Helicobacter pylori infection does not affect serum leptin concentration and body mass index (BMI) in asymptomatic subjects.
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Body Mass Index↗
Biomedical subjects
S Tsuji
Publications and source records attributed to S Tsuji.
Homozygosity and linkage disequilibrium mapping of autosomal recessive distal myopathy (Nonaka distal myopathy).
Autosomal recessive distal myopathy or Nonaka distal myopathy (NM) is characterized by its unique distribution of muscular weakness and wasting. The patients present with spared quadriceps muscles even in a late stage of the disease. The hamstring and tibialis anterior muscles are affected severely in early adulthood. We have localized the NM gene to the region between markers D9S319 and D9S276 on chromosome 9 by linkage analysis. To further refine the localization of the NM gene, we conducted homozygosity and linkage disequilibrium analysis for 14 patients from 11 NM families using 18 polymorphic markers. All of the patients from consanguineous NM families were found to be homozygous for six markers located within the region between markers D9S2178 and D9S1859. We also provided evidence for significant allelic associations between the NM region and five marker loci. Examination of the haplotype analysis identified a predominant ancestral haplotype comprising the associated alleles 199-160-154-109 (marker order: D9S2179-D9S2180-D9S2181-D9S1804), present in 60% of NM chromosomes and in 0% of parent chromosomes. On the basis of the data obtained in this study, the majority of NM chromosomes were derived from a single ancestral founder, and the NM gene is probably located within the 1.5-Mb region between markers D9S2178 and D9S1791.
Adult↗
Interaction between neuronal intranuclear inclusions and promyelocytic leukemia protein nuclear and coiled bodies in CAG repeat diseases.
Neuronal intranuclear inclusions (NIIs) are a pathological hallmark of CAG repeat diseases. To elucidate the influence of NII formation on intranuclear substructures, we investigated the relationship of NIIs with nuclear bodies in brains of dentatorubral-pallidoluysian atrophy and Machado-Joseph disease. In both diseases, promyelocytic leukemia protein, a major component of the promyelocytic leukemia protein nuclear bodies, altered the normal distribution and was rearranged around NII, forming a single capsular structure. We further demonstrated that NIIs were present in close contact with coiled bodies, a highly dynamic domain that may be involved in the biogenesis of small nuclear ribonucleoproteins. The preferential association of intranuclear polyglutamine aggregates with coiled bodies was also confirmed in the dentatorubral-pallidoluysian atrophy transgenic mouse brain and culture cells expressing mutant atrophin-1. The results suggest that the interaction between NIIs and nuclear bodies may play a role in the pathogenesis of CAG repeat diseases.
Adult↗
FcgammaRIII b and FcgammaRIIa polymorphism may affect the production of specific NA1 autoantibody and clinical course of autoimmune neutropenia of infancy.
We studied 18 children with autoimmune neutropenia (AIN) to evaluate whether there was a possible relationship between the specificity of granulocyte autoantibodies (anti-NA1,2) and the phenotype of the NA system. Direct granulocyte immunofluorescence test (D-GIFT) was positive in all patients, and indirect granulocyte immunofluorescence test (I-GIFT) was positive in 17 of these 18 patients, respectively. Fourteen of 18 patients showed preferential binding to neutrophils from NA(1+2-) phenotyped donors. Immunoblotting with anti-FcgammaRIIImAb showed that IgG prepared from 7 of 12 patients precipitated both FcgammaRIIIb from NA1 and NA2 neutrophil lysate, whereas the other 5 precipitated only NA1. Patients' IgG did not react with purified FcgammaRIIa. FcgammaRIIIb genotype were NA(1+2-) in 15 of 18 patients and NA(1+2+) in the other 3. FcgammaRIIa type of all patients were (H+R-). These distributions were significantly different from those of healthy Japanese blood donors (n = 608). The genotype of FcgammaRIIIb and FcgammaRIIa may affect the production of neutrophil specific auto-antibodies in AIN of infancy and influence its clinical course.
Age of Onset↗
Does xanthine oxidase contribute to the hydroxyl radical generation in ischemia and reperfusion of the cochlea?
We investigated the effect of a hydroxyl radical scavenger, 1,3-dimethyl-2-thiourea (dimethylthiourea), and two xanthine oxidase inhibitors, oxypurinol and allopurinol, on the threshold shift of the compound action potential (CAP) after transient ischemia of the cochlea. Transient ischemia of 30 min duration was induced in albino guinea pigs via a skull base approach. The animals were treated with perilymphatic perfusion of dimethylthiourea, oxypurinol or allopurinol from 10 min before the onset of ischemia to 4 h after the termination of ischemia. Dimethylthiourea ameliorated the CAP threshold shifts at 4 h after the onset of reperfusion in a dose-dependent manner. However, oxypurinol and allopurinol did not affect the post-ischemic cochlear dysfunction. These results imply that the hydroxyl radical plays an important role in generation of cochlear dysfunction induced by ischemia-reperfusion and that xanthine oxidase may not be the primary source of this radical.
Action Potentials↗
Ischemia-reperfusion injury of the cochlea: effects of an iron chelator and nitric oxide synthase inhibitors.
Release of free iron from cellular stores and activation of nitric oxide synthase (NOS) has been implicated in a wide variety of cochlear injuries. In order to evaluate the effects of deferoxamine (a iron chelator), 3-bromo-7-nitroindazole (a relatively selective neuronal NOS (nNOS) inhibitor) or aminoguanidine (a relatively selective inducible NOS (iNOS) inhibitor) on the post-ischemic cochlear dysfunction, albino guinea pigs were subjected to 30 min ischemia, and the threshold shifts of the compound action potential (CAP) from pre-ischemic values were compared with those of control animals 4 h after the onset of reperfusion. A statistically significant reduction in the post-ischemic CAP threshold shift was observed in the animals treated with deferoxamine or 3-bromo-7-nitroindazole. However, aminoguanidine did not affect the post-ischemic CAP threshold shift. These results suggest that free iron and nNOS play deleterious roles in the cochlear injury induced by transient ischemia.
Action Potentials↗
Cerebellar stimulation in acute cerebellar ataxia.
OBJECTIVES: To report follow-up studies of cerebellar stimulation in patients with acute cerebellar ataxia (ACA). METHODS: We studied two patients with ACA. One patient also had decreased deep sensations in the feet due to combined diseases such as diabetic polyneuropathy and lumbosacral radiculopathies. We applied the technique of electrical stimulation over the cerebellum which was reported previously (Ugawa et al., J Physiol 441 (1991a) 57). RESULTS: Conditioning stimulation over the cerebellum did not reduce the size of motor-evoked potentials to test magnetic stimulation of the motor cortex at conditioning-test intervals of 5, 6, and 7 ms in the acute stage in both patients. However, normal suppression was recognized in the recovery stage in both patients. CONCLUSIONS: This technique was useful for follow-up evaluation of cerebellar function in patients with ACA and was also useful for distinguishing cerebellar ataxia from sensory ataxia in a patient with combined diseases.
Aged↗
Somatosensory evoked high frequency oscillations recorded from subdural electrodes.
OBJECTIVES: To examine high frequency oscillations (HFOs) of somatosensory evoked potentials (SEPs) recorded directly from subdural electrodes to investigate the relationship between the primary somatosensory cortex and HFOs. METHODS: SEPs were recorded directly from subdural electrodes previously implanted in 3 patients for clinical evaluation prior to surgical treatment of intractable epilepsy. RESULTS: The primary sensory cortex (area 3b) was proposed as the source of somatosensory HFOs, because the distribution of HFOs recorded from the subdural electrodes agreed with the distribution of the N20-P20 components of the somatosensory evoked potential. The somatosensory HFOs showed a strictly somatotopic source arrangement. There was a polarity inversion of the prophase component and also the N20-P20 component of HFOs across the central sulcus. However, the phase was synchronized in the latter part of the HFOs. CONCLUSIONS: We propose that the origins of the early and latter parts of HFOs are different, and that there was a clear somatotopy.
Adult↗
Interferon gamma-producing ability in blood lymphocytes of patients with lung cancer through activation of the innate immune system by BCG cell wall skeleton.
An in vitro assay system was developed to assess the potency of the human innate immune system by measurement of IL-12, IL-18, IL-10 and IFNgamma in the supernatants of bacillus Calmette-Guerin cell wall skeleton (BCG-CWS)-stimulated blood samples. BCG-CWS is a ligand for Toll-like receptor (TLR) 2 and 4, and activates monocytes to macrophages (Mphi), and immature dendritic cells to mature antigen-presenting cells (APC). This system was found to allow the discrimination of immune suppressive states in patients with lung cancer from normal immune states in light of the cytokine profile. The following results were deduced from analyses of BCG-CWS-stimulated blood samples of lung cancer patients with reference to normal subjects. (1) The levels of production of IFNgamma and IL-10 by lymphocytes were decreased. (2) IL-12 p40 production by monocytes/Mphi was upregulated, while that of IL-10 was downregulated. (3) IL-18 was detected in all patients in a range similar to normal subjects. (4) Responses of lymphocytes to IL-2 and IL- 18 in terms of IFNgamma production were diminished. (5) The upregulated IL-12 levels were recovered to within the normal range in most patients after tumor resection. (6) Male patients showed more severe suppression of IL-12/IL-18-mediated IFNgamma production than female patients. Thus, the lesser IFNgamma production observed in patients' blood with high IL-12 p40 levels in response to BCG-CWS may reflect the production of p40 dimers or IL-23 instead of p70, or the presence of some unknown pathways to prohibit the interface between the innate and acquired immune systems. BCG-CWS-mediated Toll signaling may participate in IFNgamma induction for lymphocytes through Mphi/APC IL-12/I-18 modulation.
Adjuvants, Immunologic↗
Mitochondrial DNA reveal that domestic goat (Capra hircus) are genetically affected by two subspecies of bezoar (Capra aegagurus).
This article describes the complete sequences of the mitochondrial DNA displacement loop (D-loop) region and cytochrome b gene from domestic goats in Laos (Laos native) and wild goat "markhor" (C. falconeri). The wild goat "bezoar" (Capra aegagrus) has been considered to be the strongest candidate for the ancestor of the domestic goats (C. hircus); however, there is not sufficient molecular data to verify the hypothesis at present. In phylogenetic analyses, two wild goats, the markhor and the ibex (C. ibex), appeared as an outgroup, while the bezoar was located in a cluster of domestic goats. Mitochondrial haplotypes of Laos natives revealed two distinct major clusters: one was the same as the bezoar, the second, unique to Laos natives. The topology and calibrated levels of sequence divergence suggests that these clusters might represent at least two different subspecies of ancestral bezoars.
Animals↗
Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene.
Friedreich ataxia (FRDA), the most common autosomal recessive neurodegenerative disease among Europeans and people of European descent, is characterized by an early onset (usually before the age of 25), progressive ataxia, sensory loss, absence of tendon reflexes and pyramidal weakness of the legs. We have recently identified a unique group of patients whose clinical presentations are characterized by autosomal recessive inheritance, early age of onset, FRDA-like clinical presentations and hypoalbuminemia. Linkage to the FRDA locus, however, was excluded. Given the similarities of the clinical presentations to those of the recently described ataxia with oculomotor apraxia (AOA) linked to chromosome 9p13, we confirmed that the disorder of our patients is also linked to the same locus. We narrowed the candidate region and have identified a new gene encoding a member of the histidine triad (HIT) superfamily as the 'causative' gene. We have called its product aprataxin; the gene symbol is APTX. Although many HIT proteins have been identified, aprataxin is the first to be linked to a distinct phenotype.
Amino Acid Sequence↗
Improved preparation and crystallization of 25 kDa human fibroblast growth factor-9.
We prepared 25 kDa human fibroblast growth factor-9 (hFGF-9 N33) on a large scale after overproduction in Escherichia coli MM294 (DE3)/pTG931. The purification was performed by a combination of hydrophobic chromatography and HPLC with an ion exchange column, a heparin affinity column and a gel filtration column. This improved procedure was rapid and simple, and the purified hFGF-9 N33 was found to be homogeneous as judged by various criteria, such as amino acid analysis, N-terminal amino acid sequence, C-terminal amino acid analysis and biological activity. Furthermore, as determined by low endotoxin and DNA content, the protein was of high purity. In addition, the hFGF-9 N33 prepared in the present study was easily crystallized by the vapour diffusion method.
3T3 Cells↗
Phenytoin promotes Th2 type immune response in mice.
The effects of chronic administration of phenytoin, a common anticonvulsive drug, on immune responses were studied in mice. Anti-keyhole limpet haemocyanin (KLH) IgE antibody response after KLH-immunization was enhanced in phenytoin-treated mice. Proliferative responses of spleen cells induced with KLH, concanavalin A (ConA), lipopolysaccharide and anti-CD3 antibody were reduced in phenytoin-treated mice. Accessory function of spleen adherent cells on ConA-induced T cell proliferative response was reduced in phenytoin-treated mice. KLH-induced IL-4 production of spleen cells was enhanced, while IFN-gamma production was reduced in phenytoin-treated mice. In addition, production of IL-1 alpha, but not IL-6 and IL-12 by spleen adherent cells from phenytoin-treated mice was reduced. Natural killer cell activity was reduced in phenytoin-treated mice. These results suggest that phenytoin treatment preferentially induces a Th2 type response. We also observed that plasma ACTH and corticosterone levels were increased in phenytoin-treated mice, and speculated that phenytoin might act directly and indirectly, through HPA axis activation, on the immune system to modulate Th1/Th2 balance.
Adrenocorticotropic Hormone↗
Effects of osutidine (T-593) and its enantiomers on gastric mucosal hemodynamics and mucosal integrity in anesthetized rats.
T-593 (osutidine, CAS 140695-21-2) is a new anti-ulcer agent that consists of two enantiomers, (+)-(R)-T-593 and (-)-(S)-T-593. The present study was designed to investigate the effects of T-593, (+)-(R)-T-593 and (-)-(S)-T-593 on ethanol-induced gastric damage in rats. Rats were given intraperitoneal administration of vehicle, racemic T-593, (+)-(R)-T-593 or (-)-(S)-T-593. 30 min later, the rats intragastrically received a 1-ml solution of 40% ethanol, and 30 min thereafter, they were sacrificed for assessment of gastric damage. Gastric hemodynamics were assessed by reflectance spectrophotometry and laser Doppler flowmetry during the experiment. Gastric damage was significantly suppressed by racemic T-593 in a dose-dependent manner. While 60 mg/kg of (+)-(R)-T-593 and (-)-(S)-T-593 also suppressed ethanol-induced gastric injury, the same dose of racemic T-593 exerted the most potent anti-ulcerative activity. Both (+)-(R)-T-593 and racemic T-593 increased gastric mucosal blood flow and abolished gastric mucosal blood flow stasis induced by 40% ethanol. Although (-)-(S)-T-593, which antagonizes histamine H2-receptors, exerts an antiulcerative effect, (+)-(R)-T-593 also protects the gastric mucosa from ethanol-induced injury, possibly by influencing gastric mucosal hemodynamics. Thus racemic T-593 may protect the gastric mucosa by antagonizing H2-receptors and by enhancing gastric circulation in rats.
Anesthesia↗
A convenient method of granulocyte transfusion using a hydroxylethyl starch (HESPAN) containing a bag.
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Cell Separation↗
Molecular cloning and functional characterization of guinea pig IL-12.
IL-12 is a heterodimeric cytokine that plays a central role in cell-mediated immunity. We cloned complete cDNAs of guinea pig homologues of IL-12 p35 and p40 subunits, and compared their functional properties with human IL-12. Both p35 and p40 mRNA were constitutively expressed in the testis and peritoneal macrophages. On immunoblotting, anti-guinea pig p40 antibody detected the constitutive expression of p40 protein in the testis, while in macrophages it was induced in response to lipopolysaccharide. An unidentified 200-kDa macromolecule was also expressed in the testis. All recombinant hybrid heterodimer p70 (guinea pig p70, human p70 and two interspecies heterodimers) exerted proliferative activity toward concanavalin A-primed guinea pig and human lymphoblasts in a dose-dependent manner. A similar tendency was observed in IFN-gamma production in IL-2-treated human lymphocytes. All hybrid heterodimers also induced IFN-gamma mRNA from IL-2-treated guinea pig splenocytes. Thus, unlike the current concept that the p35 subunit determines the species incompatibility of IL-12 in humans and mice, p35 has marginal ability to define its species-specific functional expression between humans and guinea pigs. In addition, constitutive expression of IL-12 or related molecules in the testis indicated a potential role of this molecule in regulation of physiological or pathophysiological conditions in the reproductive system.
Amino Acid Sequence↗
Effects of angiotensin converting enzyme inhibitor and angiotensin II type 1 receptor blocker on cardiac dysfunction induced by isoproterenol in dogs.
We examined whether angiotensin converting enzyme (ACE) inhibitors and angiotensin II type 1 receptor blockers (ARB) prevent isoproterenol (ISO)-induced left ventricular (LV) dysfunction in dogs. The effects of a large dose of ISO, 1 microg/kg/min, 3 h infusion, were investigated in three groups with simultaneous infusion of an ACE inhibitor (quinaprilat), ARB (candesartan) or saline. ISO infusion significantly decreased LV dP/dt, LV ejection fraction and LV fractional shortening, and significantly increased tau, the time constant of isovolume relaxation of LV, and LV end diastolic pressure. All of these changes were significantly attenuated in both the ACE inhibitor and ARB groups, especially in the ARB group. Serum levels of creatinin kinase isoform MB, lactate dehydrogenase and lipid peroxide were significantly increased by ISO. However, the increases in these markers of myocardial damage were significantly diminished by simultaneous infusion of an ACE inhibitor or ARB, especially by ARB. In conclusion, an ACE inhibitor and ARB prevent LV systolic and diastolic dysfunction as well as myocardial damage induced by excess beta-adrenergic stimulation.
Adrenergic beta-Agonists↗
A case of myasthenia gravis preceded by major depression.
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Adult↗