田基黄对大鼠呼吸道及全身免疫功能的影响

目的 :研究田基黄对大鼠呼吸道及全身免疫功能的影响。方法 :将雄性重 2 0 0～ 2 5 0 g Wistar大鼠随机分成对照组与实验组 (每组 n =10 ) ,应用免疫学细胞技术 ,对大鼠呼吸道及全身免疫功能各项指标进行检测。结果 :田基黄能明显提高外周血中性粒细胞 (PMN)吞噬率 (75 .2± 3.9,83.5± 5 .1,P <0 .0 0 1)及 T淋巴细胞百分率 (6 4.8± 5 .4,72 .2± 3.1,P <0 .0 0 1) ;提高支气管肺泡灌洗液 (BAL F)中 T淋巴细胞百分率 (6 0 .4± 6 .3,6 8.8± 6 .5 ,P <0 .0 1) ;对外周血白细胞移行抑制指数 (MI) (0 .45 5± 0 .15 6 ,0 .439± 0 .148,P >0 .0 5 )及肺泡巨噬细胞 (AM)吞噬率 (4 1.8± 5 .8,48.2± 9.5 ,P >0 .0 5 )无明显影响。结论 :田基黄能提高大鼠全身的特异性和非特异性细胞免疫功能 ;对呼吸道局部免疫功能也有一定影响     

APP17肽对卵巢去势大鼠海马神经元凋亡相关因子表达的影响

为研究卵巢去势大鼠海马神经元内凋亡相关因子Fas、Fas L、NFκB、c fos、c Jun的表达及APP1 7肽对这些因子表达的影响 ,将健康雌性Wistar大鼠行双侧卵巢切除手术造模 ,并用APP1 7肽治疗 ,分别用免疫组化方法观察Fas、Fas L、NFκB、c fos、c Jun的表达 ,用TUNEL方法检测神经元的凋亡。结果发现 :卵巢去势大鼠海马神经元Fas、Fas L、c fos、c Jun的表达增高 ,而NFκB的表达则减少 ;使用APP1 7肽治疗后 ,上述蛋白质的表达恢复到正常水平 ,TUNEL检测未发现凋亡神经元。提示卵巢去势大鼠发生了海马神经元的凋亡相关蛋白的改变 ,可能是神经元处于凋亡前状态 ;APP1 7肽可改善卵巢去势大鼠海马神经元内凋亡相关蛋白的表达 ,维持神经元的正常功能     

Effect of l-carnitine supplementation on renal anemia in patients on hemodialysis: a meta-analysis

International Urology and Nephrology - l-carnitine is an amino acid derivative that is thought to be helpful for treating renal anemia in hemodialysis patients. However, the mechanism remains to be...     

小儿肾小球疾病血清微量元素测定与分析

采用原子吸收分光光度法,测定了７８ 例肾小球疾病患儿血清铜、锌、铁、镁４ 种元素。结果显示,单纯性肾病组、肾炎性肾病组、紫癜性肾病组及肾炎组血清锌均显著低于正常组（ Ｐ＜ ００５）,血清铁、镁与正常组比较无显著差异。单纯性肾病组,肾炎性肾病组血清铜显著低于正常组（ Ｐ＜ ００５）。提示血清铜、锌、铁、镁含量的变化与疾病发生和疾病状态有关。     

肾病综合征、肾小球肾炎患儿血清铜、锌、铁、镁与血清蛋白质的测定与分析

采用原子吸收分光光度法,测定50 例肾病综合征患儿、28 例肾小球肾炎患儿血清铜、锌、铁、镁元素,并探讨这些元素与上述疾病的相互关系。结果显示,肾病综合征组和肾小球肾炎组血清锌均极显著低于正常组( P< 0-01) ,血清铁、镁与正常组比较无显著性差异,血清锌浓度与血清白蛋白、球蛋白含量呈显著正相关。肾病综合征组血清铜极显著低于正常组(P< 0-01) ,肾小球肾炎组血清铜与正常组比较无显著差异,血清铜浓度与血清白蛋白、球蛋白含量呈显著正相关。提示这些变化与疾病的发生和疾病状态有关     

UFH-001 cells: A novel triple negative,CAIX-positive,human breast cancer model system

Human cell lines are an important resource for research, and are often used as in vitro models of human diseases. In response to the mandate that all cells should be authenticated, we discovered that the MDA-MB-231 cells that were in use in our lab, did not validate based on the alleles of 9 different markers (STR Profile). We had been using this line as a model of triple negative breast cancer (TNBC) that has the ability to form tumors in immuno-compromised mice. Based on marker analysis, these cells most closely resembled the MCF10A line, which are a near diploid and normal mammary epithelial line. Yet, the original cells express carbonic anhydrase IX (CAIX) both constitutively and in response to hypoxia and are features that likely drive the aggressive nature of these cells. Thus, we sought to sub-purify CAIX-expressing cells using Fluorescence Activated Cell Sorting (FACS). These studies have revealed a new line of cells that we have name UFH-001, which have the TNBC phenotype, are positive for CAIX expression, both constitutively and in response to hypoxia, and behave aggressively in vivo. These cells may be useful for exploring mechanisms that underlie progression, migration, and metastasis of this phenotype. In addition, constitutive expression of CAIX allows its evaluation as a therapeutic target, both in vivo and in vitro.     

Discovery of structure-based small molecular inhibitor of αB-crystallin against basal-like/triple-negative breast cancer development in vitro and in vivo

αB-crystallin (CRYAB) is present at a high frequency in poor prognosis basal-like breast tumours, which are largely absent of oestrogen, progesterone receptors and HER2 known as triple-negative breast cancer (TNBC). CRYAB functions as a molecular chaperone to bind to and correct intracellular misfolded/unfolded proteins such as vascular endothelial growth factor (VEGF), preventing non-specific protein aggregations under the influence of the tumour microenvironment stress and/or anti-cancer treatments including bevacizumab therapy. Directly targeting CRYAB can sensitize tumour cells to chemotherapeutic agents and decrease tumour aggressiveness. However, growing evidence shows that CRYAB is a critical adaptive response element after ischemic heart disease and stroke, implying that directly targeting CRYAB might cause serious unwanted side effects. Here, we used structure-based molecular docking of CRYAB and identified a potent small molecular inhibitor, NCI-41356, which can strongly block the interaction between CRYAB and VEGF₁₆₅ without affecting CRYAB levels. The disruption of the interaction between CRYAB and VEGF₁₆₅ elicits in vitro anti-tumour cell proliferation and invasive effects through the down-regulation of VEGF signalling in the breast cancer cells. The observed in vitro anti-tumour angiogenesis of endothelial cells might be attributed to the down-regulation of paracrine VEGF signalling in the breast cancer cells after treatment with NCI-41356. Intraperitoneal injection of NCI-41356 greatly inhibits the tumour growth and vasculature development in in vivo human breast cancer xenograft models. Our findings provide ‘proof-of-concept’ for the development of highly specific structure-based alternative targeted therapy for the prevention and/or treatment of TNBC.     

Therapeutic effects of induced pluripotent stem cells in chimeric mice with β-thalassemia

Although β-thalassemia is one of the most common human genetic diseases, there is still no effective treatment other than bone marrow transplantation. Induced pluripotent stem cells have been considered good candidates for the future repair or replacement of malfunctioning organs. As a basis for developing transgenic induced pluripotent stem cell therapies for thalassemia, β⁶⁵⁴ induced pluripotent stem cells from a β⁶⁵⁴ -thalassemia mouse transduced with the normal human β-globin gene, and the induced pluripotent stem cells with an erythroid-expressing reporter GFP were used to produce chimeric mice. Using these chimera models, we investigated changes in various pathological indices including hematologic parameters and tissue pathology. Our data showed that when the chimerism of β⁶⁵⁴ induced pluripotent stem cells with the normal human β-globin gene in β⁶⁵⁴ mice is over 30%, the pathology of anemia appeared to be reversed, while chimerism ranging from 8% to 16% provided little improvement in the typical β-thalassemia phenotype. Effective alleviation of thalassemia-related phenotypes was observed when chimerism with the induced pluripotent stem cells owning the erythroid-expressing reporter GFP in β⁶⁵⁴ mouse was greater than 10%. Thus, 10% or more expression of the exogenous normal β-globin gene reduces the degree of anemia in our β-thalassemia mouse model, whereas treatment with β⁶⁵⁴ induced pluripotent stem cells which had the normal human β-globin gene had stable therapeutic effects but in a more dose-dependent manner.     

Cerebrospinal fluid and serum prolactin in systemic lupus erythematosus with and without central nervous system involvement

Aim: Recent research has shown that prolactin (PRL) may participate in the pathogenesis of systemic lupus erythematosus (SLE), and hyperprolactinemia may be related to disease activity. The current study investigated both serum and cerebrospinal fluid (CSF) PRL in SLE patients and their possible relationship to central nervous system (CNS) involvement. Methods: Prolactin levels were determined by immunoradiometric assay. Serum PRL levels were detected in 80 patients with SLE and 25 matched healthy controls. Disease activity was scored by SLEDAI. CSF PRL levels were detected in 7 cases of CNS‐involved SLE, eight cases of non‐CNS‐involved inactive SLE and eight cases of non‐SLE CNS disorders. Results: Hyperprolactinemia was present in 40% of SLE patients. Serum PRL levels were significantly correlated with SLEDAI scores. There was no significant difference of serum PRL levels between SLE patients with or without CNS involvement, but the mean CSF PRL levels were higher in CNS‐involved SLE patients than in non‐CNS‐involved SLE and non‐SLE patients. There was no significant correlation between serum and CSF PRL levels. Conclusions: Our results suggest that high serum PRL levels correlate with active disease in SLE, but not with CNS involvement. CSF PRL levels in SLE patients correlate with CNS involvement, which indicates that CSF PRL may be involved in the pathogenesis of CNS‐SLE.     

河南“4.26”60Co源辐射事故一例受照者患非霍奇金淋巴瘤的病因探讨

关于电离辐射是否可诱发非霍奇金淋巴瘤（NHL）,目前的研究结果尚未获得一致结论。笔者报道了河南“4.26” 60Co源辐射事故中1例中度骨髓型急性放射病患者受照后第13年患NHL的病例,结合患者的受照史、病史特点、诊断及国际多项大型研究,从流行病学资料和影响因素两方面分析了患者“天”患非霍奇金淋巴瘤与电离辐射的关系,为电离辐射致NHL提供辐射流行病学依据。