PubMed Health⌕ Search

Biomedical subjects

F Lanza

Publications and source records attributed to F Lanza.

At least 91 records · Page 5Linked to original sources
PubMed1997

Comparative analysis of different permeabilization methods for the flow cytometry measurement of cytoplasmic myeloperoxidase and lysozyme in normal and leukemic cells.

Using a direct one-color (fluorescein isothiocyanate; FITC) staining method with a Facscan flow cytometer, we evaluated the intracellular expression of two granular constituents of myeloid cells [myeloperoxidase (MPO) and lysozyme] on leukemic cells from 21 patients with acute myeloid leukemia (AML), and 6 patients with acute lymphoblastic leukemia (ALL). Three different permeabilization techniques were used [FACS Lysing Solution (FLy), B.Dis; Ortho-PermeaFix (OPF); Fix and Perm (F&P), Caltag] prior to monoclonal antibody (McAb) staining, in order to verify the specificity and the sensitivity of the three labelling methods towards the two model antigens. Peripheral blood cells from 15 healthy subjects and Ortho Absolute Control served as controls. Data were expressed as percentage of positivity, net fluorescence intensity, ratio between mean fluorescence intensity (MFI) of positive cells and that of isotypic controls (P/N ratio; evaluated in both geometric and arithmetic scale), and, in 12 representatives cases (7 AML, 5 normal samples), in the form of both molecules of equivalent soluble fluorochromes (MESF) and antibody binding capacities (ABC). As far as the antigenic expression of MPO and lysozyme in normal samples is concerned, F&P resulted, in our hands, in the most specific and sensitive staining, followed by FLy solution and OPF, which showed positivity for MPO, and, to lesser extent, for lysozyme in a considerable manner of lymphocytes (means 64% and 54%, respectively, for OPF and FLy; range of ABC/cell: 0.9-5.2 x 10(3)) obtained from healthy subjects. With the reference F&P permeabilizing solution, 90% and 80% of FAB M1-M5 cases were found to be positive for MPO and lysozyme, respectively. However, M1, M2, and M3 AML FAB (French-American-British) subvarieties were characterized by a brighter expression for MPO (mean ABC/cell: 89 x 10(3)) than that of lysozyme (mean ABC/cell: 12.5 x 10(3D)), whereas blast cells from patients with M5a FAB subtypes showed higher levels of lysozyme (mean ABC/cell: 65 x 10(3)) than that of MPO (mean ABC/cell: 0.1 x 10(3)). One of five cases of FAB MO AML showed a dull positivity for MPO-7 McAb. Patients with ALL were MPO and lysozyme negative using both F&P and FLy reagents, although a certain degree of positivity was documented in some cases with OPF. Taking these data together, it can be stated that the use of anti-MPO McAbs may be of great value for the diagnosis and monitoring of acute leukemia and, along with lysozyme McAb, can provide useful information in the distinction of myeloid from monocytic leukemias and in the lineage assignment of apparently biphenotypic forms. However, the methodology used for the detection of these myeloid-associated antigens is critical for a correct interpretation of cytofluorimetric data and should be taken into account when evaluating data coming from multicenter trials dealing with leukemias. A standardization of cytofluorimetric analysis of intracellular antigens is needed in order to improve the reproducibility and comparability of results in multicenter studies.

Adult↗
PubMed1997

Gene cloning of rat and mouse platelet glycoprotein V: identification of megakaryocyte-specific promoters and demonstration of functional thrombin cleavage.

Platelet glycoprotein (GP) V is a major surface protein cleaved during thrombin-induced platelet activation. GPV associates noncovalently with the GPIb-IX complex to form GPIb-V-IX, a receptor for von Willebrand factor and thrombin. We describe the cloning of the genes coding for rat and mouse GPV and compare them with the human gene. The two rodent genes have a similar structure and resemble the human GPV gene with a coding sequence (approximately 1,700 nucleotides) entirely contained in one exon and a single intron (approximately 900 nucleotides) in the 5' untranslated region. Both genes have megakaryocyte-type promoters with conserved tandem Ets and GATA recognition motifs and lack a TATA box. The mature rat and mouse proteins comprise 551 amino acids, have 70% sequence identity, and contain an additional 8-amino acid intracellular segment as compared with the human protein. As in human GPV, there is an NH2-terminal leucine-rich region of 15 repeats and a thrombin cleavage recognition sequence. Whereas the rat and human thrombin cleavage sites are similar, the mouse cleavage site resembles that of the human thrombin receptor. Functionality of these sites was demonstrated by thrombin cleavage of synthetic peptides and analysis by high-performance liquid chromatography (HPLC) or mass spectrometry. Cleavage of native rat GPV was confirmed by means of a polyclonal antibody directed against the new NH2-terminal peptide exposed after thrombin cleavage. This antibody specifically recognized thrombin-activated rat platelets by fluorescence-activated cell sorting (FACS) analysis. In addition, we raised monoclonal antibodies specific for rat GPV (88 kD), which recognized the NH2-terminal soluble fragment (70 kD) liberated after thrombin cleavage. Knowledge of these rodent GPV genes and availability of species-specific peptides and antibodies will be essential to further studies aiming to define the exact in vivo function of platelet GPV using animal models of thrombosis and gene inactivation experiments.

Amino Acid Sequence↗
PubMed1997

PF4 inhibits thrombin-stimulated MMP-1 and MMP-3 metalloproteinase expression in human vascular endothelial cells.

We investigated whether PF4 could regulate the constitutive and thrombin-stimulated expression of metalloproteinases (MMPs) in endothelial cells (EC). PF4 inhibited the increase in the expression of MMP-1 and MMP-3 promoted by thrombin or the thrombin receptor agonist peptide SFLLRNPNDKYEPF (SFLL..) by 50% but did not modify the constitutive expression of these MMPs. This inhibitory effect was not mediated through a direct interaction of PF4 with thrombin or with the MMPs themselves. The interaction of PF4 with heparan sulfates at the surface of the EC appeared to be implicated in the inhibition mechanism of MMP-1 but not in that of MMP-3. MMP-1 transcription levels remained unchanged after PF4 treatment, whereas the increase in MMP-3 transcription induced by thrombin or SFLL.. was inhibited by approximately 50%. Expression of the tissue inhibitors of metalloproteinases TIMP-1 and TIMP-2 was not affected by PF4. The present data provide new evidence that the antiangiogenic properties of PF4 involve the inhibition of matrix breakdown and suggest that this property of PF4 could be especially relevant in the context of thrombin-regulated tissue remodelling.

Blotting, Western↗
PubMed1997

Prevention of duodenal ulcer recurrence with 15 mg lansoprazole: a double-blind placebo-controlled study. The Lansoprazole Study Group.

Although eradication of Helicobacter pylori cures duodenal ulcer, some patients are not infected and others are treatment failures. This randomized, double-blind, placebo-controlled study assessed the value of treatment with low-dose lansoprazole in preventing duodenal ulcer recurrence. One hundred eighty-six patients with endoscopic documentation of healed duodenal ulcer received 15 mg/day lansoprazole or placebo for 12 months or until ulcer recurred. Endoscopy results, symptom assessment, and fasting serum gastrin levels were obtained at multiple time points. Densities of E, EC, and G cells were assessed by biopsy when the ulcer recurred or at the final visit. Time to ulcer recurrence was significantly longer (P < 0.001) in the lansoprazole group (median >12 months) compared to placebo (median <3 months), and patients taking lansoprazole were asymptomatic longer (P < 0.05). Maintenance therapy with lansoprazole 15 mg/day suppresses acid and controls recurrence of duodenal ulcer disease.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Co-localization of CD9 and GPIIb-IIIa (alpha IIb beta 3 integrin) on activated platelet pseudopods and alpha-granule membranes.

CD9 is a 24-kDa membrane glycoprotein expressed on the surface of human platelets and potentially involved in cellular activation and adhesion functions. This protein belongs to a recently delineated family of cell-surface antigens that span the membrane four times, called tetraspans, and found mainly in leucocytes and tumour cells. As a first approach to clarify the function of CD9, we used immunoelectron microscopy to determine the localization of this antigen in human platelets, and compared its distribution with that of the GPIIb-IIIa integrin, the platelet receptor for fibrinogen. Monoclonal antibodies against CD9 (MAb7) and GPIIb-IIIa (HP1-1D) coupled to colloidal gold of different sizes (5 and 15 nm) were incubated with intact platelets in suspension or on ultrathin sections of platelets embedded in LR white. CD9 was found in association with GPIIb-IIIa on the inner face of alpha-granule membranes. These two antigens also colocalized on pseudopods of activated platelets and in contact regions between adjacent platelets. CD63, another member of the tetraspan family, was absent from alpha-granules but was associated with lysosomal structures. Flow cytometric analysis of platelet CD9 with a series of monoclonal antibodies revealed an increased expression upon thrombin stimulation, confirming the presence of an intracellular granular pool. The observation that CD9 and GPIIb-IIIa are stored in the same intracellular structures and migrate to the same activation zones after platelet stimulation lends support to previous suggestions of a close association between CD9 and GPIIb-IIIa in human platelets and of a possible involvement of CD9 in adhesive functions of platelets.

Antigens, CD↗
PubMed1997

Flow cytometry measurement of GM-CSF receptors in acute leukemic blasts, and normal hemopoietic cells.

A quantitative analysis of expression levels of GM-CSF receptors was performed by flow cytometry in different disease categories, ie AML (n = 72), ALL (n = 18), and MDS (n = 12), as well as 12 healthy volunteers, using three different unconjugated GM-CSF/R monoclonal antibodies (McAbs) (HGM-CSFR (CD116), M5D12, 4B5F5), and appropriate standards. By using the reference HGM-CSFR McAb, in healthy subjects we found detectable levels of GM-CSF/R on blood monocytes (mean MESF (molecules of equivalent soluble fluorochrome)/cell: 36.1 x 10[3]), neutrophils (mean MESF/cell: 7.4 x 10[3]), bone marrow (BM) myelo-monocytic precursors (MESF range for the myeloid component, ie promyelocytes, myelocytes, metamyelocytes: 11.7-40.5 x 10[3], and for the monocytic lineage: 25.7-69.2 x 10[3]), and in two distinct subsets of BM CD34+ progenitor cells (GM-CSF/R dim: 2.5 x 10[3] MESF/cell, GM-CSF/R bright (10% of the total number of CD34 cells: 22.0 x 10[3] MESF/cell). In these subjects, there was no correlation between the expression levels of GM-CSF/R and CFU (CFU-GM, CFU-GEMM, BFU-E) colony production. Among the AML samples, M5D12 McAb was positive in 33%, 4B5F5 McAb in 90%, and HGM-CSF/R McAb in 78% of the cases examined (range of MESF/cell for the HGM-CSFR McAb: 0.9 x 10[3]-106.7 x 10[3]). The highest MESF values were seen in the M5 FAB subvariety (mean: 39.4 x 10[3]), where all the patients tested (n = 20) showed a strong positivity for the HGM-CSFR McAb. On the contrary, all ALL samples were GM-CSF/R negative except in two patients, who displayed a dim GM-CSF/R positivity (My+ALL: 1.3 x 10[3] MESF/cell; pro-B ALL: 1.0 x 10[3] MESF/cell). In most (>70%) M1 FAB subtypes, GM-CSF/R+ blasts co-expressed CD34low, HLA-DRhigh, CD33, CD38 antigens, and had little or no capacity to form CFU-GM colonies. GM-CSF/R+ blasts from the M5 FAB category were also positive for CD14, CD11c, CD33 and CD87. Furthermore, the number of GM-CSF/R expressed by leukemic cells from five out of 72 (7%) AML patients was above the highest values seen in normal samples (>69.2 x 10[3] MESF/cell), allowing the possibility of using this marker for the monitoring of the minimal residual disease (MRD) in a subset of AML. Cell culture studies aimed at evaluating GM-CSF receptor modulation following AML blast exposure to rhGM-CSF showed two distinct patterns of response; in the first group (6/10 cases) rhGM-CSF down-modulated GM-CSF receptors, whereas in the second group (4/10 cases), rhGM-CSF treatment was associated with either an increase or no change in the number of GM-CSF/R. In conclusion, cellular GM-CSF/R expression was variable and ranged from undetectable (ALL and a minority of AML) to very high intensities in M5 AML, and were also documented in some M0 AML, thus suggesting the concept that GM-CSF/R detection may be of help in lineage assignment of undifferentiated forms. Since the number of GM-CSF/R on AML blasts may be modulated after GM-CSF treatment, it can be postulated that the clinical use of GM-CSF in this disease may be optimized by a dynamic analysis of the number and the affinity status of GM-CSF-R in blasts and normal hemopoietic cells.

Acute Disease↗
PubMed1997

CD9, a tetraspan transmembrane protein, renders cells susceptible to canine distemper virus.

Canine distemper virus (CDV), a lymphotropic and neurotropic negative-stranded RNA virus of the Morbillivirus genus, causes a life-threatening disease in several carnivores, including domestic dogs. To identify the cellular receptor(s) involved in the uptake of CDV by susceptible cells, we isolated a monoclonal antibody (MAb K41) which binds to the cell surface and inhibits the CDV infection of several cell lines from various species. Pretreatment of cells with MAb K41 reduces the number of infectious centers and the size of the syncytia. Using affinity chromatography with MAb K41, we purified from HeLa and Vero cell extracts a 26-kDa protein which contained the amino acid sequence TKDEPQRETLK of human CD9, a member of the tetraspan transmembrane or transmembrane 4 superfamily of cell surface proteins. Transfection of NIH 3T3 or MDBK cells with a CD9 expression plasmid rendered these cells permissive for viral infection and raised virus production by a factor of 10 to 100. The mechanism involved is still unclear, since we were unable to detect direct binding of CDV to CD9 by using immunoprecipitation and a virus overlay protein binding assay. These findings indicate that human CD9 and its homologs in other species are necessary factors for the uptake of CDV by target cells, the formation of syncytia, and the production of progeny virus.

3T3 Cells↗
PubMed1997

Thrombin receptor-mediated increase of two matrix metalloproteinases, MMP-1 and MMP-3, in human endothelial cells.

Matrix metalloproteinases (MMPs) are responsible for the degradation of extracellular matrix components and are secreted by a variety of cells including human endothelial cells. Because alpha-thrombin is known to interact with matrix components and has been shown to activate latent MMP-2 in human umbilical vein endothelial cells, we investigated whether human alpha-thrombin could also regulate other MMPs secreted by the human saphenous vein or mammary artery endothelial cells (EC). After treatment of EC with increasing concentrations of thrombin for different periods of time, a significantly higher gelatinolytic activity of both MMP-1 and MMP-3 was observed in addition to MMP-2 activation. The effect of thrombin was time and dose-dependent, reaching a maximum at 24 hours. After treatment with 5 NIH U/ml thrombin for 24 hours, Western blotting revealed 9.5- and 4.4-fold increases over control values for MMP-3 and MMP-1, respectively. The synthetic thrombin receptor agonist peptide SFLLRNPNDKYEPF fully reproduced the action of thrombin, whereas chemical inactivation of the catalytic site of thrombin abolished its effect on MMP-1 and MMP-3. Thrombin and SFLLRNPNDKYEPF both induced MMP-3 mRNA synthesis but had no significant influence on constitutive MMP-1 mRNA levels. These results demonstrate that thrombin not only activates latent MMP-2 but also modulates MMP-1 and MMP-3 production in EC, this latter effect being mediated by the G-protein-coupled thrombin receptor. Hence, our present data provide evidence to support the suspected role of thrombin in tissue remodeling and angiogenesis.

Blotting, Western↗
PubMed1996

Effective maintenance treatment of reflux esophagitis with low-dose lansoprazole. A randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To compare the efficacy of two doses of lansoprazole with that of placebo in preventing recurrence of erosive esophagitis in a 12-month period. DESIGN: Randomized, double-blind, parallel, placebo-controlled trial. SETTING: 25 U.S. medical centers. PATIENTS: 173 patients with documented healing of erosive esophagitis after 8 weeks of acid-suppressing therapy. INTERVENTION: Lansoprazole, 15 mg or 30 mg, or placebo once daily for as long as 12 months. MEASUREMENTS: Endoscopy and symptom evaluation after 1, 2, 3, 6, 9, and 12 months of treatment. Endoscopy was also done whenever symptoms suggested erosive changes. RESULTS: Lansoprazole was significantly superior to placebo in maintaining healing and preventing recurrence of symptoms. By month 1, 45% of placebo recipients remained healed compared with more than 90% of patients in either lansoprazole group. By month 12, only 24% of placebo recipients remained healed compared with 79% of patients receiving 15 mg of lansoprazole and 90% of patients receiving 30 mg of lansoprazole. During the same period, 35% of placebo recipients remained asymptomatic compared with 72% of recipients of 15 mg of lansoprazole and 67% of recipients of 30 mg of lansoprazole. The 15-mg and 30-mg lansoprazole doses did not differ significantly in maintaining healing and controlling symptoms. Follow-up after recurrence of erosion indicated that during the 12 months, 35% of placebo recipients and 2% of lansoprazole recipients had three or more recurrences. CONCLUSION: Lansoprazole effectively maintains healing of erosive esophagitis. The 15-mg and 30-mg lansoprazole doses did not differ significantly for use as maintenance treatment.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Polymorphonuclear neutrophils pulsed with synthetic peptides efficiently activate memory cytotoxic T lymphocytes.

Polymorphonuclear neutrophils (PMNs), traditionally considered effector cells in the inflammatory response, have recently been regarded as potential regulators of the immune response. In the present study we investigate whether PMNs are efficient antigen-presenting cells for reactivation of memory cytotoxic T lymphocytes (CTLs). PMNs were pulsed with synthetic peptides derived from Epstein-Barr virus (EBV) antigens. We have used the IVTDFSVIK (IVT) peptide derived from the Epstein-Barr virus-encoded nuclear antigen 4 protein, corresponding to the immunodominant epitope of HLA-AII-restricted CTL responses, and the CLGGLLTMV (CLG) peptide derived from the latent membrane protein 2 antigen, representing a subdominant epitope of HLA-A2-restricted CTL responses. The data indicate that peptide-pulsed PMNs selectively activate specific CTL responses to both immunodominant and subdominant epitopes. The efficiency of CTL induction by PMNs was comparable to that observed with the conventional method of EBV-specific CTL reactivation with the autologous lymphoblastoid cell line, as well as with peptide-pulsed monocyte-enriched adherent cells. On the contrary, unactivated peptide-pulsed lymphocytes failed to induce an epitope-specific CTL response. These results demonstrate that PMNs efficiently present antigens to memory virus-specific CTLs and suggest that they may have a role as antigen-presenting cells.

Amino Acid Sequence↗
PubMed1996

An Attempt to Interpret the Spread of Element Concentration in Antarctic Surface Snow: The Same Element in a Given Test Field, Several Elements in Different Sampling Fields

Sampling surface snow on a large test field always leads to a spread of analyte concentration data which partly follows a Gaussian distribution and partly a rectangular one as can be observed from the analysis of literature data. The spread depends on the nonuniformity of the air-snow interface in the field and on the extent of reproducibility of all the procedures used from sampling to analysis. Consequently a sample relevant to a restricted surface might be poorly representative of the surrounding area. Contamination of the sample during the gathering and storing steps is assumed to be the main source of nonrandom results (outliers). Using various statistical tools we were able to evaluate which part of the spread was due to the snow surface nonuniformity in the case of many samples collected in the same test field. In the case of samples gathered in different geographical areas, the possibility of finding correlations among points is greatly enhanced when three or more analytes are considered for each sample. When the same correlation is found for some analytes and a variable tentatively tested, information can be gained about the source of chemical content of snow samples. The use of UV pretreatment of snow samples has been proven to cut down the interference of organics on the electrochemical process in DPASV, allowing one to obtain accurate and reproducible data.

Journal Article↗
PubMed1996

p53 exon 5 mutations in two cases of leukemic mantle cell lymphoma.

Although p53 mutations have been described frequently in high-grade B-cell non-Hodgkin's lymphoma (NHL), they have only been reported occasionally in low-grade NHL. We therefore describe clincobiologic and molecular genetic findings in two patients with p53 mutations and leukemic mantle cell lymphoma featuring an unusually aggressive course. Circulating malignant cells showed irregularity of nuclear outline with frequent deep clefts in both cases. Immunologic studies of neoplastic cells from peripheral blood samples and from cells obtained from an involved lymph node showed a mantle B-cell phenotype (CD5+, CD19+, CD22+, CD23- or weakly+ and bright expression for surface immunoglobulins). Malignant cells were shown to be hyperdiploid by cytofluorimetric study of DNA content and the presence of the t(11;14)(q13q32) was documented in one case. An altered electrophoretic mobility of p53 exon 5 was seen in both cases, with a missense mutation at codon 158 present in one case and a CAG to TAG mutation resulting in a 167-stop codon present in the second case. The percent of reactive cells with the 1801 monoclonal antibody detecting an epitope of the p53 was 37% in one case and 1% in the second case, supporting the notion that immunologic overexpression cannot be used for a selection criterion for the detection of p53 mutations. From these findings and from data available in the literature the conclusion can be drawn that p53 gene mutations at codons 158 and 167 may be associated with lymphoproliferative disorders and that low- or intermediate-grade NHL, including leukemic mantle cell lymphoma, may frequently carry this genetic change.

Aged↗
PubMed1996

Thrombin interaction with platelet membrane glycoprotein Ib.

Platelet activation by low doses of thrombin allows the amplification thrombin formation and thereby plays an important role in the development of thrombi. Although thrombin-induced platelet activation is elicited via the cleavage of its specific receptor (TR), platelet membrane glycoprotein Ib (GPIb) is required for responses to low concentrations of thrombin, as evidenced from the observation that GPIb-deficient platelets are characterized by a decreased sensitivity to thrombin and a low rate of activation. Glycoprotein Ib is an integral membrane protein composed of two disulfide-linked chains noncovalently associated to glycoproteins IX and V. As the receptor of the von Willebrand factor (vWF), GPIb plays a main role in platelet adhesion to the subendothelium. There are 25,000 copies of GPIb at the platelet surface but only a limited number of them appear to be involved in the high-affinity binding of thrombin. The catalytic site of thrombin is not involved in the interaction with GPIb. In contrast, competitive inhibition of GPIb-thrombin interaction by the C-terminal tail of hirudin, fibrin(ogen), and thrombomodulin indicates that thrombin exosite 1 is essential for GPIb binding. A hydrophylic domain located on the 45-kd N-terminal domain of GPIb alpha is involved in thrombin binding, and in particular, a stretch of negatively charged residues appears to make ionic interactions with thrombin. The same region of GPIb also contributes to the vWF binding site that should be very close to and even overlapping the thrombin-binding site. Despite GPIb and TR both interacting with thrombin exosite 1, the soluble fragment of GPIb does not modify the hydrolysis by thrombin of its target peptidic bond on TR, indicating that these two proteins bind to discrete subsites within exosite 1 and that the promoting effect of GPIb on TR-coupled responses depends on the anchorage of these proteins to the platelet membrane.

Amino Acid Sequence↗
PubMed1996

Double-blind, multicenter evaluation of lansoprazole and amoxicillin dual therapy for the cure of Helicobacter pylori infection.

BACKGROUND: Treatment with amoxicillin plus omeprazole results in disappointing cure rates of Helicobacter pylori infection. The minimal inhibitory concentration of lansoprazole for H. pylori in vitro is lower than that for omeprazole, prompting interest in treatment with amoxicillin plus lansoprazole. MATERIALS AND METHODS: H. pylori-infected patients with endoscopically documented duodenal ulcer either currently or within the past year were randomized to 14 days of (1) lansoprazole, 30 mg bid, plus amoxicillin, 1 gm tid; (2) lansoprazole, 30 mg tid, plus amoxicillin, 1 gm tid; (3) lansoprazole, 30 mg tid alone; or (4) amoxicillin, 1 gm tid alone. Endoscopy was done at enrollment and at 4 to 6 weeks after completion of treatment or for recurrent symptoms. H. pylori status was assessed by culture and histology. Ulcer prevalence was evaluated at follow-up endoscopy. RESULTS: Two hundred sixty-two patients met enrollment criteria and were treated. By per-protocol analysis, H. pylori infection was cured in 57% of those treated with lansoprazole twice daily plus amoxicillin and in 67% of those treated with lansoprazole three times daily plus amoxicillin, compared with 0% treated with lansoprazole alone or amoxicillin alone (p < .001 for dual therapy versus either monotherapy). Amoxicillin resistance was not observed. At follow-up endoscopy, ulcer prevalence was 17% in patients treated with lansoprazole twice daily plus amoxicillin, 23% in those treated with lansoprazole three times daily plus amoxicillin, 33% in those treated with lansoprazole alone, and 35% in those treated with amoxicillin alone (p = .024; lansoprazole twice daily plus amoxicillin versus amoxicillin alone). CONCLUSIONS: Treatment with amoxicillin plus lansoprazole, 30 mg tid, led to cure of H. pylori infection in 67% of patients with active or recently healed duodenal ulcer.

2-Pyridinylmethylsulfinylbenzimidazoles↗