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T Kawanami

Publications and source records attributed to T Kawanami.

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

Different effects of trypsin inhibitors on intestinal gene expression of secretin and on pancreatic bicarbonate secretion in CCK-A-receptor-deficient rats.

The effects of oral administration of two synthetic trypsin inhibitors (camostate and ONO-3403) and soybean trypsin inhibitor (SBTI) on cholecystokinin (CCK), secretin gene expression and pancreatic secretion were examined in CCK-A-receptor-deficient (OLETF) rats. The rats were fed chow containing 0.1% trypsin inhibitors for 7 days. To examine pancreatic secretion, the rats were prepared with cannulae to drain the bile and pancreatic juice separately, a duodenal cannula and an external jugular vein cannula. The animals were maintained in Bollman cages and the experiments were conducted 4 days after surgery. The levels of CCK mRNA were significantly increased by each treatment. The levels of secretin mRNA were significantly increased by camostate and SBTI, but not by ONO-3403. Bicarbonate secretion was significantly increased in rats treated with camostate and ONO-3403, but not SBTI, while protein secretion was not affected by any treatment. These observations suggest that increased bicarbonate secretion produced by synthetic trypsin inhibitors in CCK-A-receptor-deficient rats may not be due to secretin but due to ONO-3403 in the circulation.

Allylglycine↗
PubMed1999

T-cell lymphoma showing a non-enhancing diffuse white matter lesion with marked brain atrophy.

We report an autopsy case of T-cell lymphoma with diffuse white matter infiltration. Cranial magnetic resonance (MR) images showed atrophy of the brain with a diffuse, non-enhancing, T2-high signal intensity lesion in the cerebral white matter. Intra-axial infiltration of T-cell lymphoma should be considered a differential diagnosis in patients with these MRI findings.

Adolescent↗
PubMed1999

Evaluation of the substantia nigra in patients with Parkinsonian syndrome accomplished using multishot diffusion-weighted MR imaging.

BACKGROUND AND PURPOSE: Although it is important to evaluate the substantia nigra in patients with parkinsonian syndrome, it is difficult to depict its anatomy, even by MR imaging. Using anatomic studies of the direction of nerve fibers around the substantia nigra, we attempted to depict this entity with multishot diffusion-weighted MR imaging to evaluate its topographic changes in patients with Parkinson's disease and secondary parkinsonism. METHODS: We measured the substantia nigra on 72 diffusion-weighted axial MR images obtained in 36 healthy control subjects, on 47 images obtained in 25 patients with Parkinson's disease, and on 10 images obtained in five patients with secondary parkinsonism. We considered the width of the minor axis of the substantia nigra as its "thickness," which appeared as a crescent-shaped region in the midbrain. RESULTS: Diffusion-weighted imaging portrayed the substantia nigra distinctly better than did T2-weighted imaging, because the surrounding white matter appeared as an area of high signal intensity. The mean (+/- SD) thickness values of the substantia nigra were 5.1+/-0.89 mm in control subjects, 4.8+/-0.75 mm in patients with Parkinson's disease, and 3.4+/-0.53 mm in patients with secondary parkinsonism. CONCLUSION: Multishot diffusion-weighted imaging is a better imaging technique than T2-weighted imaging for demonstrating a change in size of the substantia nigra in vivo. The substantia nigra is not reduced in size in patients with Parkinson's disease, but it is reduced in patients with secondary parkinsonism.

Adult↗
PubMed1998

Retinal degeneration in hereditary ceruloplasmin deficiency.

A 56-year-old Japanese man was diagnosed as having hereditary ceruloplasmin deficiency. His ceruloplasmin concentration was below the lower limit of detection. Serum copper and iron concentrations were below normal, but the ferritin concentration was highly elevated. An ophthalmoscopic examination showed retinal degeneration with yellowish discoloration of the fundus in both eyes. Fluorescein angiography demonstrated a dark choroid in the posterior pole. Geographic areas of window defects were seen in the midperipheral fundus. The retinal degeneration in this patient was thought to be caused by the cellular iron deposition that occurred as a result of ceruloplasmin deficiency.

Ceruloplasmin↗
PubMed1997

Islet changes in hereditary ceruloplasmin deficiency.

Diabetes mellitus (DM) is the important initial symptom of hereditary ceruloplasmin deficiency (HCD). We examined the pancreas of an autopsy case of HCD and revealed a marked reduction in insulin-containing cells in the islets despite no massive iron deposition, degeneration, nor necrosis. Non-insulin-containing cells in the islets had glucagon or somatostatin. This study indicates that DM in HCD results from depletion of insulin cells and this depletion does not seem to be caused by the direct effect of iron deposition. The present observation suggests that the defect of the ceruloplasmin gene may influence the population of islet cells.

Ceruloplasmin↗
PubMed1996

Pancreatic endocrine dysfunction in rats not expressing the cholecystokinin-A receptor.

Cholecystokinin (CCK) has been suggested to modulate insulin output. We have shown that Otsuka Long-Evans Tokushima Fatty (OLETF) rats show little or no expression of the CCK-A receptor gene in the pancreas. We examined whether the CCK-A and CCK-B receptor genes are expressed in the islets and the role of CCK-A receptor in insulin secretion. Gene expressions of CCK receptors were determined by the reverse-transcriptase polymerase chain reaction (RT-PCR) followed by Southern blot hybridization and Northern transfer analysis using LETO rats as controls. Pancreatic endocrine function was examined in perfusion (exogenous CCK stimulation) and meal ingestion (endogenous CCK stimulation) studies. CCK-A receptor mRNA was detected in the islets of LETO rats but not OLETF rats. Expression of the CCK-B receptor gene was detected in both strains by RT-PCR. Insulin secretion was impaired in OLETF rats, but the insulin contents of OLETF and LETO rats were not different. No abnormalities were detected histologically in either strain. These results suggest that the occurrence of pancreatic endocrine dysfunction in OLETF rats may be due to a defect in expression of the CCK-A receptor gene, not to insulin deficiency.

Animals↗
PubMed1996

Neurohormonal regulation of pancreatic exocrine function in rats without gene expression of the cholecystokinin-A receptor.

Otsuka Long-Evans Tokushima Fatty (OLETF) rats revealed no or reduced expression of the cholecystokinin (CCK)-A receptor gene in the pancreas and that the pancreas of this strain of rats did not respond to CCK stimulation. We examined whether the pancreatic responses to hormonal and neural stimulation except for CCK in OLETF rats were maintained. The pancreatic responses of conscious OLETF rats to various stimuli were examined in vivo and compared with those of control (Long-Evans Tokushima; LETO) rats. Moreover, the levels of expression of CCK-A and -B receptor genes in the small intestine were examined. Pancreatic responses to intravenous injection of secretin and acetylcholine and to intracerebroventricular administration of thyrotropin-releasing hormone were comparable in OLETF and LETO rats. However, responses to intravenous injection of neuromedin C, to intraduodenal injection of capsaicin, and to intragastric injection of a liquid meal were impaired in OLETF rats. CCK-A receptor mRNA was not expressed in the small intestine of OLETF rats but was in LETO rats. The pancreatic responses to various stimuli in OLETF rats were well conserved except for the involvement of CCK-A receptor function. OLETF rats are confirmed as a new experimental model deficient in CCK-A receptor gene expression and represent a useful tool for studying the physiological role of these in vivo.

Acetylcholine↗
PubMed1996

Hereditary caeruloplasmin deficiency: clinicopathological study of a patient.

A 58 year old patient with dementia, oral dyskinesia, and diabetes mellitus is described. He had an undetectable concentration of serum caeruloplasmin, as an autosomal recessive trait. Brain MRI disclosed a pronounced hypointensity in the bilateral putamina, caudate, and dentate nuclei on both T1 and T2 weighted images. Pathological findings were mainly in those regions of the brain and consisted of neuronal cell loss with gliosis, heavy iron deposition, and spheroids. Visceral organs also had iron deposition, especially severe in the liver and pancreas. The present patient and other recorded cases constitute a clinicopathological entity of hereditary caeruloplasmin deficiency, different from Wilson's disease.

Brain↗
PubMed1995

A nonsense mutation of the ceruloplasmin gene in hereditary ceruloplasmin deficiency with diabetes mellitus.

A novel mutation of the ceruloplasmin (Cp) gene was found in a patient with hereditary ceruloplasmin deficiency (HCD) with diabetes mellitus (DM). The patient had been treated for DM for about 13 years, and then his illness was diagnosed as HCD. One year later, he was found dead in his home. A decrease in insulin-immunostained cells was observed in the islets of the patient's pancreas tissue, which accounted for his DM. The polymerase chain reaction (PCR)-direct sequencing analysis of the Cp gene of his daughter revealed a novel point mutation, G to A, at nucleotide 2630 in exon 15. This mutation changes the Trp858 codon (TGG) to a stop codon (TAG) (nonsense mutation). PCR-restriction analysis for the mutation revealed that the patient as well as his daughter was a heterozygote for the mutation, indicating that the patient was a compound heterozygote.

Amino Acid Sequence↗
PubMed1995

An animal model of congenital defect of gene expression of cholecystokinin (CCK)-A receptor.

Expressions of the CCK-A and B receptor genes in fetal and adult pancreas of OLETF rats were examined by the reverse transcriptase polymerase chain reaction followed by Southern blot hybridization. The pancreatic responses to various stimulants were examined in vitro and results were compared with those of control (LETO) rats. CCK-A receptor mRNA was not expressed in the fetal pancreas of either strain or in the adult pancreas of OLETF rats, but was expressed in the adult pancreas of LETO rats. CCK-B receptor mRNA was expressed in fetal and adult pancreas in both strains. Southern blot hybridization indicated a difference in gene structure in the two strains. The maximal effective concentrations of neuromedin C, carbachol, and secretin for amylase secretion and intracellular Ca2+ movement stimulated by carbachol and neuromedin C were similar in the two strains. CCK-8 and the non-sulfated form stimulated amylase secretion only in LETO rats. These results suggest that OLETF rats are a new model of a congenital defect of the CCK-A receptor gene and should be useful for determining CCK receptor function.

Amylases↗
PubMed1995

Fine structure of the human ceruloplasmin gene.

We characterized the genomic region corresponding to the human ceruloplasmin cDNA previously reported. Using PCR-direct sequencing methods, we determined precise intron/exon boundaries and intron-exon composition of the gene in the region. The gene region spanned about 50 kb and was composed of 19 exons and 18 introns. The lengths of exons and introns range from 107 to over 267 bp and from 0.44 to 10.0 kb, respectively. The translation initiation codon and the termination codon were located in exons 1 and 19, respectively. The nucleotide sequences of the introns were also determined in the region around the intron/exon boundaries for 24-220 bp. All the sequences around the intron/exon boundaries were consistent with the 5' and 3' consensus sequences for splice junctions of transcribed genes. Putative lariat sequences were identified between -17 and -42 nucleotides from the 3' splice junction for all 18 introns.

Alternative Splicing↗
PubMed1995

Cerebellar superoxide dismutase expression in Menkes' kinky hair disease: an immunohistochemical investigation.

This comparative immunohistochemical study deals with the expression of the cytosolic Cu/Zn-binding and mitochondrial Mn-dependent superoxide dismutases (SODs) in the cerebella of five patients with Menkes' kinky hair disease (MKHD) and five age-matched controls. Several cell types, including Purkinje cells and reactive astrocytes, of all MKHD patients examined were intensely stained by an antibody to Mn SOD, but not by an anti-Cu/Zn SOD antibody. By contrast, the cells of the five controls reacted very weakly or not at all with the anti-Mn SOD antibody, but were strongly reactive with the antibody to Cu/Zn SOD. These results suggest that the increased Mn SOD immunoreactivity in MKHD reflects enzyme induction as a protective mechanism against the highly toxic superoxide anion generated under the disease conditions.

Adolescent↗
PubMed1995

Yolk sac tumor in a case of testicular feminization syndrome.

A 17 month old who had been diagnosed as having testicular feminization syndrome (noted during inguinal herniorrhaphy) was operated on because of an abdominal mass that had a high serum level of alpha-fetoprotein. Histologically, the lesion was a yolk sac tumor. The alpha-fetoprotein level normalized within 2 months of the surgery, through the administration of adjunctive chemotherapy containing cisplatinum. The patient is disease-free 4 years postoperatively. When performing inguinal herniorrhaphy in a girl, the surgeon should be prepared to deal with testicular feminization syndrome. If gonadal neoplasm is deniable at the time of diagnosis, careful follow-up examinations are needed until completion of the development of secondary sex characteristics.

Androgen-Insensitivity Syndrome↗
PubMed1995

Effect of a cholecystokinin (CCK) antagonist (CR 1505) on gene expressions of CCK and secretin in rat intestine.

The effects of intragastric administration of cholecystokinin (CCK) antagonist (CR 1505; 60-300 mg/kg/day) to rats for 3 days on the gene expressions of CCK and secretin, the plasma CCK immunoreactivity, and the CCK content in the intestinal mucosa were examined. CR 1505 increased the level of CCK mRNA in the intestine dose dependently to up to 1.6 times the level in control rats but did not affect the level of secretin mRNA. It also significantly increased the plasma CCK immunoreactivity and the amount of CCK extracted from intestine with acid dose dependently. CR 1505 tended to decrease the trypsin activity in the intestine. These results suggest that ingested CR 1505 increased the CCK mRNA level in the intestine.

Animals↗