Clinical,histological and immunophenotypic findings in a mare with a mammary lymphoma associated with anaemia and pruritus

An 18‐year‐old Quarter Horse mare presented with an 18 week history of dermatological lesions characterised by recurrent urticaria and recent signs of enlarged mammary glands, pyrexia, alopecia and intense pruritus. Haematological and serum biochemical analyses revealed anaemia, leucocytosis, thrombocytopenia and hyperfibrinogenaemia. Mammary discharge was evaluated and revealed neutrophilia. Cytological examinations of fine needle aspirates from the parotid lymph nodes were normal. Common causes of anaemia were ruled out by specific tests. The initial diagnosis was mastitis and 2 weeks later the animal returned to the hospital with worsening of clinical signs, intermittent fever, intense pruritus and generalised alopecia. Blood samples were collected for haematological and serum biochemical analyses, and the mammary gland and parotid lymph nodes were biopsied. Rectal palpation revealed a large irregular mass near the left kidney with adhesions of surrounding structures. The animal died before the laboratory results were ready. This report details the clinical, histological and immunophenotypic findings of a case of large lymphoma in a mare.     

K_(Ca)3.1通道与血管功能的研究进展

研究表明,在促进血管疾病发展的众多细胞类型中,如T细胞、B细胞、内皮细胞、成纤维细胞、巨噬细胞以及去分化的平滑肌细胞,KCa3.1都起到了一定的作用。生理上,KCa3.1已被证明在乙酰胆碱及内皮源性超极化因子(EDHF)介导下发生超极化,从而发挥控制血压的作用。病理上,KCa3.1异常则可导致血管平滑肌细胞增殖迁移。因此,从KCa3.1在内皮细胞及平滑肌细胞两方面对其作用作一总结,并对KCa3.1通道的研究进展进行综述。     

肠黏膜自然杀伤细胞的免疫功能及其调控

自然杀伤(NK)细胞是肠黏膜免疫屏障的重要组分。本文从NK细胞的发育学特征、分子表型切入,分析了其在维护肠道屏障完整性中发挥的功能,以及肠道微生物对其免疫功能的调节作用,旨在为疾病预防和肠道健康的营养调控提供理论依据。     

消化道上皮细胞中乳酸杆菌黏附配体蛋白含量的变化

利用兔抗鸡乳酸杆菌黏附配体蛋白血清,以不连续活性-PAGE电泳技术和间接ELISA方法,对不同日龄、健康和患球虫病鸡消化道不同部位乳酸杆菌黏附配体蛋白含量进行了检测。结果表明,2日龄鸡嗉囊部位产生乳酸杆菌黏附配体蛋白成分,D450nm值为0.181;1日龄鸡小肠部位产生乳酸杆菌黏附配体蛋白成分,D450nm值为0.168;5日龄乳酸杆菌黏附配体蛋白成分达到稳定,D450nm值分别为0.200和0.123。健康鸡体内嗉囊与小肠部位乳酸杆菌黏附配体蛋白含量比患球虫病鸡明显增多,D450nm值分别为：嗉囊,0.143和0.132;小肠,0.148和0.134。     

研究不同氨基酸模式对奶牛乳腺上皮细胞生长的影响

本试验以泌乳奶牛乳腺组织为原料,采用组织块培养技术,研究培养基内不同氨基酸模式对奶牛乳腺上皮细胞增殖的影响。结果表明,随着培养天数的增加,细胞数量逐渐增加,第10天各组细胞数量分别达到最高,乳腺上皮细胞生长曲线呈S形。不同氨基酸模式对乳腺细胞生长有显著影响,与氨基酸不平衡组相比,氨基酸平衡组、理想组更能促进细胞生长,各组间差异显著(P0.05)。     

Effect of Estradiol-17β on protein synthesis and degradation rates in fused bovine satellite cell cultures

Although androgenic and estrogenic steroids are widely used to enhance muscle growth and increase feed efficiency in feedlot cattle, their mechanism of action is not well understood. Further, in vivo studies indicate that estradiol (E2) affects muscle protein synthesis and/or degradation, but in vitro results are inconsistent. We have examined the effects of E2 treatment on protein synthesis and degradation rates in fused bovine satellite cell (BSC) cultures. Additionally, to learn more about the mechanisms involved in E2-enhanced muscle growth, we have examined the effects of compounds that interfere with binding of E2 or insulin-like growth factor (IGF)-1 to their respective receptors on E2-induced alterations in protein synthesis and degradation rates in BSC cultures. Treatment of fused BSC cultures with E2 results in a concentration-dependent increase (P < 0.05) in protein synthesis rate and a decrease (P < 0.05) in protein degradation rate. The pure estrogen antagonist ICI 182 780 suppresses (P < 0.05) E2-induced alterations in protein synthesis and degradation in fused BSC cultures. The G-protein coupled receptor (GPR)-30 agonist G1 does not affect either synthesis or degradation rate, which establishes that GPR30 does not play a role in E2-induced alterations in protein synthesis or degradation. JB1, a competitive inhibitor of IGF-1 binding to the Type 1 insulin-like growth factor receptor (IGFR-1), suppresses (P < 0.05) E2-induced alterations in protein synthesis and degradation. In summary, our data show that E2 treatment directly alters both protein synthesis and degradation rates in fused BSC cultures via mechanisms involving both the classical estrogen receptor (ER) and IGFR-1.     

乙酸钠对油酸诱导的BRL-3A细胞脂肪变性的影响及机制分析

通过向油酸诱导的大鼠肝成纤维细胞(BRL-3A)脂肪变性模型中添加不同浓度(2、4、8 mmol·L^-1)的乙酸钠,探讨其对脂肪变性细胞模型脂代谢的调控机理及细胞损伤的修复作用。试验方法：1)用不同浓度的油酸(0、0.03、0.06、0.12、0.24、0.48) mmol·L^-1刺激BRL-3A细胞24 h后,分别检测细胞相对活力、总脂滴面积、三酰甘油(TG)含量、天门冬氨酸氨基转移酶(AST)及丙氨酸氨基转移酶(ALT)活性,建立脂肪变性细胞模型;2)向BRL-3A细胞中添加不同浓度的乙酸钠,通过流式细胞术检测细胞凋亡率;3)用不同浓度的乙酸钠和0.12 mmol·L^-1油酸共同孵育BRL-3A细胞,试验分为4组,分别为油酸处理组、2 mmol·L^-1乙酸钠+油酸处理组、4 mmol·L^-1乙酸钠+油酸处理组和8 mmol·L^-1乙酸钠+油酸处理组,分别对细胞脂滴、TG含量、AST、ALT活性、AMPK信号通路蛋白以及脂代谢关键基因进行检测。结果显示:1)用0.12 mmol·L^-1油酸处理BRL-3A细胞24 h,成功建立BRL-3A细胞脂肪变性模型。2)不同浓度的乙酸钠对BRL-3A细胞凋亡率没有影响;3)4、8 mmol·L^-1乙酸钠处理脂肪变性细胞模型后,与油酸处理组相比,细胞总脂滴面积、每平方毫米脂滴数、TG含量、AST和ALT活性均显著(P<0.05)或极显著(P<0.01)下降,P-AMPK表达水平显著(P<0.05)或极显著(P<0.01)上升;脂合成代谢相关基因ACC、FAS以及SCD-1 mRNA表达水平均有一定程度下降;脂分解代谢相关基因CPT-1、CPT-2以及ACO mRNA表达水平均有一定程度上升。本研究表明,乙酸钠会通过AMPK通路激活脂分解代谢,减轻肝细胞脂质蓄积,并且对油酸诱导的BRL-3A细胞脂肪变性模型的损伤具有一定缓解作用。