Can proton pump inhibitors be used as bactericidal drugs in Helicobacter pylori-positive patients?
Explore the source record for details and available documents.
Helicobacter Infections↗
Biomedical subjects
M Kato
Publications and source records attributed to M Kato.
Properties of rat cone-mediated electroretinograms during light adaptation.
PURPOSE: Our aim was to better understand how to isolate the cone-mediated response in rats. Therefore, we studied the difference of ERGs in the course of light adaptation between 2 and 20 Hz stimulus frequencies. METHODS: A total of 90 rats divided into 18 different groups were used following overnight dark adaptation. ERGs were recorded against 3 different adapting field luminances (1.15, 1. 50 or 1.75 log cd/m(2)) with a combination of 3 stimulus flash intensities (0.86, 1.30 or 2.03 log cd sec/m( 2)). The responses were obtained at 2 minute intervals for 25 minutes of light adaptation. RESULTS: The response of the rat cone ERG was large despite the small number of cones. The mean amplitude increased systematically from the dark-adapted value requiring more than 15 minutes to reach an asymptote at 2 Hz stimulation, but only 10 minutes at 20 Hz stimulation. The 2 Hz adaptation curves had biphasic pattern compared to the monophasic 20 Hz curve. This second increase in the amplitude at 2 Hz appeared at around 7-8 minutes as a function of adaptation time. This tendency was most evident when using a low adapting field luminance with a high flash intensity. CONCLUSIONS: Our results suggest that the rods intrude much more during light adaptation at 2 Hz stimulation in rodents than in humans. Therefore, 20 Hz flicker stimulation can better isolate more the cone-mediated function than 2 Hz stimulation during the course of light adaptation in rats. Furthermore, the functional characteristics of the cone in rats may be different from that in humans.
Adaptation, Ocular↗
Soluble E-selectin as a marker of disease activity in pustulosis palmaris et plantaris.
In this study, we investigated a possible correlation between adhesion molecules and activity of pustulosis palmaris et plantaris (PPP). Serum levels of soluble E-selectin (sE-selectin), soluble intercellular adhesion molecules 1 (sICAM-1) and tumour necrosis factor alpha (TNF-alpha) in 30 untreated PPP patients were examined, and compared with those in 20 healthy subjects. Values in 10 PPP patients were re-examined after treatment. Serum levels of sE-selectin and TNF-alpha in untreated PPP patients were significantly higher than those in healthy subjects. There was a statistically significant correlation between the disease activity and serum levels of sE-selectin in untreated PPP patients. Furthermore, disease activity of PPP was higher in patients who smoked and during the summer, with elevation of serum sE-selectin levels. Serum levels of sE-selectin were downregulated with the recovery from PPP. These results suggest that sE-selectin may play a role in the pathogenesis of PPP and could be a reliable marker of its disease activity.
Adult↗
Roles of bone morphogenetic protein type I receptors and Smad proteins in osteoblast and chondroblast differentiation.
The biological effects of type I serine/threonine kinase receptors and Smad proteins were examined using an adenovirus-based vector system. Constitutively active forms of bone morphogenetic protein (BMP) type I receptors (BMPR-IA and BMPR-IB; BMPR-I group) and those of activin receptor-like kinase (ALK)-1 and ALK-2 (ALK-1 group) induced alkaline phosphatase activity in C2C12 cells. Receptor-regulated Smads (R-Smads) that act in the BMP pathways, such as Smad1 and Smad5, also induced the alkaline phosphatase activity in C2C12 cells. BMP-6 dramatically enhanced alkaline phosphatase activity induced by Smad1 or Smad5, probably because of the nuclear translocation of R-Smads triggered by the ligand. Inhibitory Smads, i.e., Smad6 and Smad7, repressed the alkaline phosphatase activity induced by BMP-6 or the type I receptors. Chondrogenic differentiation of ATDC5 cells was induced by the receptors of the BMPR-I group but not by those of the ALK-1 group. However, kinase-inactive forms of the receptors of the ALK-1 and BMPR-I groups blocked chondrogenic differentiation. Although R-Smads failed to induce cartilage nodule formation, inhibitory Smads blocked it. Osteoblast differentiation induced by BMPs is thus mediated mainly via the Smad-signaling pathway, whereas chondrogenic differentiation may be transmitted by Smad-dependent and independent pathways.
Activin Receptors↗
Characterization of homeodomain-leucine zipper genes in the fern Ceratopteris richardii and the evolution of the homeodomain-leucine zipper gene family in vascular plants.
The homeodomain-leucine zipper (HD-Zip) genes encode transcription factors that are characterized by the presence of both a homeodomain and a leucine zipper motif. They belong to the homeobox gene superfamily and have been reported only from flowering plants. This article is the first report on the ferm HD-Zip genes (named Crhb1-Crhb11) isolated from the homosporous ferm Ceratopteris richardii. Phylogenetic analyses of the II Crhb genes with previously reported angiosperm HD-Zip genes show that the Crhb genes belong to three of the four different angiosperm HD-Zip subfamilies (HD-Zip I, II, and IV), indicating that these subfamilies of HD-Zip genes originated before the diversification of the ferm and seed plant lineages. The Crhb4-Crhb8 and Crhb11 genes belong to the HD-Zip I subfamily but differ from angiosperm HD-Zip I genes by the presence of a seven-amino-acid indel in the leucine zipper motif. By the northern analyses, Crhb1 and Crhb3 were expressed only in gametophyte tissue. Expression of Crhb2 and Crhb11 genes could not be detected in any tissue examined, while all other Crhb genes were expressed in most sporophytic and gametophytic tissues. Although the functions of the Crhb genes in Ceratopteris are unknown, their patterns of expression suggest that they regulate developmental or physiological processes common to both the gametophyte and the sporophyte generations of the fern. Differences in the expression of Crhb1 between male gametophytes and male-hermaphrodite mixed populations of gametophytes suggests that the Crhb1 gene is involved in gametophytic sex determination.
Amino Acid Sequence↗
Molecular phylogenetic analysis among bryophytes and tracheophytes based on combined data of plastid coded genes and the 18S rRNA gene.
The basal relationship of bryophytes and tracheophytes is problematic in land plant phylogeny. In addition to cladistic analyses of morphological data, molecular phylogenetic analyses of the nuclear small-subunit ribosomal RNA gene and the plastic gene rbcL have been performed, but no confident conclusions have been reached. Using the maximum-likelihood (ML) method, we analyzed 4,563 bp of aligned sequences from plastid protein-coding genes and 1,680 bp from the nuclear 18S rRNA gene. In the ML tree of deduced amino acid sequences of the plastid genes, hornworts were basal among the land plants, while mosses and liverworts each formed a clade and were sister to each other. Total-evidence evaluation of rRNA data and plastid protein-coding genes by TOTALML had an almost identical result.
Bryopsida↗
Heritability of plasma leptin levels: a twin study.
OBJECTIVE: To examine the influence of genetic factors on plasma leptin levels. SUBJECTS AND METHODS: We measured plasma leptin levels, body mass index and body fat distribution in healthy young female monozygotic (n = 19) and dizygotic (n = 14) twins. The twin zygosity was verified by determination of short tandem repeat and amplified fragment length polymorphism systems. The genetic analysis included analysis of variance-based and maximum likelihood-based methods. RESULTS: Plasma leptin levels were correlated significantly with body mass index (r = 0.59, P < 0.001), waist circumference (r = 0.54, P < 0.001) and hip circumference (r = 0.63, P < 0.001), but not with age (r = -0.17) or the waist:hip ratio (r = 0.02). The heritability estimates derived from intraclass correlations were significant for body mass index (P = 0.001), waist circumference (P = 0.004), hip circumference (P = 0.01) and plasma leptin levels (P = 0.005), but not for the waist:hip ratio (P = 0.22). In the maximum likelihood-based path analysis, heritability was estimated at 79% for body mass index and at 73% for plasma leptin levels. After adjustment for body mass index, the heritability estimate for leptin levels from the model-fitting approach was 55%. CONCLUSIONS: Genetic factors are major determinants of plasma leptin levels in humans and may account for as much as half of the variance in leptin levels.
Adipose Tissue↗
An independent relationship between plasma leptin and heart rate in untreated patients with essential hypertension.
OBJECTIVE: To test the hypothesis that hemodynamic measurements in patients with essential hypertension are related independently to plasma leptin levels. PATIENTS AND METHODS: We measured plasma leptin, insulin, office and ambulatory blood pressure and heart rate in 60 men with untreated mild hypertension. RESULTS: Plasma leptin correlated significantly with body mass index (r = 0.43, P = 0.001), 24 h heart rate (r = 0.35, P = 0.006) and 24 h diastolic blood pressure (r = 0.27, P = 0.04) but not with age (r = 0.03; P = 0.85) or 24 h systolic blood pressure (r = -0.08, P = 0.56). Plasma leptin levels adjusted for body mass index correlated significantly with 24 h heart rate (r = 0.36, P = 0.005) but not with 24 h diastolic blood pressure (r = 0.19, P = 0.15). We divided the patient population into tertiles of body mass index-adjusted plasma leptin levels. Age, plasma insulin, blood pressure, smoking status and physical activity habits were similar across the adjusted leptin tertiles. Patients from the third tertile of adjusted plasma leptin distribution (those with leptin levels higher than would be expected on the basis of body mass index) had significantly faster ambulatory heart rates than subjects from both the first and the second tertiles. The difference in heart rate across the three tertiles was most pronounced for the night-time values. CONCLUSIONS: In patients with essential hypertension, heart rate is faster in those patients with higher plasma leptin levels. This relationship is independent of age, body mass index, insulin levels, blood pressure level, smoking status and physical activity.
Adipose Tissue↗
Recent weight gain in patients with newly diagnosed obstructive sleep apnea.
OBJECTIVE: Patients with obstructive sleep apnea are often obese. Obesity may contribute to both sleep apnea itself and to the cardiovascular risk associated with sleep apnea. Weight loss in obese patients with sleep apnea may alleviate symptoms and decrease the severity of sleep apnea. Whether patients with obstructive sleep apnea are indeed predisposed to recent weight gain, as compared with similarly obese subjects without sleep apnea, is not known. PATIENTS AND METHODS: We compared 1-year weight histories in 53 male and female patients newly diagnosed with obstructive sleep apnea, compared with 24 controls matched for gender, age, body mass index, and percent body fat. Sleep apnea patients had never been treated. Control subjects were proven to be free of sleep-disordered breathing by overnight polysomnography. RESULTS: Patients with obstructive sleep apnea (n = 53) had a significant recent weight gain of 7.4 +/- 1.5 kg compared with a weight loss of 0.5 +/- 1.7 kg (P = 0.001) in similarly obese controls (n = 24). Male patients with obstructive sleep apnea (n = 28) had a history of significant weight gain (6.8 +/- 2.3 kg) over the year preceding the study compared with male control subjects (n = 13), in whom average weight fell by 0.58 +/- 2.4 kg (P = 0.03). Female patients (n = 25) with obstructive sleep apnea had an 8.0 +/- 1.9 kg weight gain compared with female controls (n = 11) who had a history of weight loss of 0.46 +/- 2.6 kg (P = 0.02). CONCLUSION: These findings support the concept that patients with obstructive sleep apnea may be susceptible to increasing obesity in the period preceding the diagnosis of obstructive sleep apnea.
Adipose Tissue↗
The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation.
OBJECTIVE: There is limited information on the mechanisms mediating the deleterious effects of passive smoke exposure. Cross-sectional studies indicate that nonsmokers exposed chronically to passive smoke have impaired endothelium mediated vasodilation. We tested the hypothesis that acute exposure to sidestream (passive) smoke impairs endothelium-dependent vasodilation in healthy nonsmokers. METHODS AND RESULTS: We studied 12 healthy nonsmokers (aged 27 +/- 5 years, nine men and three women). We obtained measurements of blood pressure, heart rate, and bilateral forearm blood flow (FBF). Each individual was studied twice, following a randomized, placebo-controlled design. The effects of passive smoke were studied on one day and the effects of vehicle (room air) on a separate day. Acetylcholine (ACh) and sodium nitroprusside (SNP) were infused into the left brachial artery before and after 15 min of exposure to either passive smoke (carbon monoxide concentration between 20 and 40 p.p.m.) or vehicle (room air). The order of ACh and SNP, and smoke or vehicle, was randomized between individuals. Smoke exposure increased carboxyhemoglobin from 0.5 +/- 0.1 % to 0.8 +/- 0.1% (P= 0.002). Neither passive smoke nor vehicle changed baseline measurements of heart rate, blood pressure and forearm vascular resistance (FVR). The vasodilatory responses to ACh and SNP were very similar, both before and after exposure to passive smoke and before and after vehicle. CONCLUSION: Our data demonstrate that acute exposure to passive smoke does not alter either endothelium-dependent or independent vasodilatory responses in healthy nonsmoking individuals. Hence, impaired endothelial vasodilatory responses in nonsmokers chronically exposed to passive smoke most likely reflect chronic functional and/or structural changes in responses to cigarette smoke, rather than the acute effects of cigarette smoke toxicity on endothelial function.
Acetylcholine↗
Monoclonal antibody to human midkine reveals increased midkine expression in human brain tumors.
We produced a rat IgG2a monoclonal antibody against the carboxyl terminal region of human midkine (MK), a novel growth factor. This monoclonal antibody was used in immunohistochemical studies to compare the expression of MK, proliferating cell nuclear antigen (PCNA) and p53 protein in 133 primary brain tumors and 21 carcinoma metastases to the central nervous system. Approximately half of the glioblastomas multiforme (GBMs) (19/32), medulloblastomas (8/14), primitive neuroectodermal tumors (PNETs) (5/11), breast carcinoma metastases (Br-Mts) (6/10) and lung carcinoma metastases (L-Mts) (5/11) as well as some astrocytomas (2/14) had tumor cells that expressed MK; however, oligodendrogliomas, ependymomas, schwannomas, meningiomas, and pituitary adenomas did not express MK. The values of the PCNA-labeling index were statistically higher in GBMs, medulloblastomas, PNETs, Br-Mts, and L-Mts that expressed MK than in those that did not (Wilcoxon rank-sum test, p < 0.05). There was no correlation between MK and p53 protein in all tumor types. Normal and non-neoplastic brain tissues were negative for MK, PCNA, and p53 protein. We conclude that primary and metastatic tumors of the brain express MK and that the MK expression in brain tumors may depend, in part, on the proliferating potential.
Animals↗
Effect of inhalational anesthesia on cerebral circulation in Moyamoya disease.
To clarify the effects of inhalational anesthesia on cerebral circulation in patients with Moyamoya disease, the authors measured regional cortical blood flow (CoBF), jugular bulb oxygen saturation (SjO2), and frontal regional oxygen saturation (rSO2) by near infra-red spectroscopy under total intravenous and inhalational anesthesia in 13 patients undergoing revascularization procedures. Cortical blood flow decreased in some regions under inhaled anesthesia in all cases, and the mean value decreased significantly (p<0.01). Patients' SjO2 levels rose during inhalational anesthesia in 10 of 11 cases (p<0.01). Frontal rSO2 declined in 9 of 11 cases. Regional CoBF levels may be decreased by inhaled anesthesia in patients with Moyamoya disease, and such anesthesia may provoke intracerebral steal. Total intravenous anesthesia, however, lacked these effects.
Adolescent↗
Purification and characterization of caffeine synthase from tea leaves.
Caffeine synthase (CS), the S-adenosylmethionine-dependent N-methyltransferase involved in the last two steps of caffeine biosynthesis, was extracted from young tea (Camellia sinensis) leaves; the CS was purified 520-fold to apparent homogeneity and a final specific activity of 5.7 nkat mg-1 protein by ammonium sulfate fractionation and hydroxyapatite, anion-exchange, adenosine-agarose, and gel-filtration chromatography. The native enzyme was monomeric with an apparent molecular mass of 61 kD as estimated by gel-filtration chromatography and 41 kD as analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The enzyme displayed a sharp pH optimum of 8.5. The final preparation exhibited 3- and 1-N-methyltransferase activity with a broad substrate specificity, showing high activity toward paraxanthine, 7-methylxanthine, and theobromine and low activity with 3-methylxanthine and 1-methylxanthine. However, the enzyme had no 7-N-methyltransferase activity toward xanthosine and xanthosine 5'-monophosphate. The Km values of CS for paraxanthine, theobromine, 7-methylxanthine, and S-adenosylmethionine were 24, 186, 344, and 21 microM, respectively. The possible role and regulation of CS in purine alkaloid biosynthesis in tea leaves are discussed. The 20-amino acid N-terminal sequence for CS showed little homology with other methyltransferases.
Affinity Labels↗
Structure of the histidine-containing phosphotransfer (HPt) domain of the anaerobic sensor protein ArcB complexed with the chemotaxis response regulator CheY.
The three-dimensional structure of the HPt domain of ArcB complexed with CheY has been determined using the molecular-replacement method. The structure was refined to a crystallographic R factor of 18.3% at 2.68 A resolution. The final model included 1899 protein atoms (117 residues from the HPt domain and 128 residues from CheY), one sulfate ion and 44 solvent molecules. In the crystal, CheY molecules stacked along the a axis of the cell with no interactions between neighbouring rows and the HPt domain bridged the CheY molecules. The phosphodonor residue His715 was fully exposed to the solvent region, even though the HPt domain was in contact with four molecules of CheY. CheY showed significant conformational change. This indicates that the HPt domain has a rigid structure when complexed with CheY.
Bacterial Proteins↗
Refined structure of the histidine-containing phosphotransfer (HPt) domain of the anaerobic sensor kinase ArcB from Escherichia coli at 1.57 A resolution.
The crystal structure of the histidine-containing phosphotransfer (HPt) domain of the anaerobic sensor kinase ArcB from Escherichia coli has been refined to 1.57 A resolution, using the coordinates of the earlier 2.06 A structure as a starting model. The final model contained 956 protein atoms, one zinc ion and 156 water molecules, with an R factor of 19.0%. The high-resolution electron-density maps clearly revealed additional solvent molecules and seven discrete rotamers in the protein side chains. One residue, Met755, was fully buried but was able to occupy the space in the hydrophobic core by means of the two-state conformation of its side chain. One water molecule was buried in the protein core and contributed to the rigidity of the HPt domain, cooperating in the coordination of the zinc ion.
Anaerobiosis↗
Differential regulation of MMP-9 and TIMP-2 expression in malignant melanoma developed in metallothionein/RET transgenic mice.
We recently established a metallothionein-I(MT)/RET transgenic mouse line in which skin melanosis, benign melanocytic tumor and malignant melanoma develop stepwise. Malignant melanoma cells but not benign melanocytic tumor cells had metastatic ability in transgenic mice. In the present study, we investigated the expression of several matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs), including MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MT1-MMP, TIMP-1 and TIMP-2, in these tumors. Western and northern blot analyses revealed that malignant transformation of melanocytic tumors developed in MT/RET transgenic mice accompanied with upregulation of MMP-9 and downregulation of TIMP-2. Expression of other MMP and TIMP genes examined was very low or undetectable in both benign and malignant tumors. Since activation of MMP-9 in malignant tumors was detected by gelatin zymography, these results suggest that imbalance of expression of the MMP-9 and TIMP-2 genes might be associated with metastatic ability of melanoma cells developed in MT/RET transgenic mice.
Animals↗
Complete regression of recurrent esophageal carcinoma with reduced expression of glutathione S-transferase-pi by treatment with continuous infusion of 5-fluorouracil and low-dose cisplatin infusion.
The mortality rate of recurrent esophageal carcinoma remains high because of its resistance to chemotherapy and radiation therapy. We present a patient with recurrent esophageal carcinoma, which dramatically disappeared after treatment with the combination of continuous infusion of 5-fluorouracil and low-dose cis-Diamminedichloroplatinum-II (cisplatin) infusion (FP therapy). Furthermore, we immunohistologically found that glutathione S-transferases (GST)-pi, a marker of resistance to cisplatin, was faintly expressed both in the endoscopical biopsy specimens of recurrent tumor and in the resected specimens of esophageal carcinoma and metastatic lymph nodes. FP therapy was suggested to be effective for recurrent esophageal carcinoma. Immunostaining for GST-pi might be a prospective marker for the sensitivity of esophageal carcinoma to FP therapy, particularly cisplatin.
Antimetabolites, Antineoplastic↗
Intracellular signaling of the TGF-beta superfamily by Smad proteins.
TGF-beta is a potent inhibitor of cell growth, and accumulating evidence suggests that perturbation of the TGF-beta signaling pathway leads to tumorigenesis. Smads are recently identified proteins that mediate intracellular signaling of the TGF-beta superfamily. Smads 2 and 3 are phosphorylated by the TGF-beta type I receptor. Smad4 was originally identified as a candidate tumor suppressor gene in pancreatic cancers. Smads 2 and 3 form complexes with Smad4 upon TGF-beta stimulation. The heteromeric Smad complexes translocate into the nucleus, where they activate expression of target genes. Our recent study demonstrated that Smads exist as monomers in the absence of TGF-beta. Smads 2 and 3 form homo- as well as hetero-oligomers with Smad4 upon ligand stimulation. Both homo-oligomers and hetero-oligomers directly bind to DNA, suggesting that the signaling pathway of Smads may be multiplex. Smads 2 and 3 associate with transcriptional coactivators such as p300 in a ligand-dependent manner, p300 enhances transactivation by TGF-beta, suggesting that coactivators link Smads to the basal transcriptional machinery. A missense mutation of Smad2 identified in colorectal and lung cancers was introduced to Smad3. The mutant, Smad3(DE), blocked the activation of wild-type Smad2 and Smad3. Thus, the missense mutation not only disrupts the function of the wild-type Smad but also creates a dominant-negative Smad, which could actively contribute to oncogenesis.
Animals↗