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T Ogihara

Publications and source records attributed to T Ogihara.

At least 469 records · Page 26Linked to original sources
PubMed1995

Sjögren's syndrome with pleural effusion.

Sjögren's syndrome (Sjs) can cause many organic changes, but is rarely accompanied by pleuritis. We report here a 62-year-old patient with subclinical Sjs who developed unilateral pleuritis with moderate effusion. He was diagnosed to have subclinical Sjs based on the positivity of anti SS-A/SS-B antibodies and the biopsy findings of minor salivary glands which revealed lymphocyte infiltration around the duct. In the pleural effusion, both increased lymphocytes and anti SS-A/SS-B antibodies were observed. He showed no signs of infection nor malignancy. There was no direct evidence that he had other collagen diseases which cause pleuritis. We conclude that the pleuritis was caused by Sjs. In patients with Sjs, activated polyclonal B lymphocytes and autoantibodies are considered to cause systemic tissue damage. This case indicates that these factors can cause pleuritis in Sjs patients.

Biopsy↗
PubMed1995

Leukemia developing after 131I treatment for thyroid cancer in a patient with Werner's syndrome: molecular and cytogenetic studies.

A 40-year-old female patient with Werner's syndrome (WS) suffering from thyroid cancer and myelodysplastic syndrome (MDS) is reported. She had been diagnosed as having WS complicated with thyroid cancer seven years previously. Total thyroidectomy and radioactive iodine (131I, 100 mCi/year) therapy for seven years had slowed the progression of thyroid cancer. She suffered a sudden onset of MDS at the age of 40 years. After six months she died from overt leukemia. We found an additional chromosome aberration of chromosome 10 in the progression of leukemia from MDS.

Adenocarcinoma, Papillary↗
PubMed1995

Gastric blood flow in ulcer diseases.

BACKGROUND: Gastric blood circulation maintains the structure and functions of the stomach, and thereby is closely associated with the pathogenesis and the healing of gastrointestinal lesions. Gastric mucosal blood flow, regulated by systemic neural and humoral factors, is also modified by local metabolic factors such as prostaglandins, leukotrienes. PAF and other endogenous chemical mediators in mucosa. Endothelium-derived factors that are produced by vascular endothelial cells, inducing relaxation or contraction of the blood vessels, are also recognized as basic mediators that regulate the circulation in the stomach. RESULTS: The regionally disturbed gastric circulation in combination with the presence of acid is closely associated with the pathogenesis of NSAIDs and ethanol-induced gastric lesions. Blood flow and oxygenation in the surface mucosa surrounding the peptic ulcer change during healing, depending on the quality of the ulcer healing process: an increased blood circulation with increased oxygen supply to the ulcer margin is important for rapid ulcer healing shown by reflectance spectrophotometry. Factors altering the blood flow during the ulcer healing are discussed.

Animals↗
PubMed1995

[Perceived quality of life and social factors in elderly hypertensive patients].

We conducted a cross-sectional study of elderly outpatients with hypertension to examine the relationship between quality of life (QOL) scores and social background factors. The subjects consisted of 516 outpatients (267 females), age of 60 or over, at nine clinics of major hospitals which participated in the National Cardiovascular Center Research Project. The perceived QOL was evaluated by the QOL scale originally based on Japanese patients with cardiovascular diseases. The scale consisted of the following 5 subscales; difficulty due to disease, psychological stability, independence, satisfaction in daily living and vitality. The background factors included family structure, socioeconomic factors and work status, and physical activity of daily living (ADL). After adjusting for age, sex, administered drugs and complicating conditions such as ischemic heart disease and/or apoplexy, a significant odds ratio of a low score of difficulty due to disease, psychological stability, satisfaction in daily living and vitality was found in the impaired physical ADL group with low socioeconomic class, and a significant odds ratio of low score of independence were found in the impaired physical ADL group who had lost jobs due to illness and had no children.

Aged↗
PubMed1995

[Genetic analysis of Werner syndrome in a family].

Werner syndrome (WRN) is a rare autosomal recessive disorder, one of the progeroid syndromes, and is characterized by features of premature aging. The incidence of WRN in the Japanese population, 1 in 200,000, is higher than than that in the Caucasian population. The genetic defect of WRN is unknown. But genetic linkage to several markers on the short arm of chromosome 8 has been reported recently. Here, we studied one family with WRN in which an affected individual had a papillary thyroid carcinoma and myelodysplastic syndrome. Using 4 microsatellites closely located to the WRN locus: D8S360, D8S1055, D8S339 and ANK1, we analyzed the genotypes of this patient, her three siblings and her parents, who were first cousins. The mutative haplotype, identified through the generations in pedigree, helps detect a carrier or a presymptomatic patient. The eldest sister inherited two normal haplotypes, but the second sister inherited one mutative haplotype. There was no difference in clinical signs and symptoms between these sisters. when the WRN gene is isolated, it will help us understand the mechanism of aging.

Adult↗
PubMed1995

Role of parathyroid hormone-related protein in the proliferation of vascular smooth muscle cells.

Human parathyroid hormone-related protein(1-34) [hPTHrP(1-34)] inhibited [3H]thymidine incorporation into DNA of cultured vascular smooth muscle cells (VSMC) and increased intracellular cAMP accumulation, both in a concentration-dependent manner. The potency of hPTHrP(1-34) was similar to that of human parathyroid hormone(1-34) [hPTH(1-34)], but their antagonists, hPTHrP(7-34) and hPTH(3-34), showed no effect on VSMC DNA synthesis. The inhibitory effect of PTHrP on VSMC DNA synthesis was mimicked by dibutyryl-cAMP but not by dibutyryl-cGMP. These results suggest that PTHrP, as an autocrine and/or paracrine regulator, may inhibit VSMC DNA synthesis mediated at least partly by cAMP, a second messenger which has also been proposed to mediate vascular relaxation.

Animals↗
PubMed1995

[Acute lymphoblastic leukemia accompanied by severe hypercalcemia; successful treatment with bisphosphonate].

A 62-year-old woman was admitted to the hospital because of bone pain. Laboratory data showed blasts in the peripheral blood, hypercalcemia (corrected calcium 15.1 mg/dl) and an increased level of parathyroid hormone related-protein (PTHrP). Bone marrow aspiration revealed increased lymphoblasts (96.5%), indicating acute lymphoblastic leukemia (ALL, L1). Subsequent radiological examination disclosed bone infiltration of ALL. Although the hypercalcemia was successfully treated with bisphosphonate, the PTHrP level remained high. After chemotherapy, the blasts in the peripheral blood disappeared and the PTHrP level normalized. We hypothesize that in the present case the production of PTHrP by lymphoblasts resulted in the hypercalcemic state. Although ALL is rarely accompanied by hypercalcemia, this case might help us to understand the relationship between ALL and hypercalcemia.

Diphosphonates↗
PubMed1995

[Molecular genetics of myotonic dystrophy].

The gene for myotonic dystrophy (DM) was found to be an expansion of an unstable CTG repeat located in the 3'-UTR of the putative protein kinase gene. In the general population 5 approximately 37 copies of the repeat are present, but in DM patients the repeat number varies from 50 up to thousands of copies. We have determined the copy number of the CTG repeat and made a haplotype using the closely linked markers to the CTG repeat in 93 Japanese DM families. The absolute linkage disequilibrium was observed in patients from both populations, between the DM gene and the linked markers. These data strongly suggest a common origin of Caucasian and Japanese DM alleles. The genetic analysis of apparently sporadic occurrence of DM in a family in which two asymptomatic members have been shown to have a number of repeats corresponding to premutation alleles, 44 and 46 CTG alleles. These data strongly suggest that (CTG) 19 approximately 37 may act as a predisposing allele for successive DM generations and that there is a premutation allele for DM, as predicted in a multistep model for etiology of this disorder.

Alleles↗
PubMed1995

[Motilin].

Explore the source record for details and available documents.

Humans↗
PubMed1995

The effect of central amino acid neurotransmitters on the antihypertensive response to angiotensin blockade in spontaneous hypertension.

OBJECTIVE: To investigate the effects of central amino acid neurons on the antihypertensive action of a newly developed angiotensin II type 1 receptor (AT1) antagonist, CV 11974. MATERIALS AND METHODS: We measured the release of various amino acids in the rostral ventrolateral medulla using the brain microdialysis technique. A microdialysis probe was inserted into the exposed rostral ventrolateral medulla in male spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats anaesthetized with urethane. Mean arterial pressure and the release of amino acids (glutamate, glycine, glutamine, taurine and gamma-aminobutyric acid) were monitored before and after intravenous administration of CV 11974 (5 mg/kg), nitroglycerin (5 mu g/kg per min) or vehicle. RESULTS: In SHR, CV 11974 decreased mean arterial pressure (-40 +/- 6 mmHg) accompanied by significant increases in the release of inhibitory amino acids, glycine (411 +/- 83%) and gamma-aminobutyric acid (363 +/- 71%) in the rostral ventrolateral medulla, whereas intravenous nitroglycerin produced a decrease in mean arterial pressure (-35 +/- 4 mmHg) without changes in amino acid release. In WKY rats, both intravenous CV 11974 and intravenous nitroglycerin produced smaller but significant decreases in mean arterial pressure (CV 11974, -18 +/- 5 mmHg; nitroglycerin, -20 +/- 7 mmHg) without change in the release of amino acids in the rostral ventrolateral medulla. Selective perfusion of glycine or gamma-aminobutyric acid into the rostral ventrolateral medulla caused a larger mean arterial pressure reduction in SHR than in WKY rats. Furthermore, the use of a specific antagonist of glycine or of the gamma-aminobutyric acid receptor in the rostral ventrolateral medulla attenuated the antihypertensive response induced by the intravenous AT1 antagonist in SHR. CONCLUSION: The present results suggest that the release of the inhibitory amino acids glycine and gamma-aminobutyric acid in the rostral ventrolateral medulla contributes to the depressor action of this AT1 receptor antagonist in the genetic hypertensive rat model.

Angiotensin Receptor Antagonists↗
PubMed1995

Effect of angiotensinogen on blood pressure regulation in normotensive rats: application of a loss of function approach.

OBJECTIVE: To investigate the effect of plasma angiotensinogen on blood pressure regulation in normotensive rats, by a loss of function approach using antisense oligonucleotides. DESIGN AND METHODS: Eight-week-old male Wistar rats were transfected with antisense, sense or scrambled oligonucleotides using liposomes containing viral agglutinins, which are reported to be highly efficient in promoting fusion with target cells. The abdomen was opened with a median incision, and the liver and portal vein were exposed. Then 2.5 ml of hemagglutinating virus-liposome complex containing oligonucleotides was introduced into the liver by multiple direct injections or infusion via the portal vein. Blood pressure, plasma angiotensinogen and angiotensin II levels were measured after transfection. The hepatic angiotensinogen level was examined by Northern blotting and radioimmunoassay. RESULTS: The in vivo injection of antisense oligonucleotides against rat angiotensinogen by the hemagglutinating virus-liposome gene transfer method into normotensive rats resulted in a transient fall in blood pressure from day 1 to day 4 after injection. This was accompanied by a decrease in plasma angiotensinogen and hepatic angiotensinogen messenger RNA levels on day 2. No significant changes were noted in untreated rats or those treated with sense or scrambled oligonucleotides. Plasma angiotensin II concentration was also reduced by antisense treatment, but not sense or scrambled treatment. CONCLUSIONS: In vivo administration of antisense angiotensinogen oligonucleotides resulted in a transient decrease in blood pressure accompanied by a decrease in plasma angiotensinogen and angiotensin II levels, which suggests that angiotensinogen plays a pivotal role in the regulation of blood pressure in normotensive rats.

Angiotensin II↗
PubMed1994

Pharmacokinetics of antisense oligodeoxyribonucleotides (cyclin B1 and CDC 2 kinase) in the vessel wall in vivo: enhanced therapeutic utility for restenosis by HVJ-liposome delivery.

Using a highly efficient viral HVJ (hemagglutinating virus of Japan) liposome-mediated transfer method, we examined the cellular fate of antisense oligodeoxyribonucleotides (oligos) in the vessel wall in vivo. Direct transfer of unmodified FITC (fluorescein isothiocyanate)-labeled oligos into injured rat carotid arteries showed, localized in the medial layer, fluorescence that disappeared within 1 day. In contrast, transfection of unmodified FITC-oligos by the HVJ-liposome method showed, concentrated in the medial layer, high levels of fluorescence that were sustained for at least 1 week. Moreover, we demonstrated nuclear localization and accumulation of fluorescence in the vessel wall using this method. To examine the therapeutic utility of this method, we transferred antisense phosphorothioate oligos against cyclin B1- and CDC2 kinase-encoding genes into balloon-injured rat carotid artery as a potential therapy for experimental restenosis. Two weeks after transfection, antisense oligo treatment directed against either CDC2 kinase or cyclin B1 resulted in a partial, but significant, inhibition in neointima formation. In contrast, transfection of either sense or scrambled control oligos had no effect. Interestingly, co-transfection of antisense oligos against CDC2 kinase and cyclin B resulted in further inhibition of neointima formation, as compared to blockade of either gene target alone. These results demonstrate that: (i) the HVJ-liposome method enhances the half life and nuclear localization of antisense oligos in the vessel wall in vivo; and (ii) HVJ-mediated administration of antisense CDC2 kinase and cyclin B1 oligos produces a sustained inhibition of neointima formation after balloon angioplasty.

Animals↗
PubMed1994

Elastase enhances cAMP accumulation and the inhibition of DNA synthesis induced by OP-41483, a stable prostacyclin analogue, in vascular smooth muscle cells.

To define the physiological roles of elastase in the vascular wall, we examined whether elastase at low concentrations can modulate the proliferation of vascular smooth muscle cells (VSMC). Elastase itself at low concentrations from 1 to 50 ng/ml inhibited DNA synthesis dose-dependently in VSMC. However, phenylmethylsulfonyl fluoride-inactivated elastase failed to induce this inhibition. OP-41483, a stable analogue of prostacyclin, inhibited DNA synthesis and stimulated accumulation of cAMP in VSMC. Preincubation of VSMC for 24 h with 50 ng/ml elastase enhanced both inhibition of DNA synthesis and the accumulation of cAMP induced by OP-41483. Preincubation of VSMC with 12-O-tetradecanoylphorbol 13-acetate, an activator of protein kinase C (PKC), also enhanced cAMP accumulation induced by OP-41483. On the other hand, elastase failed to enhance OP-41483-induced cAMP accumulation in PKC down-regulated cells. Furthermore, coincubation with chelerythrine, an inhibitor of PKC, inhibited the enhancement of cAMP accumulation induced by preincubation with elastase. These results suggest that elastase at low concentrations can enhance the inhibition of VSMC proliferation induced by prostacyclin through the activation of protein kinase C.

Animals↗
PubMed1994

Augmentation by converting enzyme inhibition of accelerated endothelin release from rat mesenteric arteries following nephrectomy.

We investigated the release of endothelin-1 (ET) from rat mesenteric arteries to clarify its pathophysiological role in the sustained hypertension of spontaneously hypertensive rats (SHR) following nephrectomy and the regulatory mechanism of the ET release which might be modified by vascular angiotensins and bradykinins. Nephrectomy increased the plasma level of ET and enhanced the ET release in both SHR and Wistar-Kyoto rats (WKY). CV-11974, an angiotensin II receptor antagonist, did not affect the ET release from arteries of nephrectomized rats. On the contrary, infusion of captopril, a converting enzyme inhibitor, further enhanced the ET release in both intact and nephrectomized rats. These findings suggest that the release of ET from mesenteric arteries may be regulated by bradykinins, but not by angiotensins. This pressor substance does not contribute to the sustained hypertension because the enhanced production of ET observed in both SHR and WKY. However, there is a possibility that the exaggerated responsiveness of vascular ET may in part account for local vascular tone and vascular remodeling in renal dysfunction.

Analysis of Variance↗
PubMed1994

Glyburide enhances insulin gene expression and glucose-induced insulin release in isolated rat islets.

Long-term glyburide therapy has been reported to improve glucose-induced insulin secretion in patients with NIDDM. We examined the effects of glyburide on the synthesis and release of insulin and insulin gene expression in isolated islets in vitro. Incubation with glyburide (500 ng/ml) significantly increased insulin release without affecting the insulin content. The PPI mRNA level was not increased after incubation for 1 h but was increased after incubation for 20 h. Incubation with 5 ng/ml of glyburide for 1 h or 20 h had no effect on the content or release of insulin, but incubation with 5 ng/ml of glyburide for 20 h significantly increased the PPI mRNA level and enhanced insulin release induced by 11 mM glucose. These results suggest that a high concentration of glyburide stimulates insulin release directly, while a low concentration of glyburide increases the PPI mRNA level and may thereby enhance glucose-induced insulin release.

Animals↗
PubMed1994

Percutaneous transgastric intestinal decompression: the management of malignant bowel obstruction without nasal intubation.

We inserted a long intestinal tube via the percutaneous transgastric route in three patients with an inoperable malignant bowel obstruction. The percutaneous endoscopic gastrostomy technique facilitated this method. The main purpose of our procedure is to achieve direct intestinal decompression without nasal intubation, which is not always possible by venting gastrostomy alone. Palliative intestinal decompression proved to be effective in all patients. This alternative therapeutic strategy for managing bowel obstruction in terminal cancer patients is herein presented.

Cecal Neoplasms↗