三氧化二砷对骨髓增生异常综合征粒单系细胞体外作用的研究

为了探讨三氧化二砷（Ａｓ２Ｏ３）对骨髓增生异常综合征（ＭＤＳ）粒单系细胞的体外作用,用半固体、液体培养及ＡＰＡＡＰ法检测不同浓度Ａｓ２Ｏ３对２４例ＭＤＳ患ＣＦＵ－ＧＭ和ＣＤ３３,ＣＤ１５,ｂｃｌ－２表达的影响,结果发现,Ａｓ２Ｏ３随着浓度的增加对ＣＦＵ－ＧＭ的抑制作用增强;０．３８８μｍｏｌ／Ｌ时对丛的抑制大于集落,其中低危组７０．７８％对３４．０５％,高危组８６．７６％对６５．８６％（Ｐ〈０．０１）;０．１９４μｍｏｌ－Ｌ时使低危组丛减少,而使集落增加,高危组丛减少,集落不变。高浓度（１．９４μｍｏｌ／Ｌ）时ＣＤ３３与ＣＤ１５表达降低,ｂｃｌ－２表达减少,细胞出现核染色质固缩,低浓度（０．１９４μｍｏｌ／Ｌ）时低危组ＣＤ３３减少,ＣＤ１５增加,高危组ＣＤ３３减少,ＣＤ１５不变,ｂｃｌ－２减少,且出现上述细胞     

“神农33”注射液治疗急性肾衰34例疗效观察

目的：观察中药“神农33”注射液（简称“神农33”）治疗急性肾功能衰竭（ARF）的疗效及作用机理。方法：将64例急性肾功能衰竭病人随机分为治疗组（Ⅰ组）和对照组（Ⅱ组）,Ⅰ组在西医综合治疗基础上加用“神农33”静脉点滴,Ⅱ组仅采用西医综合治疗。结果：有效率Ⅰ组为91.18%,Ⅱ组为73.33%,两组差异显著（P〈0.05）。血肌酐（Scr）、尿素氮（BUN）恢复正常所需治疗时间,两组差异极显著（P〈0.01）。少尿总时间、治疗后少尿持续时间、尿蛋白转阴时间以及血液透析平均次数,两组差异显著（P〈0.05）。结论：“神农33”注射液对于急性肾功能衰竭具有良好的治疗作用。     

解整合素-金属蛋白酶33基因T1位点多态性与哮喘相关性研究

目的 探讨解整合素-金属蛋白酶33(ADAM33)基因中的T1位点不同基因型及等位基因的分布频率,与支气管哮喘及血浆IgE水平的相关性.方法 对122例陕西关中地区汉族哮喘儿童(哮喘组)及137例对照儿童(对照组)应用聚合酶链反应结合限制性片段长度多态性(PCR-RFLP)方法检测位点多态性;通过ELISA法检测血浆IgE水平.结果 与对照组相比,哮喘组血浆总IgE水平显著上升(P ＜ 0.001).在该地区儿童中只检测到T1位点的2种基因型(TT和CT),哮喘组2种基因型的分布频率分别为85.2%和14.8%,对照组分别为86.1%和13.9%,两组分布频率差异无统计学意义(χ2 ＝ 0.041,P ＞ 0.05);哮喘组的T等位基因和C等位基因频率分别为92.6%、7.4%,对照组分别为93.1%、6.9%,两组分布差异也无统计学意义(χ2 ＝ 0.038,P ＞ 0.05).259例(包括对照组和哮喘组)样本和122例哮喘样本的血浆IgE水平在不同基因型均无差异.结论 在陕西关中地区汉族儿童中,ADAM33基因T1位点基因多态性与哮喘不相关,也不影响血浆IgE水平.     

DIFF33H参与TRAIL诱导的人Jurkat T淋巴细胞白血病细胞凋亡调控

目的：研究DIFF33H在人T淋巴细胞白血病细胞Jurkat凋亡中的表达规律及其生物学功能。方法：采用PCR扩增DIFF33H cDNA，Northern blot分析DIFF33H的mRNA表达，MTT法测定细胞凋亡。结果：在重组可溶性TRAIL诱导的人T淋巴细胞白血病细胞Jurkat凋亡过程中，DIFF33H mRNA的表达水平随着Jurkat细胞的凋亡而下降，并对重组可溶性TRAIL的作用具有浓度和时间的依赖性。在抗肿瘤药物5-FU诱导肿瘤细胞凋亡过程中，DIFF33H的mRNA表达水平也显著下降。结论：DIFF33H参与人T淋巴细胞白血病细胞Jurkat凋亡的调控。     

Plasma adiponectin response to acute exercise in healthy subjects

Adipose tissue secretes adiponectin, an adipocytokine that is involved in the regulation of insulin sensitivity. Following acute exercise, insulin sensitivity has been shown to increase. Increased adiponectin following exercise may be related to the change in insulin sensitivity. The purpose of the present study was to characterize the effect of a single cycle exercise session on adiponectin and to compare the exercise effects between healthy male and female subjects. Plasma concentrations of adiponectin, tissue necrosis factor-alpha (TNF-), insulin, glucose, and leptin were assessed before and immediately after a 60-minute stationary cycle ergometry session at 65% of O_2max. Male and female subjects were matched for cardiorespiratory fitness and body composition and dietary intake was controlled for the three days prior to the exercise trial. At rest, adiponectin concentration was not associated with percentage body fat, body mass index (BMI), fitness, or resting plasma variables (P>0.05). Following exercise, neither male nor female subjects exhibited changes in adiponectin or leptin concentrations (P>0.05). TNF- exhibited a time main effect increase with exercise (P<0.05), but there were no gender differences. These results suggest that plasma adiponectin concentrations do not change with exercise in healthy male or female subjects. Results are given as mean (SE).     

DFNB79: reincarnation of a nonsyndromic deafness locus on chromosome 9q34.3

Genetic analysis of an inbred Pakistani family PKDF280, segregating prelingual severe to profound sensorineural hearing loss, provided evidence for a DFNB locus on human chromosome 9q34.3. Co-segregation of the deafness trait with marker D9SH159 was determined by a two-point linkage analysis (LOD score 9.43 at θ=0). Two additional large families, PKDF517 and PKDF741, co-segregate recessive deafness with markers linked to the same interval. Haplotype analyses of these three families refined the interval to 3.84 Mb defined by D9S1818 (centromeric) and D9SH6 (telomeric). This interval overlaps with the previously reported DFNB33 locus whose chromosomal map position has been recently revised and assigned to a new position on chromosome 10p11.23–q21.1. The nonsyndromic deafness locus on chromosome 9q segregating in family PKDF280 was designated DFNB79. We are currently screening the 113 candidate DFNB79 genes for mutations and have excluded CACNA1B, EDF1, PTGDS, EHMT1, QSOX2, NOTCH1, MIR126 and MIR602.     

Loss of heterozygosity at 9q32-33 (DBC1 locus) in primary non-invasive papillary urothelial neoplasm of low malignant potential and low-grade urothelial carcinoma of the bladder and their associated normal urothelium

Tumour recurrence has a major impact on patients with non-invasive papillary urothelial tumours of the bladder. To explore the role of DBC1 (deleted in bladder cancer 1 locus), a candidate tumour suppressor gene located at 9q32-33, as prognostic marker we have performed loss of heterozygosity (LOH) testing in 49 patients with primary papillary urothelial tumours and associated normal urothelium. Data from the 38 tumours and 11 specimens of normal urothelium that were informative in the LOH study (D9S195 marker) showed that LOH in urothelium (45.4%) but not in non-invasive tumours (60.5%) was associated with tumour recurrence (p = 0.026) but not to grade or progression. Also, tumours whose normal urothelium had LOH were larger (p = 0.020) and showed cyclin D1 over-expression (p = 0.032). Non-significant increased expression of p53, p21Waf1, apoptotic index and tumour proliferation, and decreased expression of p27Kip1 or cyclin D3 also characterized tumours whose normal urothelium had LOH. The expression of these G1-S modulators, apoptotic index and tumour proliferation was more heterogeneous in papillary urothelial tumours, irrespective of having retained heterozygosity or LOH. Also, Bax expression decreased in papillary urothelial tumours having LOH (p = 0.0473), but Bcl-2 was unrelated to LOH status. In addition, FGFR3 protein expression decreased in LOH tumours (p = 0.036) and in those having LOH in their normal urothelium (p = 0.022). FGFR3 immunohistochemical expression was validated by western blot in selected cases. The survival analysis selected LOH in normal urothelium as a marker of disease-free survival (log-rank 5.32, p = 0.021), progression-free survival (log-rank 3.97, p = 0.046) and overall survival (log-rank 4.26, p = 0.038); LOH in tumours was significant in progression-free survival (log-rank 3.83, p = 0.042). It is concluded that LOH at the DBC1 locus in normal urothelium seems to be relevant in the prognosis of non-invasive papillary tumours of the bladder via selecting cases with increased proliferation, frequent alterations of the G1-S phase modulators, and decreased FGFR3 protein expression.     

IL-1, IL-18, and IL-33 families of cytokines

Summary: The interleukin-1 (IL-1), IL-18, and IL-33 families of cytokines are related by mechanism of origin, receptor structure, and signal transduction pathways utilized. All three cytokines are synthesized as precursor molecules and cleaved by the enzyme caspase-1 before or during release from the cell. The NALP-3 inflammasome is of crucial importance in generating active caspase-1. The IL-1 family contains two agonists, IL-1α and IL-1β, a specific inhibitor, IL-1 receptor antagonist (IL-1Ra), and two receptors, the biologically active type IL-1R and inactive type II IL-1R. Both IL-1RI and IL-33R utilize the same interacting accessory protein (IL-1RAcP). The balance between IL-1 and IL-1Ra is important in preventing disease in various organs, and excess production of IL-1 has been implicated in many human diseases. The IL-18 family also contains a specific inhibitor, the IL-18-binding protein (IL-18BP), which binds IL-18 in the fluid phase. The IL-18 receptor is similar to the IL-1 receptor complex, including a single ligand-binding chain and a different interacting accessory protein. IL-18 provides an important link between the innate and adaptive immune responses. Newly described IL-33 binds to the orphan IL-1 family receptor T1/ST2 and stimulates T-helper 2 responses as well as mast cells.     

IL-33及其受体ST2在炎症性肠病中免疫调节作用的研究新进展

IL-33是近年来发现的一种IL-1家族的细胞因子,其受体为ST2.IL-33具有双重作用,既能作为分泌性细胞因子,参与调节Th2型免疫应答,诱导前炎性因子的表达,又能作为核因子,定位于细胞核内,起抑制转录作用,阻遏前炎性基因表达.在慢性炎症性肠病(IBD)患者的肠道组织中可查到该细胞因子的表达.研究IL-33及ST2受体有助于进一步了解IBD发病机制,寻找治疗IBD的新靶点.