[Diagnosis of Helicobacter pylori infection: comparison with gold standard].

Marshall and Warren were the first to succeed in culturing Helicobacter pylori (H. pylori) from the gastric mucosa of patients with gastritis in 1983. H. pylori is a spiral-shaped bacterium that resides in the gastric mucosa and is one of the most common infections worldwide. H. pylori infection causes gastritis and peptic ulcers and is associated with the development of gastric cancer and MALT lymphoma. Now, a variety of accurate diagnostic tests are widely available. Both invasive tests (bacterial culture, histopathology, and RUT) and non-invasive tests (UBT and serological test) are conducted for the diagnosis of H. pylori infection. This review provides a general overview of the diagnostic methods and tests the characteristics (sensitivity and specificity) for H. pylori infection.

Attenuated stress-induced catecholamine release in mice lacking the vasopressin V1b receptor.

Vasopressin V(1b) receptor is specifically expressed in the pituitary and mediates adrenocorticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the V(1b) receptor gene (V(1b)R(-/-) mice) vs. wild-type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), was increased in wild-type mice, whereas the increases in NE and DA were not observed in V(1b)R(-/-) mice. In wild-type mice, E, but not NE or DA, was increased in response to social isolation stress, whereas the increase in E was not observed in V(1b)R(-/-) mice. These results suggest that the V(1b) receptor regulates stress-induced catecholamine release. Because it has been suggested that arginine-vasopressin (AVP) is related to the development of depression, we also evaluated immobility time in the forced swimming test, and we found no significant change in V(1b)R(-/-) mice. Taken together, these findings suggest that, in addition to the previously elucidated effect on the hypothalamic-pituitary-adrenal axis, vasopressin activity via V(1b) receptors regulates stress-induced catecholamine release.

Antidiuretic effects of a novel nonpeptide vasopressin V(2)-receptor agonist, OPC-51803, administered orally to dogs.

We elucidated the pharmacological properties of a novel nonpeptide vasopressin V(2)-receptor agonist, OPC-51803 ((5R)-2-[1-(2-chloro-4-(1-pyrrolidinyl)benzoyl-2,3,4,5-tetrahydro-1H-1-benzazepine-5-yl]-N-isopropylacetamide), via both in vitro binding experiments incorporating canine kidney and platelet membrane fractions and in vivo experiments that would determine the compound's antidiuretic effects after oral administration to water-loaded dogs. OPC-51803 displaced [(3)H]arginine vasopressin (AVP) binding to canine V(2) and V(1a) receptors, as determined by resulting K(i) values of 15.2 +/- 0.6 nM (n = 4) and 653 +/- 146 nM (n = 4), respectively. These data indicate that OPC-51803 was about 43 times more selective for V(2) receptors than for V(1a) receptors. Antidiuretic studies showed that orally administered doses of OPC-51803 (0.03 to 0.3 mg x kg(-1)) decreased urine volume and increased urinary osmolality in a dose-dependent manner in water-loaded dogs. Intravenous OPC-51803 infusions (0.3 and 3 microg x kg(-1) x min(-1)) did not affect renal or systemic hemodynamics in anesthetized dogs. Since these results confirm that OPC-51803 shows antidiuretic action in dogs, the compound may be useful for treating AVP-deficient pathophysiological states.

Analysis of risk factors for hepatocellular carcinoma in patients with HBs antigen- and anti-HCV antibody-negative alcoholic cirrhosis: clinical significance of prior hepatitis B virus infection.

BACKGROUND: The hepatitis B virus (HBV) or hepatitis C virus (HCV) markers frequently are detected in alcoholic patients with hepatocellular carcinoma (HCC). However, risk factors for the development of HCC in patients with HBs antigen (Ag)- and anti-HCV antibody (anti-HCV)-negative alcoholic cirrhosis have not been clearly documented. The present study was conducted to elucidate the occurrence rates of HCC in HBs Ag- and anti-HCV-negative male alcoholic cirrhosis and to assess the risk factors for hepatocellular carcinogenesis. METHOD: We prospectively studied 91 consecutive patients with HBs Ag- and anti-HCV-negative alcoholic cirrhosis for 0.5 to 12.5 years (median 5.9 years). Potential risk factors assessed for liver carcinogenesis included the following six variables: age, total alcohol intake, association of continuing alcohol intake after diagnosis, indocyanine green retention rate at 15 min, anti-HB core antibodies (anti-HBc), and association of diabetes mellitus. RESULTS: Cumulative occurrence rates of HCC were 6.4%, 18.9%, and 28.7% at the end of the 5th, 7th and 10th years, respectively. When classified by anti-HBc, the occurrence rates of HCC in 31 patients with anti-HBc and 60 patients without anti-HBc were 15.6% and 2.9% at the 5th year, 28.4% and 13.5% at the 7th year, and 40.4% and 22.1% at the 10th year, respectively. The occurrence rates of HCC were also significantly related to the cumulative alcohol intake. Cox proportional hazard model identified that cumulative alcohol intake (p = 0.0047) and positive anti-HBc antibodies (p = 0.0598) were independently associated with the occurrence rates of HCC. CONCLUSION: These epidemiologic results suggest that heavy cumulative alcohol intake and prior exposure to HBV infection are risk factors for the development of HCC in patients with HBs Ag- and anti-HCV-negative alcoholic cirrhosis.

Effects of OPC-51803, a novel, nonpeptide vasopressin V2-receptor agonist, on micturition frequency in Brattleboro and aged rats.

We assessed the effects of OPC-51803 ((5R)-2-[1-(2-chloro-4-(1-pyrrolidinyl)benzoyl)-2,3,4,5-tetrahydro-1H-1-benzazepin-5-yl]-N-isopropylacetamide), a nonpeptide vasopressin V(2)-receptor agonist, on micturition frequency in female homozygous Brattleboro rats (strain carries hereditary diabetes insipidus) and aged male Sprague-Dawley rats with polyuria. Female homozygous Brattleboro rats exhibited more diuresis and a larger micturition frequency over a 24-h period than did the heterozygous controls. In Brattleboro rats, an oral administration of OPC-51803 at 0.03 and 0.3 mg/kg significantly decreased urinary frequency and was accompanied by decreased urine volume. However, little effect was seen in the mean and maximal micturition volume. Aged male Sprague-Dawley rats (25-month-old) showed a significant increase in urine volume throughout a 0- to 24-h period compared with mature (6-month-old) rats. Orally administered OPC-51803 at 0.3 mg/kg decreased not only urine volume but also urinary frequency in aged rats. Furthermore, OPC-51803 prolonged the time prior to the first micturition. Therefore, OPC-51803 decreased micturition frequency in both rat species by reducing urine outflow. This suggests that the compound will be useful for treating micturition disorders that result in frequent micturition, such as that from polyuria, nocturnal polyuria, and some kinds of urinary incontinence.

Oxygen radicals mediate ultrastructural and metabolic protection of preconditioning in vivo in pig hearts.

Ischemic preconditioning (PC) preserves myocardial high-energy phosphate metabolites and intracellular pH during subsequent sustained ischemia. Generation of reactive oxygen species may be required to mediate PC, as seen in vitro. In the present study, the effects of inhibiting reactive oxygen species generation during a PC protocol in vivo using an open-chest porcine model were examined. Myocyte ultrastructural changes assessed by electron microscopy were correlated with phosphorus nuclear magnetic resonance spectroscopy data. Open-chest pigs underwent 60 min of left anterior descending coronary artery occlusion. PC was elicited by a single episode of 5 min occlusion and 5 min reperfusion. The cell-diffusible hydroxyl radical and superoxide radical scavenger, N-2-mercapto-propionyl glycine (MPG, 20 mg/kg), or placebo saline were infused for 40 min, starting 30 min before PC (PC plus MPG group, n=10; and PC group, n=9). After PC, ATP and intracellular pH were significantly preserved through 25 min of ischemia (control versus PC, 46+/-3% versus 55+/-5% of baseline [P<0.05]; and control versus PC, 6.18+/-0.08 versus 6.42+/-0.03 [P<0.05], respectively). Phosphocreatine was significantly preserved through 20 min of ischemia (control versus PC, 0+/-0% versus 7+/-2% of baseline [P<0.05]). The preservation of high-energy phosphate metabolites and intracellular pH was abolished by inhibiting the generation of reactive oxygen species with MPG. Preservation of high-energy phosphate metabolites with PC was associated with reduced ultrastructural damage, as seen by electron microscopy, including less myocyte swelling, myofibrillar disruption and nuclear chromatin margination. The present study demonstrates the importance of reactive oxygen species generation in mediating PC preservation of myocyte ultrastructure and high-energy phosphate metabolites during prolonged ischemia in vivo.