短程兰索拉唑、克拉霉素和阿莫西林三联疗法根除幽门螺杆菌在东南亚患者中的

测定和比较含兰索拉唑、克拉霉和阿莫西林的5日tid疗法和7日bid疗法根除幽门螺杆菌（H.pylori)疗效,方法：本研究为随机,双盲,对照研究。胃窦和胃体部活检经组织学检查和快速尿素酶试验确诊为H．pylori感染的患者内入研究,患者分别接受克拉霉素500mgtid,阿莫西林500mgtid和兰索拉唑每日30mg治疗5天（LAC5组）或克拉霉素500mgbid,阿莫西林500mgbid和兰索拉唑每日30mg治疗7天（LAC7组）。治疗结束至少4周后,用组织学检查和快速尿酶素试验评估H．pylori是否成功除,胃窦和胃体部活检H．pylori阴性定义为H．pylor根除,结果：108例胃患者纳入研究,LAC5组有4例患者失访;LAC7组2例患者失访,2例患者对药物不能依从。按意图治疗分析,LAC5组的根除率为85．2％[46/54,95%可信区间（CI):72.9%,93.4%],LAC7组的根除率为87．0％（47／54,95％CI：75．1,94.6%).按方案分析,LAC5组的根除率为92．90％（46／50,95％CI：80．8％,97．8％）,LAC7组的根除率为94．0％（47／50,95％CI：83.5%,98.7%),两种疗效对患者均很适宜,除LAC7组2例外,其余患者均服完规定的药物,两种疗法的副作用均较轻微,没有患者因对药物不耐受而中断治疗,最常见的副作用是味觉改变（LAC5组：64．7％,LAC7组：78．8％）。少数患者有腹泻,恶心和厌食,结论：LAC5tid疗法和LAC7bid疗法均有具有良好受性的治疗方案,根除H．pylor的疗效高。     

慢性胃病脾虚患者胃窦粘膜胃泌素细胞和分泌生长抑素细胞的变化及其意义

目的：观察以慢性胃病为主的脾虚患者胃窦粘膜分泌胃泌家(Gas)细胞(G细胞)、生长抑素(SS)细胞(D细胞)与脾虚证发生的关系。方法：将84例脾虚患者分为脾胃虚寒组、脾虚夹热组、胃阴不足组、脾胃湿热组、肝胃不和组，应用免疫组化技术标记胃窦粘膜G、D细胞，并定量分析。结果：以慢性胃病为主的脾虚证患者G、D细胞数均减少，D细胞面积缩小，G/D细胞数和细胞面积比值均增高(P＜0．05)。结论：G、D细胞的变化可能是慢性胃病脾虚证胃肠功能障碍的一个重要病理机制。     

KAI407, a Potent Non-8-Aminoquinoline Compound That Kills Plasmodium cynomolgi Early Dormant Liver Stage Parasites In Vitro

Preventing relapses of Plasmodium vivax malaria through a radical cure depends on use of the 8-aminoquinoline primaquine, which is associated with safety and compliance issues. For future malaria eradication strategies, new, safer radical curative compounds that efficiently kill dormant liver stages (hypnozoites) will be essential. A new compound with potential radical cure activity was identified using a low-throughput assay of in vitro-cultured hypnozoite forms of Plasmodium cynomolgi (an excellent and accessible model for Plasmodium vivax). In this assay, primary rhesus hepatocytes are infected with P. cynomolgi sporozoites, and exoerythrocytic development is monitored in the presence of compounds. Liver stage cultures are fixed after 6 days and stained with anti-Hsp70 antibodies, and the relative proportions of small (hypnozoite) and large (schizont) forms relative to the untreated controls are determined. This assay was used to screen a series of 18 known antimalarials and 14 new non-8-aminoquinolines (preselected for blood and/or liver stage activity) in three-point 10-fold dilutions (0.1, 1, and 10 μM final concentrations). A novel compound, designated KAI407 showed an activity profile similar to that of primaquine (PQ), efficiently killing the earliest stages of the parasites that become either primary hepatic schizonts or hypnozoites (50% inhibitory concentration [IC₅₀] for hypnozoites, KAI407, 0.69 μM, and PQ, 0.84 μM; for developing liver stages, KAI407, 0.64 μM, and PQ, 0.37 μM). When given as causal prophylaxis, a single oral dose of 100 mg/kg of body weight prevented blood stage parasitemia in mice. From these results, we conclude that KAI407 may represent a new compound class for P. vivax malaria prophylaxis and potentially a radical cure.     

Radiographic damage in large joints in early rheumatoid arthritis: relationship with radiographic damage in hands and feet, disease activity, and physical disability

An assessment of the onset of radiographic damage in the large joints (hip, knees, shoulders, elbows, ankles and tarsus) in patients with early rheumatoid arthritis, and the relationship of the progression of large joint damage with joint damage in hands and feet, with physical disability, and with cumulative disease activity, was performed in a prospective 6 yr follow-up study. Large joint damage appeared to be an early phenomenon with 20% of the patients having some damage in at least one large joint within 1 yr, and 50% of the patients within 6 yr after disease onset. Radiographic damage in large joints was significantly related to the damage in hands and feet, the physical disability index, and the cumulative disease activity. The initial disease activity at study entry was the only prognostic factor that reached significance.      

Interleukin-12 inhibits murine graft-versus-host disease

Interleukin-12 (IL-12) is a potent immunostimulatory cytokine and an inducer of type-1 T-helper cell activity and of cytotoxic T lymphocyte and natural killer cell function. We report here the paradoxical observation that a single injection of 4,900 IU of recombinant murine IL-12 inhibits acute graft-versus-host disease (GVHD) in a fully major histocompatibility complex (MHC) plus multiple minor antigen-mismatched bone marrow transplantation (BMT) model (A/J-->B10). The protective effect was enhanced by administration of T-cell-depleted host-type BM cells, and complete donor-type lymphohematopoietic reconstitution was observed in most animals. Treatment with a protective course of IL-12 led to increased serum interferon-gamma (IFN-gamma) levels as compared with those for GVHD controls at early time points, when IFN-gamma was produced predominantly by host-type natural killer cells, but led to almost complete inhibition of the later GVHD-associated increase in serum IFN-gamma levels, when IFN-gamma is produced predominantly by CD4+ T cells. Furthermore, IL-12 treatment was associated with marked alterations in the kinetics of donor T-cell expansion. Reductions in donor CD4+ and CD8+ T cells were observed in the spleen on day 4 post- BMT, but a marked increase in donor CD8+ cells was observed on day 7. Unlike broadly immunosuppressive methods for inhibiting GVHD, which are associated with loss of antileukemic effects, IL-12 has the potential to mediate antileukemic effects of its own; therefore, the GVHD- inhibitory effects of IL-12 described here suggest a potential application for this cytokine in clinical BMT.     

The in vitro effects of Newcastle disease virus on the metabolic and antibacterial functions of human neutrophils

Live Newcastle disease virus (NDV) was used to investigate the in vitro effects of a viral infection on phagocytosis, chemiluminescence generation, superoxide production, oxygen consumption, NADPH-oxidase activity, and intracellular killing of bacteria by Ficoll-Hypaque separated human neutrophils. Phagocytosis of oil red O particles by NDV- treated PMN was inhibited by 50%. Chemiluminescence by PMN was inhibited 79% after zymosan stimulation and 86% after tetradeconyl phorbol acetate stimulation. Superoxide generation was inhibited by 68%. Oxygen consumption was inhibited in the presence of NDV by 37% after stimulation with phorbol myristate acetate, while membrane- associated NADPH-enzyme activity was decreased by 19%. The percent of surviving intracellular S. aureus was significantly elevated in NDV- treated PMN after 60 and 120 min of incubation. Purified bacterial neuraminidase markedly suppressed chemiluminescence, while neuraminic acid blocked the effects of the virus. These observations suggest that infections with myxoviruses may suppress a number of vital neutrophil functions. It appears that the effects may be partly mediated by the interaction of viral neuraminidase with the external neutrophil membrane.