Neuropathy in igMλ paraproteinemia

Summary In axonal neuropathies associated with IgM paraproteinemia, reports of antigen specificity of the M-protein are few. A patient with IgM paraproteinemia presented with progressive mononeuritis multiplex. IgM was found deposited in striking amounts in endoneurium and shown to bind specifically to neural proteins and chondroitin sulfates. Direct immune mechanisms, as well as the physical effects of IgM deposition, likely contributed to the development of the neuropathy.     

矿泉“851”对抗疟治疗的非特异性免疫作用

感染伯氏疟原虫(P.berghe ANKA株)小鼠,经矿泉“851”及与抗疟酮合用治疗后,腹腔巨噬细胞吞噬百分率和吞噬指数明显高于感染对照组(P<0.01)。两组药均能提高小鼠单核巨噬细胞系统(MPS)对碳微粒的廓清率,其K值与对照组相比,P<0.01,MPS活性的增强程度与其疟原虫的抑制率成正相关。     

Nanoparticle albumin-bound-paclitaxel: a limited improvement under the current therapeutic paradigm of pancreatic cancer

Nanoparticle albumin-bound (nab)-paclitaxel is paclitaxel linked to albumin nanoparticles, which makes it soluble and is an example of an application of nanotechnology for cancer treatment. The development of nanotechnology as a delivery system for nab-paclitaxel has improved the pharmacokinetics and pharmacodynamics of paclitaxel, in part by decreasing its hydrophobicity. Nab-paclitaxel in combination with gemcitabine has slightly improved survival in pancreatic cancer, compared to gemcitabine alone, as demonstrated in Phase III clinical trials. Cell cycle phase-specific drugs, such as nab-paclitaxel, which target cells in the G₂/M phase of the cell cycle, can only have limited efficacy since the vast majority of cells in a tumor are quiescent in G₀/G₁ phase. Recent advances in our laboratory on how to decoy cancer cells to cycle and then trap them in a sensitive phase of the cell cycle, can, in the hopefully near future, allow drugs such as nab-paclitaxel to have high efficacy, even in a treatment-resistant tumor such as pancreatic cancer.     

放射后鼻咽癌细胞株C666-1存活亚克隆高表达miR-181a

目的：：初步分析miR-181a与鼻咽癌细胞系C666-1放射敏感的相关性。方法：首先使用大剂量8 Gy的X射线照射C666-1,挑选三个大的存活亚克隆并命名为 C666-1-R1,C666-1-R2和 C666-1-R3,然后应用MTT等技术分析亚克隆及对照母本C666-1细胞系放射敏感性的差异,最后采用实时荧光定量PCR 法,分析三个存活亚克隆及对照C666-1的miR-181 a表达水平。结果：通过MTT比色法检测细胞增殖：6 Gy照射后,三个亚克隆C666-1-R1,C666-1-R2和C666-1-R3的细胞存活率均高于对照细胞C666-1,尤其C666-1-R2在48、72和96 h的存活率增高均有显著性差异(P<0.05),提示C666-1-R2具有放射抗拒性。另一方面,各亚克隆及对照细胞的 miR-181a 的2-△△Ct值如下：C666-1-R1=0.693,C666-1-R2=0.486,C666-1-R3=0.762,C666-1=1。提示放射后存活的三个亚克隆均高表达 miR-181a,尤其放射抗拒亚克隆C666-1-R2的 miR-181a表达更高。结论：miR-181a与鼻咽癌存活亚克隆的放射抗拒性密切相关。miR-181a可能是评估鼻咽癌放射敏感性的一个新分子,miR-181a 与鼻咽癌放射抗拒的相关性值得深入研究。     

CCMD—2—R精神分裂症诊断标准的临床应用与ICD—10、DSM—Ⅳ的比较

为了评价CCMD-2-R精神分裂症诊断标准与ICD-10、DSM-Ⅳ之间在临床应用中的一致性及其差异,检验CCMD-2-R的效度,本文选取50例临床诊断确定为“精神分裂症”的住院病人,通过SCAN检查与参阅住院病历相结合的方式收集病史,然后分别用CCMD-2-R、ICD-10、DSM-Ⅳ精神分裂症诊断标准去诊断,比较它们在框架内容、亚型诊断频度、亚型诊断符合率与症状标准内容方面的一致性。发现CCMD-2-R精神分裂症诊断标准与临床经验诊断、ICD-10之间有很好的一致性(K>0.75),与DSM-Ⅳ之间也有一定的一致性(K>0.40),提示CCMD-2-R精神分裂症诊断标准有良好的经验效度和平行效度。说明CCMD-2-R更加完善了我国精神分裂症诊断标准。     

李振华胃脘痛辨证规律探讨

胃脘痛,是以上腹胃脘部近心窝处发生疼痛的病证。它既是一个独立的病症,又是脾胃系多种疾病的一个症状。现代医学的急、慢性胃炎,胃、十二指肠溃疡病,胃痉挛,胃神经官能症,胃癌等以上腹胃脘部疼痛为主症者,均属中医学“胃脘痛”范畴。首批国家级名老中医李振华教授多年从事脾胃病的诊治和研究,尤其对胃脘痛的诊断,辨证审慎、要点明晰、机法圆活,且形成了付诸临床颇具效验的的辨证规律。本文以“十五”国家科技攻关计划“名老中医学术思想及经验传承研究”纵向课题“李振华学术思想及临证经验研究”及河南省新世纪优秀人才支持计划项目“名老…     

Prior in vitro exposure to GLP-1 with or without GIP can influence the subsequent beta cell responsiveness

Glucagon-like peptide-1 (7-36) amide (GLP-1) and glucose-dependent insulinotropic peptide (GIP) potentiate glucose-induced insulin release when present at the time of nutrient stimulation. This study examines whether they can also influence rat beta cell responsiveness to subsequent stimulations. When rat beta cells were cultured for 24 h with 1 nM GLP-1, they progressively desensitized to subsequent GLP-1 stimuli, as evidenced by cellular cAMP production. This GLP-1-induced desensitization did not occur when the incretin was only present during three periods of 1 h at 10 mM glucose that alternated with 6-9 h culture at 3 mM glucose. After these 24h, the beta cells exhibited the same secretory response to glucose (10 mM) and GLP-1 (10 nM at 10 mM glucose), whether GLP-1 was present during the pulses or not. Similarly the presence of 1 nM GIP during these one hour pulses did not influence subsequent secretory responses to glucose and GLP-1. However, when both GLP-1 and GIP, each at 0.5 nM, were added to the one hour pulses, they not only amplified insulin release during the pulses, as was the case with their single addition, but also increased the secretory response to a subsequent stimulation by glucose and GLP-1. These data distinguish between a desensitization effect of a prolonged exposure to GLP-1 and a positive priming effect of a discontinuous exposure to a combination of GLP-1 plus GIP. They may have to be taken into account in drug treatment strategies aiming the mimicking of physiologic patterns in the regulation of insulin release.