周围神经源性良性肿瘤的超声特性

目的通过分析周围神经源性良性肿瘤的超声特性,评价超声在周围神经源性良性肿瘤中的诊断作用。方法采用回顾性调查方法收集2000—2011年我院收治的有完整临床资料的良性周围神经肿瘤65例患者的术前超声检查、手术图片及病理检查结果,其中58例肿瘤患者同时包含彩色多普勒超声检查结果,由2位有丰富临床经验的超声影像医师对患者的术前超声图像进行回顾分析,评估肿瘤超声特性包括肿瘤的形状、大小、边界、包膜、内部回声特性、后方回声情况与周围神经的关系以及血流情况。结果本组65例良性周围神经源性肿瘤70处病变的超声检查结果显示42处病变(60%)为内部回声均匀的实质性低回声结构;28处病变(40%)为回声不均的低回声结构,其中18处(26%)病变为低回声结构内部可见高回声区,10处(14%)病变为低回声结构内部可见液性暗区;36处病变与知名周围神经相连。58例肿瘤彩色多普勒超声检查显示24例肿瘤(41%)有丰富血流信号,22例肿瘤(38%)有少量血流信号,12例(21%)肿瘤无血流信号。65例患者70处病变均行手术切除,术中见54处病变来源于知名的周围神经,16处病变位于肌肉内,无知名神经纤维连结。超声检查显示病变与神经相连的阳性率为67%(36/54)。65例肿瘤手术切除后病理检查结果显示,62例肿瘤为神经鞘膜瘤,2例为神经纤维瘤,1例为神经纤维瘤病。结论超声检查能提供良性神经源性肿瘤较详细的形态、内部结构、边界、包膜以及肿瘤与周围组织的关系的信息,还能显示肿瘤与周围神经的联系以及血流情况等,检查方便易行,检查费用低廉,患者易于接受。     

Evaluation of drugs for elimination of leukemic cells from the bone marrow of patients with acute leukemia

Relatively nonmyelotoxic drugs and drug combinations were investigated for their ability to eliminate malignant cells from human bone marrow. In vitro 90% inhibitory concentration (IC90) doses were established on granulocyte macrophage colony-forming units (GM-CFU) in culture of bone marrow by using the GM-CFU assay for the following drugs: 4- hydroperoxycyclophosphamide (4-HC), Adriamycin, L-asparaginase, bleomycin, hydrocortisone, VP-16, spirogermanium, Taxol, and vincristine. The leukemic cell kill efficiency of these drugs at IC90 doses was compared with that of 4-HC on acute lymphoid leukemia (ALL) cell lines by using the limiting-dilution assay. Under these conditions, no single drug was superior to 4-HC. To increase the in vitro effect in leukemic cell kill, combinations of vincristine with hydrocortisone, Adriamycin, VP-16, and 4-HC were investigated. Vincristine at 1 to 5 micrograms/mL increased the marrow cytotoxicity of hydrocortisone, Adriamycin, and VP-16, but it was protective (subadditive) with 4-HC. Vincristine and 4-HC in combination was additive to supraadditive on ALL cell lines, increased the leukemic cell kill by one to two logs above 4-HC alone at IC90 doses (P less than .05), and was not affected by the addition of excess marrow cells. The recommended doses for chemopurging in clinical studies are vincristine, 1 to 5 micrograms/mL, plus 4-HC, 5 micrograms/mL.     

甘草泻心汤治疗溃疡性结肠炎机制及临床研究进展

溃疡性结肠炎（UC）是一种慢性、非特异性炎症性肠病,病因与环境、遗传、感染和肠道微生物等多种因素相关。甘草泻心汤出自《伤寒论》,由炙甘草、黄芩、黄连、干姜、人参、半夏、大枣组成,具有调和寒热,消痞止利的功效。现代研究发现,甘草泻心汤单独或联合西药治疗UC具有显著疗效,其作用机制包括调节炎症因子、保护肠道黏膜和改善肠道菌群。通过查阅相关文献,对近年来甘草泻心汤及其单体治疗UC的相关机制与临床研究进行梳理与总结,以期为中医及中西医结合治疗UC提供理论依据并拓展治疗思路。     

Chromosome 7 long arm deletion in myeloid disorders: a narrow breakpoint region in 7q22 defined by molecular mapping

The involvement of the erythropoietin (EPO), plasminogen activator inhibitor type I (PAI1), and multi-drug resistance (MDR2) genes located in chromosomal region 7q21-22 was studied in patients with myeloid disorders and with or without a chromosome 7 abnormality. Separated blood mononuclear cells and granulocytes from 21 patients were used in restriction fragment length polymorphism (RFLP) studies with gene- specific DNA probes. A marked weakness of one of the allelic bands was observed in granulocyte-derived DNA from heterozygous patients with monosomy 7. In four patients with a partial deletion of chromosome 7 long arm (7q-), marked weakness of an allelic band was observed in granulocyte-derived DNA with PAI1 probe (four heterozygous patients) and MDR2 probe (one heterozygous patient), implying deletion of these genes. In contrast, the EPO gene was not deleted in these patients, as demonstrated by the presence of two allelic bands of equal strength in granulocyte-derived DNA (two patients) or by gene dosage estimation (two patients). Two allelic bands of equal strength were also observed in three heterozygous patients with an arbitrary probe (pKV13) located in 7cen-q21.3. Unexpected hemizygosity or hybridization bands were not observed in any patient. We conclude that PAI1 and MDR2 are located distally of EPO in 7q22, and that none of these genes is commonly rearranged in myeloid disorders. The chromosome 7 long arm deletion breakpoint is located in a relatively narrow segment between the PAI1 and EPO genes in different patients. The deletion may involve a specific site in DNA, since the genetic distance between the PAI1 and EPO genes is only 3 cM.