Recurrent ulcer after successful treatment with cimetidine or antacid

This study was designed to compare the rates of duodenal ulcer healing and recurrence after treatment with cimetidine or antacid. Patients with endoscopically documented duodenal ulcer received cimetidine, 1200 mg daily, or Mylanta II, 7 oz daily, in a randomized, double-blind trial. For the 69 patients in each group who completed the healing phase of the trial, endoscopic ulcer healing was almost identical. At 2, 4, and 6 wk, the cumulative percent healed on antacid was 33%, 64%, and 80%, and on cimetidine it was 25%, 62%, and 86%. The 114 patients with healed ulcer were observed on no therapy and underwent additional endoscopy to detect recurrences when symptomatic or at 3, 6, and 12 mo. There was no difference in the frequency of recurrences between treatments. At 3 and 6 mo, the cumulative percentages of patients with recurrence were 29% and 56% after antacid therapy and 36% and 55% after cimetidine therapy. Some patient variables were associated with delayed ulcer healing or ulcer recurrence. These included sex, pain frequency, smoking, disease duration, and acid secretion.     

A randomized study of high-dose cytarabine in induction in acute myeloid leukemia [see comments]

High-dose cytarabine (ara-c) may overcome cytarabine resistance in leukemic blasts. It has been used as a successful salvage and in postremission therapy but not as initial induction treatment. Patients aged 15 to 60 years, presenting with newly diagnosed acute myeloid leukemia (AML) were randomized to receive either high-dose cytarabine, 3 g/m2 12 hourly on days 1, 3, 5, and 7 for 8 doses, daunorubicin 50 mg/m2 days 1 to 3, etoposide 75 mg/m2 days 1 to 7, (HIDAC-3-7) or standard dose cytarabine 100 mg/m2 continuous intravenous infusion for 7 days with daunorubicin and etoposide at the same dose and schedule as above (7-3-7). Patients could receive a second or third induction course if complete remission (CR) was not achieved. All patients received the same postinduction consolidation therapy (5-2-5) for 2 courses. Eligible patients had no prior chemotherapy or myelodysplastic disease. Patients have been followed for a median of 4.5 years. Of 301 patients treated, complete response (CR) was achieved in 71% with HIDAC- 3-7 and 74% with 7-3-7. For patients in CR, the estimated median remission duration was 45 months with HIDAC-3-7 and 12 months with 7-3- 7 (P = .0005 univariate analysis, P = .0004 multivariate analysis). The estimated percentage of patients relapse free 5 years after achieving a CR was 49% on HIDAC-3-7 and 24% on 7-3-7. Patients in CR tended to survive longer with HIDAC-3-7 but there were no overall survival differences between the two arms. HIDAC-3-7 was associated with significantly more toxicity in induction with more leukopenia, thrombocytopenia, nausea, and vomiting and eye toxicity (all P < .001) but a similar incidence of severe central nervous system and cerebellar toxicity compared to 7-3-7. The consolidation treatment was the same in both arms but caused significantly more leukopenia and thrombocytopenia in patients previously treated with HIDAC-3-7 induction (P < .0001). We conclude that a dose-effect exists for cytarabine in AML and that HIDAC- 3-7 prolongs remission duration and disease-free survival and is tolerable when used as initial induction therapy in patients with de novo AML.     

A2 gene of Old World cutaneous <Emphasis Type="Italic">Leishmania</Emphasis> is a single highly conserved functional gene

Background  

Leishmaniases are among the most proteiform parasitic infections in humans ranging from unapparent to cutaneous, mucocutaneous or visceral diseases. The various clinical issues depend on complex and still poorly understood mechanisms where both host and parasite factors are interacting. Among the candidate factors of parasite virulence are the A2 genes, a family of multiple genes that are developmentally expressed in species of the Leishmania donovani group responsible for visceral diseases (VL). By contrast, in L. major determining cutaneous infections (CL) we showed that A2 genes are present in a truncated form only. Furthermore, the A2 genomic sequences of L. major were considered subsequently to represent non-expressed pseudogenes [1]. Consequently, it was suggested that the structural and functional properties of A2 genes could play a role in the differential tropism of CL and VL leishmanias. On this basis, it was of importance to determine whether the observed structural/functional particularities of the L. major A2 genes were shared by other CL Leishmania, therefore representing a proper characteristic of CL A2 genes as opposed to those of VL isolates.     

Platelet-melanoma cell interaction is mediated by the glycoprotein IIb- IIIa complex

A human malignant melanoma cell line (M3Dau) was observed by electron microscopy to interact directly with human platelets and induced platelet aggregation. Fab fragments of a monoclonal antibody MoAb (LYP18), directed against the platelet glycoprotein (GP) IIb-IIIa complex, inhibited platelet-melanoma interactions and platelet-platelet aggregation. M3Dau melanoma cells bind LYP 18 and synthesize IIb-IIIa- like GPs. When the melanoma cells were preincubated with LYP 18, tumor- platelet interaction did not occur, suggesting that the interaction may be mediated by the IIb-IIIa-like GPs present on the melanoma cell surface. Glanzmann's thrombasthenic platelets, lacking GPIIb and IIIa, did not interact with melanoma cells, indicating that the platelet GPIIb-IIIa complex is also necessary for the platelet-melanoma cell interaction. This work demonstrates the importance of the IIb-IIIa-like GPs, present on M3Dau melanoma cells, in mediating tumor-platelet interactions.     

Metabolic activity of phagocytosing granulocytes in chronic granulocytic leukemia: ultrastructural observation of a degranulation defect

The functional capacities of granulocytes in patients with chronic granulocytic leukemia are still a subject of controversy, probably due to the heterogeneity of the abnormalities observed from patient to patient. For a better definition of these abnormalities, 14 patients with untreated chronic granulocytic leukemia were studied. The patients were divided into three groups on the basis of the functional activities of their phagocytosing granulocytes. In four patients (group I), the granulocytes were normal in respect to particle ingestion, nitroblue tetrazolium (NBT)-stimulated reduction, cyanide-insensitive oxygen (O2) consumption, superoxide anion (O2-)-stimulated production, hydrogen peroxide (H2O2) production, and iodination. They also had a normal myeloperoxidase (MPO) content. In four patients (group III), the granulocytes were significantly defective in all of these activities. In the six remaining patients (group II), all the initial metabolic steps of the phagocytosing granulocytes (ingestion, NBT reduction, O2 consumption, O2-production, H2O2 production) were normal, as were the MPO content of the granulocytes, while iodination was strikingly decreased. These metabolic features suggested a degranulation defect which was observed ultrastructurally in the only patient studied among these six. The phagocytosing granulocytes of this patient did not degranulate and no deposits of MPO activity were seen in the phagosomes.     

TCR gamma delta bearing lymphocyte clones with lymphokine-activated killer activity against autologous leukemic cells

Activated T lymphocytes with the T-cell receptor (TCR) gamma delta (CD3+ and TCR delta 1+) exhibit strong cytotoxic activity against the standard natural killer (NK) and lymphokine-activated killer (LAK) sensitive target cells. In order to test the cytotoxic activity of gamma delta T lymphocytes against autologous leukemic cells, 84 clones of gamma delta T lymphocytes were obtained from the peripheral blood of three acute lymphoblastic leukemia (ALL) patients. Forty-four of these T-cell clones were active against an LAK-sensitive cell line and the other 40 were active against K562, an NK target cell line. In each of the three patients, cytotoxic clones against autologous leukemic cells were obtained. Among the 84 clones, ten were able to kill autologous tumor cells, including eight that lyse the LAK-sensitive target and two with NK activity. The clones were highly cytotoxic, stable, and easily expanded in large quantity.     

图形翻转视觉诱发电位在视神经管减压后视神经损伤不同时期的变化特征

目的:观察视神经损伤动物模型在损伤后和不同时期视神经管减压后视觉诱发电位的变化,了解创伤性视神经损伤的手术时机与疗效的关系。方法:实验于2005-03/05在解放军南京军区南京总医院动物实验中心完成。①实验分组:30只新西兰白兔随机分为正常对照组、术后2d减压组、术后7d减压组、术后14d减压组、术后不减压组,每组6只。②造模:除正常对照组外,其余各组在视神经孔中塞入一细端为2mm直径的圆锥软硅胶,阻塞视神经孔,造成视神经的挤压伤。③指标检测:采用图形翻转视觉诱发电位检测损伤前、损伤后1h、减压前1h、减压后2周视功能变化,记录NPN曲线主波(P波)的绝对潜伏期、绝对波幅。正常对照组仅采集一组数据作为对照。结果:30只实验动物均进入结果分析。①正常对照组家兔图形翻转视觉诱发电位检查均引出典型NPN波型曲线,视神经挤压伤后1hNPN波形低阔扁平,P波潜伏期延长,波幅降低。②P波潜伏期:术后2d减压组减压后短于减压前[(71.25±8.51),(86.47±14.28)ms,P<0.05];术后7d减压组减压前后比较差异无显著性(P>0.05);术后14d减压组减压后明显长于减压前[(158.73±15.16),(116.35±17.13)ms,P<0.05]。术后2d减压组和术后7d减压组短于术后不减压组(P<0.01)。术后7,14d减压组和术后不减压组明显长于正常对照组(P<0.01)。③P波波幅:术后2d减压组减压后高于减压前[(5.25±0.78),(4.42±0.42)μV,P<0.05]。术后2d减压组减压后低于术后7d减压组、术后14d减压组(P<0.01),术后14d减压组低于术后7d减压组(P<0.05);术后7d减压组、术后14d减压组、术后不减压组低于正常对照组(P<0.01)。结论:神经元继发性损伤是视功能进行性下降的重要原因,视神经减压术有利于减轻视神经间接损伤,较早期(损伤后48h以内)减压可阻止轴突继发性损伤,避免视功能进一步下降,并在一定程度上逆转视功能的损害。     

三维CT评估发育性髋关节脱位的骨性形态学特征

目的:通过使用CT三维测量髋臼发育情况及髋臼对股骨头覆盖率对比性观察,整体反映髋臼发育情况。方法:①观察对象:选择2003-06/2005-04对41例发育性髋关节脱位患者55个髋关节。其中男12例,女29例;年龄18个月～6岁。患髋右侧23例,左侧32例,其中双侧12例。健康侧27髋。患儿家属均知情同意。②实验方法:所有患儿使用PQ6000型多层螺旋CT扫描,扫描数据进行骨组织三维重建。将测量数据制成图表,显示三维的髋臼发育情况,并量化表示髋臼的缺损情况。③实验评估:计算不同截面正常侧髋臼指数、中心边缘角(假设符合正态分布)的均数、标准差、分布范围及95%可信区间。观察发育性髋关节脱位术前术后骨骼形态学变化。分别在术前、术后测量患者患侧髋臼指数、中心边缘角和前倾角,测量值均分别与正常值进行对比。结果:患侧55个髋,健康侧27髋,均进入结果分析。①发育性髋关节脱位术前术后骨骼形态学变化:术前55侧发育性髋关节脱位髋关节脱位程度为,参照T"nnis分类方法,Ⅰ度5髋(9.1%),Ⅱ度11髋(20%),Ⅲ度32髋(58.2%),Ⅳ度7髋(12.7%)。术后患者均表现髋臼α角均>90°,头臼呈同心圆对位,Shenton线连续,股骨头较术前明显发育,原先未出现头骺的患者,出现头骺,但较正常仍偏小;髋臼口呈类圆形,髋臼边缘欠光滑,髋臼整体呈一定程度前倾。②术前术后髋臼指数、中心边缘角和前倾角变化对比:术后患者的髋臼指数和前倾角与正常对照组之间差异无显著性(P>0.05),术后患者的中心边缘角大于正常对照组[(33.4±2.6)°(29.1±2.0)°,P<0.01],术后患者的髋臼指数和前倾角测量值均小于术前(P<0.01)。结论:介绍了一种对髋臼形态测量的新方法,它能够全面反映髋臼的发育情况,不但增加了对中心边缘髋臼病理改变的认识程度,还为手术提供了精确的可信度较高的矫形设计方案。