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W Fuchs

Publications and source records attributed to W Fuchs.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Leptospirosis (Weil's syndrome) with renal failure, severe jaundice, disseminated hemorrhages and xanthopsia].

We report a case of a 48-year-old man from western Austria with severe leptospirosis. This disease occurs worldwide but predominates in the tropics. The infectious urine of a wide variety of domestic and wild animals mediates transmission of the infection, which characteristically has a biphasic pattern. It begins with the "leptospiraemic phase" with high fever, conjunctival suffusion, muscle pain and headache. Hepatitis, nephritis and haemorrhages may follow. The second "immune phase" has a greater variety of clinical manifestations. Fever and the initial symptoms may recur and the central and peripheral nervous system may be involved. The patient reported showed all major characteristics except conjunctival suffusion. The outcome was favourable despite some conditions with a poor prognosis (jaundice, renal failure, haemorrhages). The extreme severity of jaundice and the xanthopsia (yellow vision) make the case unique.

Color Vision Defects↗
PubMed1999

Short-term triple therapy with lansoprazole 30 mg or 60 mg, amoxycillin and clarithromycin to eradicate Helicobacter pylori.

BACKGROUND: We investigated the efficacy of 30 vs. 60 mg lansoprazole daily in a 1-week triple therapy for eradication of Helicobacter pylori in a prospective randomized study. METHODS: Two hundred and fifteen consecutive out-patients with peptic ulcer disease or non-ulcer dyspepsia, in whom H. pylori infection was confirmed by histology and/or a urease biopsy test, were randomly assigned to a 1-week treatment with either 15 mg lansoprazole b.d. (LAC15 group) or 30 mg lansoprazole b.d. (LAC30 group) in combination with 1 g amoxycillin b.d. and 500 mg clarithromycin b.d. RESULTS: Eradication of H. pylori was successful in 87% (per protocol) and 82% (intention-to-treat) of the patients with LAC15 and in 94% (per protocol) and 87% (intention-to-treat) of the patients with LAC30. The difference was not significant. In both treatment groups, all peptic ulcers were healed at the check-up. Adverse effects were seen in 11 patients of the LAC15 group and 10 patients of the LAC30 group: they caused discontinuation of the therapy in four of the LAC15 group and two patients of the LAC 30 group. CONCLUSIONS: A 7-day triple therapy using lansoprazole (LAC15) is an efficient and economical regimen for the eradication of H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Effect of 7-day therapy with different doses of the proton pump inhibitor lansoprazole on the intragastric pH in healthy human subjects.

BACKGROUND: Systematic, randomized, and controlled studies on the effect of low to high doses of the proton pump inhibitor lansoprazole on intragastric acidity and plasma gastrin levels have not previously been performed. METHODS: We investigated the effect of 7-day therapy with different doses of lansoprazole (15 mg once or twice daily, 30 mg once or twice daily, and 15 mg three times daily) on intragastric acidity and meal-stimulated daytime plasma gastrin levels in 12 healthy Helicobacter pylori-negative human subjects in a randomized, double-blind, placebo-controlled, 6-way crossover study. On days 1, 2, and 7 of the study 24-h intragastric pH-metry and 12-h integrated daytime plasma gastrin determinations were done. RESULTS: Lansoprazole in a dose regimen of 1 x 30 mg/day, 3 x 15 mg/daily, and 2 x 30 mg/day significantly (P < 0.05) increased the intragastric 24-h median pH on days 1, 2, and 7 of therapy as compared with placebo. Lansoprazole in doses of 1 x 15 mg/day and 2 x 15 mg/day significantly increased the intragastric 24-h median pH on days 2 and 7 but not on day 1 of therapy. Doses of 3 x 15 mg and 2 x 30 mg lansoprazole daily significantly increased the intragastric 24-h median pH on days 2 and 7 of treatment as compared with 1 x 30 mg lansoprazole daily. Except for 1 x 15 mg lansoprazole on day 1 of therapy, all given dose regimens of lansoprazole (15-60 mg/day) significantly (P < 0.05) stimulated the 12-h integrated meal-stimulated daytime plasma gastrin response (pM x min) on days 1, 2, and 7 of therapy as compared with placebo. CONCLUSION: A dose of 1 x 30 mg/day is nearly as potent as higher dose regimens of lansoprazole. Thus it most likely is the optimum dose for therapy of gastric and duodenal peptic lesions. A dose of 1 x 15 mg lansoprazole daily is a potent inhibitor of gastric acid output and could be a therapeutic dose for prevention of peptic lesions (that is, reflux oesophagitis or ulcers).

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1998

Gene arrangement within the unique long genome region of infectious laryngotracheitis virus is distinct from that of other alphaherpesviruses.

The genome of the avian alphaherpesvirus infectious laryngotracheitis virus (ILTV) comprises ca. 155 kbp of which ca. one-third have been sequenced so far. To gain additional sequence information we analyzed two stretches of 15.5 and 1.9 kbp of the ILTV unique long (U(L)) genome region. The larger fragment contains homologs of the herpes simplex virus (HSV) UL23 (thymidine kinase) and UL22 (glycoprotein H) genes followed by five open reading frames (ORF) encoding putative proteins of 334 to 410 amino acids which exhibit no homology to any known herpesvirus protein. RNA analyses showed that these unique ILTV genes are indeed expressed. An origin of replication separates this cluster of unique genes from a conserved gene cluster consisting of the UL45, UL46, UL48, UL49, UL49.5, and UL50 homologs. The absence of UL47 from this position coincides with the localization of a UL47-homologous ORF within the unique short (U(S)) region of the ILTV genome (M. Wild, S. Cook, and M. Cochran, Virus Genes 12:107-116, 1996). Within the second analyzed region the ILTV UL21 homolog was found adjacent to the UL44 gene. We thus identified five novel herpesvirus genes in ILTV and present evidence for a large internal inversion in the ILTV U(L) region, in contrast to the collinear genomes of other alphaherpesviruses. Interestingly, a similar inversion is also present in the porcine alphaherpesvirus pseudorabies virus.

Alphaherpesvirinae↗
PubMed1998

Infectious laryngotracheitis herpesvirus expresses a related pair of unique nuclear proteins which are encoded by split genes located at the right end of the UL genome region.

Avian infectious laryngotracheitis virus (ILTV) possesses an alphaherpesvirus type D DNA genome of ca. 155 kbp. Completion of our previous sequence analyses (W. Fuchs and T. C. Mettenleiter, J. Gen. Virol. 77:2221-2229, 1996) of the right end of the unique long (UL) genome region revealed the presence of two adjacent, presumably ILTV-specific genes, which were named UL0 and UL[-1] because of their location upstream of the conserved UL1 (glycoprotein L) gene. Transcriptional analyses showed that both genes are abundantly expressed during the late phase of the viral replication cycle and that both mRNAs are spliced by the removal of short introns close to their 5' ends. Furthermore, the deduced gene products exhibit a moderate but significant homology of 28% to each other. The newly identified ILTV genes encode proteins of 63 kDa (UL0) and 73 kDa (UL[-1]), which both are predominantly localized in the nuclei of virus infected chicken cells. In summary, our results indicate that duplication of a spliced ILTV-specific gene encoding a nuclear protein has occurred during evolution of ILTV.

Animals↗
PubMed1997

Nitrate removal from drinking water using a membrane-fixed biofilm reactor.

Biological treatment of drinking water is a cost-effective alternative to conventional physico/chemical processes. A new concept was tested to overcome the main disadvantage of biological denitrification, the intensive post-treatment process to remove microorganisms and remnant carbon source. The biological reaction zone and carbon supply were separated from the raw water stream by a nitrate-permeable membrane. Denitrification takes place in a biofilm, which is immobilized at the membrane. In a series of bench-scale runs, different types of membranes and reactor configurations were investigated. The best denitrification rates achieved were 1230 mg NO3(-)-N m-2 day-1. In one run, raw water containing 100 mg NO3- 1-1 was completely freed from nitrate. The membrane and the attached biofilm also represent a barrier against the passage of the C source and nutrients into the raw water. At concentrations of 20 mg 1-1 ethanol and 15 mg 1-1 phosphate in the bioreactor no diffusion through the membrane into the treated water was observed. Without any post-treatment, the effluent met nearly all the relevant criteria for drinking water; only the colony count was slightly increased.

Biofilms↗
PubMed1997

Identification and transcriptional analysis of pseudorabies virus UL6 to UL12 genes.

We determined the nucleotide sequence of an 11059 bp fragment of the pseudorabies virus genome located in the right part of genomic BamHI fragment 3 and the adjacent part of BamHI fragment 6. Within this region eight open reading frames were identified whose deduced amino acid sequences exhibited homology to the UL6, UL7, UL8, UL8.5, UL9, UL10, UL11, and UL12 protein products of herpes simplex virus type 1. Transcriptional analyses indicated presence of 3'-coterminal mRNAs for genes UL8, UL8.5, and UL9 as well as for genes UL6 and UL7, respectively, while UL10 was represented by a very abundant unique transcript. Both gene arrangement and transcriptional organization within this region of the pseudorabies virus genome thus parallels the situation found in other alphaherpesviruses.

Amino Acid Sequence↗
PubMed1997

Lansoprazole versus omeprazole: influence on meal-stimulated gastric acid secretion.

AIMS: To investigate, by means of meal-stimulated acid secretion, the extent to which differences in plasma half-life, bioavailability and the recommended therapeutic dose can influence the antisecretory potency of lansoprazole and omeprazole. METHODS: In this double-blind, placebo-controlled, crossover study, 10 healthy male volunteers received 15 mg or 30 mg lansoprazole, 20 mg or 40 mg omeprazole or placebo for 5 days, in a randomized order. Meal-stimulated acid secretion was determined by means of a homogenized test meal and intragastric titration. RESULTS: On day 1, meal-stimulated acid secretion was decreased by 35% and 45% after administration of 15 mg or 30 mg lansoprazole, and by 16% and 42% after 20 mg or 40 mg omeprazole. After 3 and 5 days of dosing the decreases were 53% and 48% with 15 mg lansoprazole, 82% and 82% with 30 mg lansoprazole, 43% and 39% with 20 mg omeprazole, and 76% and 83% with 40 mg omeprazole. At all measuring points during the 5-day dosing periods, lansoprazole 15 mg and 30 mg proved superior to 20 mg omeprazole in inhibiting meal-stimulated gastric acid secretion, but the differences were only statistically significant for the lansoprazole 30 mg dose, 30 mg lansoprazole and 40 mg omeprazole proved equipotent. On day 1 only 30 mg lansoprazole was significantly better than placebo. CONCLUSION: This study demonstrated the following order of antisecretory potency: 30 mg lansoprazole = 40 mg omeprazole > 15 mg lansoprazole approximately 20 mg omeprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Pseudorabies virus glycoprotein L is necessary for virus infectivity but dispensable for virion localization of glycoprotein H.

Herpesviruses contain a number of envelope glycoproteins which play important roles in the interaction between virions and target cells. Although several glycoproteins are not present in all herpesviruses, others, including glycoproteins H and L (gH and gL), are conserved throughout the Herpesviridae. To elucidate common properties and differences in herpesvirus glycoprotein function, corresponding virus mutants must be constructed and analyzed in different herpesvirus backgrounds. Analysis of gH- mutants of herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PrV) showed that in both viruses gH is essential for penetration and cell-to-cell spread and that its presence is required for virion localization of gL. Since gH homologs are found complexed with gL, it was of interest to assess the phenotype of gL- mutant viruses. By using this approach, HSV-1 gL has been shown to be required for entry and for virion localization of gH (C. Roop, L. Hutchinson, and D. Johnson, J. Virol. 67:2285-2297, 1993). To examine whether a similar phenotype is associated with lack of gL in another alphaherpesvirus, PrV, we constructed two independent gL- PrV mutants by insertion and deletion-insertion mutagenesis. The salient findings are as follows: (i) PrV gL is required for penetration of virions and cell-to-cell spread; (ii) unlike HSV-1, PrV gH is incorporated into the virion in the absence of gL; (iii) virion localization of gH in the absence of gL is not sufficient for infectivity; (iv) in the absence of gL, N-glycans on PrV gH are processed to a greater extent than in the presence of gL, indicating masking of N-glycans by association with gL; and (v) an anti-gL polyclonal antiserum is able to neutralize virion infectivity but did not inhibit cell-to-cell spread. Thus, whereas PrV gL is essential for virus replication, as is HSV-1 gL, gL- PrV mutants exhibit properties strikingly different from those of HSV-1. In conclusion, our data show an important functional role for PrV gL in the viral entry process, which is not explained by a chaperone-type mechanism in gH maturation and processing.

Animals↗
PubMed1997

Functional complementation of UL3.5-negative pseudorabies virus by the bovine herpesvirus 1 UL3.5 homolog.

The UL3.5 gene is positionally conserved but highly variable in size and sequence in different members of the Alphaherpesvirinae and is absent from herpes simplex virus genomes. We have shown previously that the pseudorabies virus (PrV) UL3.5 gene encodes a nonstructural protein which is required for secondary envelopment of intracytoplasmic virus particles in the trans-Golgi region. In the absence of UL3.5 protein, naked nucleocapsids accumulate in the cytoplasm, release of infectious virions is drastically reduced, and plaque formation in cell culture is inhibited (W. Fuchs, B. G. Klupp, H. Granzow, H.-J. Rziha, and T. C. Mettenleiter, J. Virol. 70:3517-3527, 1996). To assay functional complementation by a heterologous herpesviral UL3.5 protein, the UL3.5 gene of bovine herpesvirus 1 (BHV-1) was inserted at two different sites within the genome of UL3.5-negative PrV. In cells infected with the PrV recombinants the BHV-1 UL3.5 gene product was identified as a 17-kDa protein which was identical in size to the UL3.5 protein detected in BHV-1-infected cells. Expression of BHV-1 UL3.5 compensated for the lack of PrV UL3.5, resulting in a ca. 1,000-fold increase in virus titer and restoration of plaque formation in cell culture. Also, the intracellular block in viral egress was resolved by the BHV-1 UL3.5 gene. We conclude that the UL3.5 proteins of PrV and BHV-1 are functionally related and are involved in a common step in the egress of alphaherpesviruses.

Animals↗
PubMed1997

The UL20 gene product of pseudorabies virus functions in virus egress.

The UL20 open reading frame is positionally conserved in different alphaherpesvirus genomes and is predicted to encode an integral membrane protein. A previously described UL20- mutant of herpes simplex virus type 1 (HSV-1) exhibited a defect in egress correlating with retention of virions in the perinuclear space (J. D. Baines, P. L. Ward, G. Campadelli-Fiume, and B. Roizman, J. Virol. 65:6414-6424, 1991). To analyze UL20 function in a related but different herpesvirus, we constructed a UL20- pseudorabies virus (PrV) mutant by insertional mutagenesis. Similar to HSV-1, UL20- PrV was found to be severely impaired in both cell-to-cell spread and release from cultured cells. The severity of this defect appeared to be cell type dependent, being more prominent in Vero than in human 143TK- cells. Surprisingly, electron microscopy revealed the retention of enveloped virus particles in cytoplasmic vesicles of Vero cells infected with UL20- PrV. This contrasts with the situation in the UL20- HSV-1 mutant, which accumulated virions in the perinuclear cisterna of Vero cells. Therefore, the UL20 gene products of PrV and HSV-1 appear to be involved in distinct steps of viral egress, acting in different intracellular compartments. This might be caused either by different functions of the UL20 proteins themselves or by generally different egress pathways of PrV and HSV-1 mediated by other viral gene products.

Animals↗
PubMed1997

[Studies on the protective effect of lansoprazole on human gastric mucosa against low-dose acetylsalicylic acid. An endoscopic controlled double-blind study].

In a randomized double-blind parallel study the gastroduodenal tolerability of 300 mg acetylsalicylic acid (ASA) daily has been evaluated in the presence of placebo, 15 mg lansoprazole (CAS 103577-45-3, Agopton) and 300 mg ranitidine daily (8 a.m.) in 30 healthy volunteers using upper gastrointestinal tract endoscopy. The treatment periods lasted 14 days. Endoscopic controls were performed at entry and repeated at day 14. At entry, the mean endoscopic score averaged 1.0 +/- 0.0 (+/- SEM) in the ASA/placebo (n = 10), in the ASA/ lansoprazole 15 mg (n = 10) and the ASA/300 mg ranitidine group. In the placebo experiments 300 mg ASA daily induced marked gastroduodenal lesions at day 14 (lesion score of 10.1 +/- 1.4) (+/- SEM). Concomitant administration of 15 mg lansoprazole daily offered significant protection against 300 mg ASA daily on day 14 (3.6 +/- 1.2) (p < 0.05), 300 mg ASA plus 300 mg ranitidine daily reduced the damaging score to 5.8 +/- 1.3 (p n.s. vs ASA/placebo). Our data suggest that co-administration of 15 mg lansoprazole daily reduces significantly gastroduodenal lesions evoked by 300 mg ASA.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

DNA sequence and transcriptional analysis of the UL1 to UL5 gene cluster of infectious laryngotracheitis virus.

We have cloned and sequenced the KpnI L and M restriction fragments of infectious laryngotracheitis virus (ILTV, gallid herpesvirus 1) DNA, which are localized adjacently at the right end of the unique long region of the genome. Within the 6930 bp DNA sequence six complete open reading frames (ORFs) were identified. The predicted amino acid sequences of four of them exhibit significant homologies to the UL5 (helicase), UL4, UL3 and UL2 (uracil-DNA glycosylase) genes, which are conserved in similar arrangement in all alphaherpesvirus genomes characterized up to now. A short ORF of 72 codons between UL3 and UL4 of ILTV is positionally homologous to the UL3.5 gene present in the genomes of different members of the Varicellovirus genus of alphaherpesviruses, but not in herpes simplex virus. The predicted ILTV protein encoded upstream of UL2 possesses limited sequence homology to the UL1 gene product of herpesviruses, the structural glycoprotein L. The presence of a N-terminal signal sequence, a conserved N-glycosylation site and two conserved cysteine residues indicates a similar function of the putative ILTV protein. Upstream of the UL1 gene of ILTV the C-terminal part of an additional ORF designated as ULO was identified, which exhibits no significant homology to known herpesvirus genes. RNA analyses indicate the expression of all detected ILTV genes including ULO.

Amino Acid Sequence↗
PubMed1996

Identification and characterization of the pseudorabies virus UL3.5 protein, which is involved in virus egress.

Alphaherpesvirus genomes exhibit a generally collinear gene arrangement, and most of their genes are conserved among the different members of the subfamily. Among the exceptions is the UL3.5 gene of pseudorabies virus (PrV) for which positional homologs have been detected in the genomes of varicella-zoster virus, equine herpesvirus 1, and bovine herpesvirus 1 but not in the genomes of herpes simplex virus types 1 and 2. To identify and characterize the predicted 224 amino acid UL3.5 protein of PrV, a rabbit antiserum was prepared against a UL3.5 fusion protein expressed in Escherichia coli. In Western blot (immunoblot) analyses the antiserum detected a 30-kDa protein in the cytoplasm of PrV infected cells which was absent from purified virions. For functional analysis, UL3.5-expressing cell lines were established and virus mutants were isolated after the rescue of defective, glycoprotein B-negative PrV by insertion of the complementing glycoprotein B-encoding gene of bovine herpesvirus 1 at two sites within the UL3.5 locus. A PrV mutant carrying the insertion at codon 159 and expressing a truncated UL3.5 protein was still capable of efficient productive replication in noncomplementing cells. In contrast, a PrV mutant carrying the insertion at codon 10 of the UL3.5 gene did not express detectable UL3.5 protein and exhibited a dramatic growth deficiency on non-complementing cells with regard to plaque formation and one-step replication. Electron microscopical studies showed an accumulation of unenveloped capsids in the vicinity of the Golgi apparatus. This defect could be compensated by propagation on complementing UL3.5-expressing cell lines. Our results thus demonstrate that the PrV UL3.5 gene encodes a nonstructural protein which plays an important role in virus replication, presumably during virus egress. The functionally relevant domains appear to be located within the N-terminal part of the UL3.5 protein which also comprises the region exhibiting the highest level of homology between the predicted UL3.5 homologous proteins of other alphaherpesviruses.

Animals↗
PubMed1995

Mutations affecting the UL21 gene contribute to avirulence of pseudorabies virus vaccine strain Bartha.

Analysis of the live attenuated pseudorabies virus (PrV) vaccine strain Bartha indicated location of a major determinant for PrV neurovirulence within the genomic BamHI fragment 4 (B. Lomniczi et al., 1984, J. Virol. 52, 198-205). To more precisely localize the defect, marker rescue experiments were performed using cloned subfragments of BamHI-4. Rescuants were analyzed after intracerebral infection for their virulence in chicken, as well as after intranasal infection for virulence in pigs. We show that the defect associated with attenuation in strain Bartha is located in a 3.8-kb subfragment of BamHI-4 which encompasses the PrV UL20 and UL21 genes and a putative origin of replication (B. Klupp, H. Kern, and T. C. Mettenleiter, 1992, Virology 191, 900-908). Sequence analysis of this region of the strain Bartha genome and comparison with the corresponding region in wild-type PrV strain Ka revealed the presence of eight point mutations. Four nucleotide exchanges reside within the UL21 gene with three of them leading to amino acid substitutions; one is located in the intergenic region between the UL20 and UL21 genes and three are localized downstream from the UL21 gene. Neither the UL20 gene nor the putative origin sequence was affected. Insertional inactivation of the UL21 gene in wild-type PrV strain Ka led to a marked attenuation of the virus for pigs infected by the intranasal route. In summary, our data show that the PrV UL21 gene is a major determinant of PrV virulence and that point mutations affecting the UL21 gene of live vaccine strain Bartha contribute to its attenuated phenotype.

Amino Acid Sequence↗
PubMed1995

Comparison of the safety and efficacy of delapril with captopril in outpatients with congestive heart failure.

In this study delapril and captopril were compared in outpatients with congestive heart failure (CHF), New York Heart Association (NYHA) classes III and IV, in a double-blind study of efficacy and safety. Efficacy was evaluated by monitoring changes in the NYHA classification, exercise work, hemodynamic parameters, Kostuk's classification, and clinical signs and symptoms. Safety was monitored by a variety of laboratory tests, including renal and hepatic function, urinalysis, routine hematology testing, and the reporting of adverse events. Analysis of the data obtained revealed that delapril and captopril exhibit equal efficacy over the dosage ranges studied. There was a greater improvement of NYHA classification in terms of CHF signs and symptoms and ergometric workload in the delapril group; however, this did not reach statistical significance. The safety of the 2 drugs was also comparable, with no significant differences in any of the parameters measured at the start and end of the study. There was no statistically significant difference in the reporting of adverse events between the 2 drugs, although the sample size studied was small. There were no significant differences between the 2 drugs in terms of their effects on arterial blood pressure and no difference between prestudy and post-treatment arterial blood pressure measurements.

Administration, Oral↗
PubMed1995

Influence of lansoprazole on intragastric 24-hour pH, meal-stimulated gastric acid secretion, and concentrations of gastrointestinal hormones and enzymes in serum and gastric juice in healthy volunteers.

Twelve healthy volunteers (6 females, 6 males) between 26 and 36 years of age were enroled in this double-blind, randomized, placebo-controlled, three-way cross-over study. The objective was to determine the influence of lansoprazole (Agopton, Takeda Pharma GmbH, Aachen), a novel proton pump inhibitor, in doses of 30 and 60 mg, on the intragastric pH, on meal-stimulated gastric acid secretion and on the concentration of gastrointestinal hormones and enzymes in serum and gastric juice. Active drug or placebo had to be taken as single daily morning doses on an empty stomach for 7 days. Each wash-out period between drug application periods was 2 weeks long. Lansoprazole induced a dose-related increase in intragastric pH as well as a relevant reduction of basal acid output, meal-stimulated acid output and meal-stimulated secretion volume. 60 mg lansoprazole was significantly superior to 30 mg in increasing intragastric pH. The basal secretion volume in volunteers on 30 and 60 mg lansoprazole were lower than in volunteers on placebo. Serum gastrin and serum pepsinogen concentrations increased in a dose-dependent manner. Pepsin output and pepsin activity in gastric juice were slightly decreased in volunteers on 30 mg lansoprazole and markedly suppressed in volunteers on 60 mg lansoprazole 2 h after meal stimulation. Intrinsic factor concentration increased in volunteers on lansoprazole with a clear dose relationship. The evaluation of laboratory data and reported nonserious adverse events proved the relative safety of this new antiulcer agent.

2-Pyridinylmethylsulfinylbenzimidazoles↗