture at jing-well point combined with educational training can effectively improve the intelligence level of children with severe mental retardation and its curative effect is better than that of simply education and training.     

股总动脉医源性损伤1例

临床资料患者男,72岁。主因突发右足疼痛、发凉2 d入院。查体:右足皮色苍白,未见青紫发花,双下肢皮温低,以右下肢为甚,左股动脉搏动良好,左腘动脉搏动弱,右股动脉搏动弱,右腘动脉、双侧足背动脉及胫后动脉未触及搏动。     

The role of nerve fibers and their neurotransmitters in regulating intervertebral disc degeneration

Intervertebral disc degeneration (IVDD) has been the major contributor to chronic lower back pain (LBP). Abnormal apoptosis, senescence, and pyroptosis of IVD cells, extracellular matrix (ECM) degradation, and infiltration of immune cells are the major molecular alternations during IVDD. Changes at tissue level frequently occur at advanced IVD tissue. Ectopic ingrowth of nerves within inner annulus fibrosus (AF) and nucleus pulposus (NP) tissue has been considered as the primary cause for LBP. Innervation at IVD tissue mainly included sensory and sympathetic nerves, and many markers for these two types of nerves have been detected since 1940. In fact, in osteoarthritis (OA), beyond pain transmission, the direct regulation of neuropeptides on functions of chondrocytes have attracted researchers’ great attention recently. Many physical and pathological similarities between joint and IVD have shed us the light on the neurogenic mechanism involved in IVDD. Here, an overview of the advances in the nervous system within IVD tissue will be performed, with a discussion on in the role of nerve fibers and their neurotransmitters in regulating IVDD. We hope this review can attract more research interest to address neuromodulation and IVDD itself, which will enhance our understanding of the contribution of neuromodulation to the structural changes within IVD tissue and inflammatory responses and will help identify novel therapeutic targets and enable the effective treatment of IVDD disease.     

原发丘脑区生殖细胞瘤1例

病例男,18岁,主因视物成双2月,无明显诱因出现右侧肢体麻木、无力1周入院。查体：神清语利,复视,视力无明显下降,双瞳孔正大等圆,双侧对光反射灵敏,双侧视野无偏盲。右侧肢体轻瘫,右侧肢体肌张力增高,右侧踝阵挛阳性。影像学检查：CT平扫：左侧丘脑区可见一大小约为3.5 cm×3.1 cm×4.1 cm的类圆形稍高密度肿块影,边界清楚,     

IL-10 ameliorates PM2.5-induced lung injury by activating the AMPK/SIRT1/PGC-1α pathway

Exposure to fine particulate matter with a diameter ≤2.5 μm (PM2.5) can cause a number of respiratory diseases. However, there is currently no safe treatment for PM2.5-induced lung damage. This study investigated the protective effect of IL-10 against lung injury and the possible involvement of AMPK/SIRT1/PGC-1α signaling. The mean diameter, particle size distribution, and zeta potential of PM2.5 samples were assessed using a Zetasizer Nano ZS90 analyzer. Thereafter, Wistar rats were exposed to PM2.5 (1.8, 5.4, or 16.2 mg/kg) alone or high-dose PM2.5 with recombinant rat IL-10 (rrIL-10; 5 μg/rat). Treatment with rrIL-10 ameliorated PM2.5-induced acute lung injury, reduced mitochondrial damage, and inhibited inflammation, oxidative stress, and apoptosis in the PM2.5-treated rats. Moreover, the mRNA and protein expression of AMPK, SIRT1, and PGC-1α were upregulated by rrIL-10 treatment. In conclusion, rrIL-10 protected lung tissues against PM2.5-induced inflammation by reducing oxidative stress and apoptosis via activating AMPK/SIRT1/PGC-1α signaling.     

髂静脉闭塞、髂股动静脉瘘合并下肢动脉硬化闭塞症1例

1 临床资料 患者女,68岁.主因左下肢间歇水肿伴足部胀痛半年,于2019年4月23日就诊于我院.查体:左下腹可见腹壁浅静脉,左下肢肿胀,以小腿为著,足靴区可见明显色素沉着,皮肤张力高,左侧足背及胫后动脉未触及搏动,左下肢肌力4级,右下肢查体未见明显阳性体征.入院后查D-二聚体为:1.22 mg/L FEU,余检验结果...     

苏拉明防治兔外伤性增生性玻璃体视网膜病变的研究

目的研究生长因子抑制剂苏拉明对外伤性增生性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)玻璃体中生长因子的影响及防治作用。方法将40只健康新西兰大白兔随机平均分为5组,除空白组外,其余均制备外伤性PVR模型。然后分别将生理盐水(0.1mL)和浓度分别为40g.L-1、60g.L-1和80g.L-1苏拉明(0.1mL)注入模型组和实验1、2、3组玻璃体腔内,空白组不进行注射。对眼底连续观察28d并对PVR进行分级,采用双抗夹心ELISA法和放射免疫方法分别检测玻璃体液中肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)和表皮生长因子(epidermal growth factor,EGF)的含量。结果造模后第28天,空白组、模型组及实验1、2、3组玻璃体腔中TNF-α含量分别为(0.245±0.346)μg.L-1、(3.984±0.302)μg.L-1、(3.024±0.163)μg.L-1、(2.038±0.239)μg.L-1、(1.285±0.151)μg.L-1;EGF含量分别为(0.180±0.385)μg.L-1、(1.025±0.092)μg.L-1、(0.540±0.073)μg.L-1、(0.274±0.069)μg.L-1、(0.242±0.322)μg.L-1。实验1、2、3组和空白组玻璃体腔中TNF-α和EGF含量均低于模型组,差异均有显著统计学意义(均为P<0.01)。实验1、2、3组玻璃体腔中TNF-α的含量均高于空白组,差异均有统计学意义(P<0.01或P<0.05)。实验1组玻璃体腔中EGF的含量高于空白组,差异有显著统计学意义(P<0.01)。实验2、3组玻璃体腔中EGF的含量与空白组比较,差异无统计学意义(P>0.05)。实验2、3组玻璃体腔中TNF-α和EGF含量均低于实验1组,差异均有统计学意义(均为P<0.05)。形态学上未发现明显视网膜毒副作用。结论苏拉明玻璃体腔注射安全有效,通过降低玻璃体中细胞因子TNF-α和EGF的含量,有效抑制了兔外伤性PVR的发展,为以后临床应用提供可靠的理论依据。     

Control of peroxyntrite -induced production of inducible nitric oxide synthase isoforms and antagonism of cholecystokinin octapeptide-8 in retinal pigment epithelial cells in vivo

· AIM: To explore if peroxyntrite (ONOO-) induced iNOS via Fas/ Fas/L pathway in diabetic rats and the effection of cholecystokinin octapeptide-8 (CCK-8) as therapeutic agent for decrease diabetic retinopathy. · METHODS: Thirty-six rats were taken as control group, seventy two were given (streptozotocin) STZ (45mg/kg) and then divided into ONOO-group and CCK-8 group (peritoneal injection CCK-8). STZ-induced diabetic rats were treated with CCK-8 for 60 days. Western blotting analysis, DNA ladder, RT-PCR, immunohistochemistry and flow cytometry were used for determining the expression of nitrotyrosine (NT, the foot print of ONOO-); apoptosis and inducible nitric oxide synthase (iNOS) mRNA as well as Fas/Fasl signal transduction in RPE cells. · RESULTS: Both RPE cells in ONOO- and CCK-8 group developed apoptosis and expressed NT, iNOS mRNA and Fas/Fasl. But latter delayed the all changes in a time-dependent manner compared with control and ONOO- group (P<0.001). iNOS and Fas/Fasl were up-regulated and associated with an increase of expression of ONOO-in vivo. · CONCLUSION: The study suggested that apoptosis of RPE was partly induced by ONOO- may be the new way of oxidative damage to the RPE cells. CCK-8 decreased RPE cells apoptosis partly induced by ONOO- and is a potential drug for therapy of diabetic retinopathy. The mechanism of CCK-8 dealing with RPE cells may be related to its direct inhibition of the formation of iNOS to produce ONOO- and antagnism of damage of ONOO- to RPE cells. ·