Development of multifocal duodenal erosions after anti-Helicobacter pylori triple therapy.

BACKGROUND AND PURPOSE: Anti-Helicobacter pylori triple therapy is effective for healing duodenal ulcer (DU) diseases and reducing disease recurrence. However, multifocal duodenal erosions or shallow ulcers may develop after triple therapy. The purpose of this study was to investigate the incidence and outcome of duodenal erosions that developed after triple therapy. METHODS: A total of 106 Taiwanese with active DU and with H. pylori infection were enrolled in this study. All patients received anti-H. pylori triple therapy (i.e., 2 weeks of antimicrobial agents combined with treatment for 4 to 6 weeks with acid suppression agents). Follow-up endoscopy was performed immediately after stopping treatment. The incidence of multifocal erosions or shallow ulcers over the bulb and/or second portion of the duodenum was studied. Additional acid suppression agent was given for 4 weeks whenever duodenal erosions or shallow ulcers were found. RESULTS: Out of 106 patients, 11 (10.4%) were found to have multifocal duodenal erosions and/or shallow ulcers on the duodenal bulb and/or second portion of the duodenum at the end of treatment. Ten of the 11 patients with newly developed erosions had healed DU in the S1 or S2 stage, and all 11 had successful H. pylori eradication. The duodenal erosions and/or shallow ulcers of these 11 patients were healed after an additional 4 weeks of histamine-2-receptor antagonist therapy. CONCLUSIONS: Multifocal duodenal erosions and/or shallow ulcers were noted in around 10% of Taiwanese DU patients who received anti-H. pylori triple therapy. An additional 4 weeks therapy with acid suppression agents healed these lesions.     

Suppressive effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the high-affinity antibody response in C57BL/6 mice.

In the humoral immune response to an invasion of foreign antigens, B cells differentiate into low-affinity antibody-forming cells (AFCs) that mainly secrete IgM or, through germinal center (GC) formation, into high-affinity AFCs that secrete IgG-class antibodies with a higher affinity for the antigen. Previous studies have established the suppressive effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on low-affinity antibody responses to antigens. However, whether and how TCDD affects the high-affinity antibody response to antigens has not yet been clarified. In this paper we investigate the effects of TCDD on GC formation, high-affinity AFC generation, and high-affinity antibody production in the primary humoral immune response. C57BL/6 mice were orally administered 0 or 20 microg/kg of TCDD and subsequently immunized with alum-precipitated ovalbumin (OVA) on day 0. Then the GC formation in the spleen and OVA-specific antibodies in the plasma, was evaluated until day 14 postimmunization. TCDD exposure reduced the production of OVA-specific IgG1 on days 10 and 14. GC formation in the spleen was also suppressed by TCDD exposure, and the suppression persisted from day 7 until day 14. In TCDD-administered mice, on day 7, cellular proliferation in the GCs was significantly suppressed, although apoptosis was not markedly affected. In order to measure high-affinity antibody and high-affinity AFCs, the mice were administered TCDD followed by immunization with alum-precipitated (4-hydroxy-3-nitrophenyl) acetyl linked to chicken gamma-globulin (NP-CG). The frequency of high-affinity NP-specific AFCs that bind to low-haptenated antigen was clearly shown to be reduced in the spleen on days 10 and 14. Furthermore, the high-affinity anti-NP IgG1 levels on days 10 and 14 postimmunization were significantly reduced by TCDD exposure. Taken together, the results of this paper demonstrate that TCDD exposure inhibits the generation of high-affinity AFCs and high-affinity antibody production during the primary humoral immune response and suggest that these alterations were caused by the suppression of antigen-responding B-cell proliferation induced by TCDD during GC formation.     

Anti-inflammatory effect of methoxyphenamine compound in rat model of chronic obstructive pulmonary disease

AIM: To evaluate the anti-inflammatory effect of methoxyphenamine compound (MC) on chronic obstructive pulmonary disease (COPD) in rats by measurement of proinflammatory cytokines, total and differential white cell counts (WCC) of bronchroalveolar lavage fluid (BALF). METHODS: Adult rat model of COPD (COPD group) was induced by intratracheal instillation of lipopolysaccharides and exposure to cigarette smoke. Treatment groups received different dosage of MC (3, 9, and 27 mg daily, MC group) or prednisone (0.25 mg daily, P group) respectively. Tumor necrosis factor alpha (TNF-α), interleukin 1beta (IL-113), interleukin-6 (IL-6), transforming growth factor β (TGF-β) of BALF were determined by ELISA. Total and differential WCC were performed after Giemsa staining. RESULTS: The levels of TNF-α, IL-1β, IL-6, TGF-β, total and differential WCC in BALF of MC groups were significantly decreased than that of COPD group (P<0.01), and there was no significant difference among MC groups. There was no significa     

Possible dominant-negative mutation of the SHIP gene in acute myeloid leukemia.

The SH2 domain-containing inositol 5'-phosphatase (SHIP) is crucial in hematopoietic development. To evaluate the possible tumor suppressor role of the SHIP gene in myeloid leukemogenesis, we examined primary leukemia cells from 30 acute myeloid leukemia (AML) patients, together with eight myeloid leukemia cell lines. A somatic mutation at codon 684, replacing Val with Glu, was detected in one patient, lying within the signature motif 2, which is the phosphatase active site. The results of an in vitro inositol 5'-phosphatase assay revealed that the mutation reduced catalytic activity of SHIP. Leukemia cells with the mutation showed enhanced Akt phosphorylation following IL-3 stimulation. K562 cells transfected with the mutated SHIP-V684E cDNA showed a growth advantage even at lower serum concentrations and resistance to apoptosis induced by serum deprivation and exposure to etoposide. These results suggest a possible role of the mutated SHIP gene in the development of acute leukemia and chemotherapy resistance through the deregulation of the phosphatidylinositol-3,4,5-triphosphate (PI(3,4,5)P3)/Akt signaling pathway. This is the first report of a mutation in the SHIP gene in any given human cancer, and indicates the need for more attention to be paid to this gene with respect to cancer pathogenesis.     

跨声门癌50例观察

为确立一种原发喉室的跨声门癌，选择肿瘤主体以喉室为中心经全喉切除手术的标本５０例，火棉胶包埋，连续切片观察。结果发现①跨声门癌的肿瘤原发部位在喉室，５０例中有Ｔ２３例。②肿瘤以深层浸润为主占９０％（４５／５０），易侵及声门旁间隙（８２％，４１／５０）和甲状软骨（６４％，３２／５０），临床分期与病理分期不符达４８％（２４／５０）。结论：原发喉室的跨声门癌是声门上型癌的一种特殊类型。     

新生儿窒息综合评分法的临床研究

探讨新生儿窒息的评分方法，为新生儿窒息的诊断提供可靠依据。方法随机选择100例正常儿和138例窒息儿作为研究对象。在Apgar评分基础上，经反复筛选提出9项参数作为新生儿窒息综合评分的指标。结果新生儿窒息综合评分的指标分别为呼吸（R）、心率（HR）、肤色（SC）、血氧饱和度（SAT）、血氧分压（PaCO2）．二氧化碳分压（PaO2）、脐血pH值（UB－pH）．无创血压（N－BP）及胎儿监护（CTG）等。初评方案Ⅰ由R、P、SC、SAT、CTG和UB－pH组成，初评方案Ⅱ由R、P、SC、CTG、PaO2和PaCO2组成．复评方案由pH、PaO2、PaCO2、SaO2、N－BP和Silverman呼吸评分组成。Apgar评分正常的新生儿采用初评方案Ⅰ、Ⅱ评价，分别有5％、8％的新生儿存在轻度窒息。Apgar评分属于窒息者，采用初评方案Ⅰ、Ⅱ评分均正常者4例，初评方案Ⅰ为正常者6例，初评方案Ⅱ为正常者8例。结论采用Apgar评分诊断新生儿窒息存在假阳性和假阴性。采用初评方案Ⅰ诊断新生儿窒息具有简便、快速、准确、重复性好等优点。     

HPLC测定佛手增乳膏中阿魏酸的含量

佛手增乳膏经乙醚，2％碳酸钠液萃取后，用HPLC测定阿魏酸的含量。方法简便，快速，准确。     

喉近全切除喉功能重建术

目的 为了减少喉全切除率并重建喉功能。方法 自１９９１￣１９９６年作喉近全切除喉功能重建术１９例。男８例，女１１例。年龄最大７４岁，最小４０岁，平均５７．６岁。临床分期Ⅱ期２例，Ⅲ期９例，Ⅳ期８例。手术特点是：切除舌骨，保留环状软骨及一侧杓状软骨，将五状软骨前缘与舌根切缘吻合，增强了舌根对新喉口的遮盖作用，减轻了误咽．结果 全部病例术后发音功能良好，多数病例误咽不重。５例拔除套管经喉呼吸。１４例新