Efficacy of short‐course lansoprazole with clarithromycin and amoxicillin in the eradication of Helicobacter pylori in South‐East Asian patients: 5‐day t.d.s. versus 7‐day b.d. treatment regimens

OBJECTIVE : To determine and compare the efficacy of 5‐day t.d.s and 7‐day b.d. treatment regimens comprising lansoprazole, clarithromycin and amoxicillin in the eradication of Helicobacter pylori. METHODS : Patients with unequivocal evidence of H. pylori infection based on histology and rapid urease tests of both antrum and corpus biopsies were recruited for the study. The study was a randomized, investigator‐blind, comparative study. Patients received either 500 mg clarithromycin t.d.s. and 500 mg amoxicillin t.d.s. for 5 days (LAC5) or 500 mg clarithromycin b.d. and 500 mg amoxicillin b.d. for 7 days (LAC7) together with 30 mg lansoprazole (both groups) daily for either 5 or 7 days, depending on the treatment group. Patients were assessed for the successful eradication of H. pylori, defined as the absence of bacteria based on histology and urease tests on both antral and corporeal biopsies, carried out at least 4 weeks after completion of the therapy. RESULTS : One hundred and eight patients were recruited for the study. In the LAC5 treatment group, four patients failed to return for follow up and in the LAC7 group, two failed to return for follow up and two were not compliant with medications. Eradication rates based on an intention‐to‐treat analysis were: 46/54 for LAC5 (85.2%; 95% CI = 72.9–93.4) and 47/54 for LAC7 (87.0%; 95% CI = 75.1–94.6). Based on a per protocol analysis, the rates were: 46/50 for LAC5 (92.0%; 95% CI = 80.8–97.8) and 47/50 for LAC7 (94.0%; 95% CI = 83.5–98.7). Both treatment regimens were convenient for patients and except for two patients in the LAC7 group, all patients reported taking 100% of all prescribed medications. The side‐effects encountered were uniformly mild and no patient discontinued treatment because of intolerance to medications. The most common side‐effects were altered taste (LAC5 64.7%; LAC7 78.8%). Diarrhea, nausea and anorexia were reported in a minority of patients. CONCLUSIONS : Both the LAC5 t.d.s. and the LAC7 b.d. treatment regimens were well tolerated by patients and were highly effective in the eradication of H. pylori.     

von Willebrand disease in the RIIIS/J mouse is caused by a defect outside of the von Willebrand factor gene [published erratum appears in Blood 1995 Sep 15;86(6):2461]

An animal model for human type I von Willebrand disease (vWD) has been previously described in the inbred mouse strain RIIIS/J. Murine vWD is characterized by a prolonged bleeding time, normal von Willebrand factor (vWF) multimer distribution, autosomal dominant inheritance, and proportionately decreased plasma vWF antigen, ristocetin cofactor, and factor VIII (FVIII) activities. To study the molecular genetics of murine vWD, a portion of the vWF gene surrounding exon 28 was cloned, sequenced, and used to develop two informative DNA sequence polymorphisms for rapid genotyping by DNA polymerase chain reaction. RIIIS/J mice were crossed with PWK/Ph mice, an inbred line of Mus musculus musculus, and the F1 progeny backcrossed to the parental PWK/Ph strain. vWF antigen levels in F1 mice were not significantly different from the parental RIIIS/J strain but were markedly decreased compared with the parental PWK/Ph mice. Genetic linkage analysis of 104 backcross progeny showed no correlation between vWF antigen level and vWF genotype. These data indicate that murine vWD is caused by a defect at a novel genetic locus, distinct from the murine vWF gene. The distribution of vWF antigen levels among backcross progeny suggests the presence of one major dominant vWD gene in the RIIIS/J mouse with possible modifying contributions from one or more additional minor loci. These observations may provide new insights into the molecular basis and variable expressivity of human vWD.     

Neutrophil deactivation by influenza A viruses: mechanisms of protection after viral opsonization with collectins and hemagglutination-inhibiting antibodies

Bacterial superinfections are a major cause of morbidity and mortality during influenza A virus (IAV) epidemics. Depression of phagocyte functions resulting from attachment of the IAV hemagglutinin (HA) to cell surface sialo-glycoproteins is a likely contributory cause of these infections. We have proposed that the group of collagenous lectins (termed collectins) present in blood and pulmonary surfactant play a role in initial host defense against IAV. We used here several recombinant human surfactant protein D (RhSP-D) preparations to determine the mechanism through which opsonization of IAV with collectins protects neutrophils against the deactivating effects of IAV on cellular respiratory burst responses in vitro. RhSP-D was markedly more potent than antibodies that inhibited viral hemagglutination activity (anti-HA antibodies) at protecting neutrophils in this assay. Unlike the anti-HA antibodies, RhSP-D was protective at concentrations that minimally inhibited viral hemagglutination activity. Two related features of SP-D--the degree of multimerization and the ability to cause aggregation of IAV particles--were critical determinants of the ability of SP-D to protect neutrophils against deactivation. Similarly SP-D-induced viral aggregate formation resulted in enhanced IAV binding to neutrophils and potentiated the ability of the virus itself to trigger neutrophil respiratory burst responses. In contrast to the case of IAV-antibody complexes, SP-D-IAV complexes attached to and activated neutrophils through a neuraminidase-sensitive mechanism (ie, similar to unopsonized IAV). These results indicate that collectin-mediated viral aggregation per se may be an important host defense mechanism not only by virtue of reducing the number of infectious viral particles, but also by promoting phagocyte responsiveness.     

Quantitative and cell-cycle differences in progenitor cells mobilized by recombinant human interleukin-7 and recombinant human granulocyte colony-stimulating factor

Administration of recombinant human interleukin-7 (rhIL-7) to mice increases the exportation of myeloid progenitors (colony-forming unit [CFU]-c and CFU-granulocyte erythroid megakaryocyte macrophage [CFU- GEMM]) from the bone marrow (BM) to peripheral organs, including blood, and also increases the number of primitive progenitor and stem cells in the peripheral blood (PB). We now report that combined treatment of mice with rhIL-7 and recombinant human granulocyte-colony stimulating factor (rhG-CSF) stimulates a twofold to 10-fold increase in the total number of PB CFU-c, and a twofold to fivefold increase in the total number of PB CFU-spleen at day 8 (CFU-S8) over the increase stimulated by rhIL-7 or rhG-CSF alone. In addition, the quality of mobilized cells with trilineage, long-term marrow-repopulating activity is maintained or increased in mice treated with rhIL-7 and rhG-CSF compared with rhIL- 7 or rhG-CSF alone. These differences in mobilizing efficiency suggest qualitative differences in the mechanisms by which rhIL-7 and rhG-CSF mobilize progenitor cells, in fact, the functional status of progenitor cells mobilized by rhIL-7 differs from that of cells mobilized by rhG- CSF in that the incidence of actively cycling (S-phase) progenitors obtained from the PB is about 20-fold higher for rhIL-7-treated mice than for mice treated with rhG-CSF. These results suggest the use of rhIL-7-mobilized progenitor/stem cells for gene-modification and tracking studies, and highlight different functions and rates of repopulation after reconstitution with PB leukocytes obtained from mice treated with rhIL-7 versus rhG-CSF.     

End-of-Life Medical Costs of Medicaid Cancer Patients

ObjectivesTo quantify end-of-life (EOL) medical costs for adult Medicaid beneficiaries diagnosed with cancer.ConclusionsMedicaid cancer patients incur substantially higher EOL costs than noncancer patients. This increased cost may reflect the cost of palliative care. Future studies should assess the types and timing of services provided to Medicaid cancer patients at the EOL.     

胼胝体损伤预测临床孤立综合征的复发

背景:大多数多发性硬化(MS)患者的首发症状为临床孤立综合征(GIS).目前MS的诊断主要依据临床表现、Barkhof MRI指标和脑脊液分析.