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681.
682.
目的 通过观察FeCl2皮层注射致损伤性癫痫(PTE)模型大鼠海马、额叶突触蛋白P38的表达变化.探讨突触可塑性在PTE发病机制中的作用. 方法 健康成年雄性SD大鼠采用随机数字表法分为正常对照组(n=5)、假手术组(n=12)、模型组(n=20).采取立体定向皮层注射FeCl2(0.1 moL/L,10μL)建立PTE模型,假手术组注入等量生理盐水,正常对照组不做处理.观察各组大鼠EEG的变化并应用免疫组织化学方法 检测大鼠造模后不同时间点(1 h、7 d、14 d、30 d)海马、额叶P38的表达. 结果大多数模型组大鼠在注射FeCl2后不久记录到癫痫样放电;与假手术组比较,模型组不同时间点右侧额叶P38表达减少.差异有统计学意义(P<0.05);与正常对照组和假手术组比较,致痫1h后,CA3区多形层、辐射层、腔隙层和齿状回(DG)分子层P38表达均无明显变化,7 d后P38表达增加,维持到30d,差异均有统计学意义(P<0.05). 结论 与突触蛋白P38表达相关的突触可塑性变化在PTE的发病机制中可能起重要作用. 相似文献
683.
Recent clinical and laboratory studies have shown that the effects of naltrexone for alcoholism may be moderated by the Asn40Asp single-nucleotide polymorphism (SNP) of the μ-opioid receptor gene (OPRM1). Allele frequencies for this polymorphism, however, have been shown to vary substantially as a function of ethnic background, such that individuals of Asian descent are more likely to carry the minor (Asp40) allele. The objective of this study is to test the naltrexone pharmacogenetic effects of the Asn40Asp SNP in a sample of Asian Americans. This study consists of a double-blinded, randomized, placebo-controlled laboratory trial of naltrexone. Participants (n=35, 10 females; 13 Asn40Asn and 22 Asp40 carriers) were non-treatment-seeking heavy drinkers recruited from the community. After taking naltrexone or placebo, participants completed an intravenous alcohol administration session. The primary outcome measures were subjective intoxication and alcohol craving. Results suggested that Asp40 carriers experienced greater alcohol-induced sedation, subjective intoxication, and lower alcohol craving on naltrexone, as compared to placebo, and to Asn40 homozygotes. There results were maintained when controlling for ALDH2 (rs671) and ADH1B (rs1229984) markers and when examining the three levels of OPRM1 genotype, thereby supporting an OPRM1 gene dose response. These findings provide a much-needed extension of previous studies of naltrexone pharmacogenetics to individuals of Asian descent, an ethnic group more likely to express the minor allele putatively associated with improved biobehavioral and clinical response to this medication. These findings help further delineate the biobehavioral mechanisms of naltrexone and its pharmacogenetics. 相似文献
684.
目的 应用网络药理学分析金藤清痹颗粒治疗急性痛风性关节炎(acute gouty arthritis,AGA)的作用机制,并建立AGA大鼠模型进行验证。方法 在清热解毒、活血止痛治法指导下,通过TCMSP数据库搜集金藤清痹颗粒的活性成分及靶点,利用GeneCards、NCBI数据库等搜集AGA相关靶点,与金藤清痹颗粒作用靶点整合后,构建共有靶点蛋白质-蛋白质相互作用(protein-protein interaction,PPI)网络和“金藤清痹颗粒-中药-活性成分-靶点-AGA”网络,并进行基因本体(gene ontology,GO)功能及京都基因与基因组百科全书(Kyoto encyclopedia of genes and genomes,KEGG)通路富集分析。雄性SD大鼠随机分为空白组、模型组、秋水仙碱(0.3 mg/kg)组和金藤清痹颗粒低、中、高剂量(1.05、2.10、4.20 g/kg)组,每组6只,踝关节注射单钠尿酸盐(monosodium urate,MSU)晶体建立AGA大鼠模型。采用游标卡尺测量大鼠踝关节直径,计算踝关节肿胀度;采用全自动生化仪检测血清尿酸(serum uric acid,SUA)、C反应蛋白(C-reactive protein,CRP)水平;采用苏木素-伊红(HE)染色观察踝关节组织病理变化;采用qRT-PCR、ELISA和Western blotting检测踝关节组织及血清中关键靶点和信号通路的表达。结果 共检索到金藤清痹颗粒110种活性成分、212个作用靶点,272个AGA治疗靶点,共有靶点29个,关键靶点有白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子(tumor necrosis factor,TNF)及IL-6,涉及TNF信号通路、IL-17信号通路和NOD样受体信号通路等。大鼠踝关节注射MSU晶体后明显肿胀(P<0.01),SUA及CRP显著升高(P<0.05、0.01),滑膜组织增生明显、结构紊乱,有大量炎症细胞浸润,NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)、NIMA相关蛋白激酶7(NIMA-related kinases 7,NEK7)、凋亡相关斑点样蛋白(apoptosis-associated speck-like protein containing a CARD,ASC)、半胱氨酸天冬氨酸蛋白酶-1(cystein-asparate protease-1,Caspase-1)、消皮素D(gasdermin D,GSDMD)、IL-18、IL-1β、IL-6及TNF-α表达水平明显升高(P<0.01);秋水仙碱或金藤清痹颗粒治疗后,有效缓解踝关节肿胀(P<0.05、0.01),SUA及CRP均显著降低(P<0.05、0.01),关节滑膜增生、炎症细胞浸润均得到改善,同时显著抑制IL-1β、TNF-α及IL-6等靶点和NOD样受体信号通路的表达(P<0.05、0.01)。结论 金藤清痹颗粒对AGA大鼠具有明显的保护作用,其机制可能与抑制NOD样受体信号通路的异常激活,降低炎症因子水平,改善关节滑膜增生、炎症细胞浸润有关。 相似文献
685.
Fabrizio Romano Marisa Molinaro Susanne Schibli Philipp KA Agyeman Ruth Mari Lllgen 《Clinical Case Reports》2021,9(8)
Jaundice should be considered as a first clinical sign preceding severe invasive bacterial infection or sepsis in patients of all ages including childhood and adolescence. Early laboratory investigations and MR imaging studies for osteomyelitis or myositis are paramount to avoid progression to life‐threatening sepsis and significant morbidity and mortality. 相似文献
686.
687.
James R. Berenson Daisy Martinez Tahmineh Safaie Ralph Boccia Honghao Yang Mehdi Moezi Stephen Lim Gary Schwartz Shahrooz Eshaghian Regina Swift Benjamin M. Eades Sean Bujarski Bernard Regidor Clara Kim Susanna Kim Robert Vescio 《British journal of haematology》2023,200(6):722-730
Although Janus kinase (JAK) inhibitors have demonstrated efficacy for treating autoimmune disorders and myeloproliferative neoplasms, their efficacy in treating other types of cancer has not been clearly demonstrated. We evaluated oral ruxolitinib (15 mg twice daily) with oral methylprednisolone (40 mg every other day) for multiple myeloma (MM) patients with progressive disease who had received a proteasome inhibitor, lenalidomide, glucocorticosteroids and three or more prior regimens. All of the planned 29 patients had been enrolled with follow-up until 28 April 2022. Median lines of prior therapy were 6 (range 3–12). Cytogenetics and fluorescent in situ hybridization were evaluable in 28 patients; 9 (32%) and 17 (70%) patients showed high-risk cytogenetics and/or 1q+, respectively. The overall response rate was 31%. The median duration of response was 13.1 (range 2.8–22.0) months. Median progression-free survival rate was 3.4 (range 0.5–24.6) months, Overall, the treatment was well tolerated. The combination of ruxolitinib and methylprednisolone demonstrated significant clinical activity among previously heavily-treated MM patients, and responses were achieved among patients who had high-risk cytogenetics. This is the first clinical study to show activity of JAK inhibitors in combination with steroids for MM patients and expands the potential use of these drugs to those with cancers other than myeloproliferative neoplasms. 相似文献
688.