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Biomedical subjects

T Terano

Publications and source records attributed to T Terano.

At least 19 recordsLinked to original sources
PubMed2001

A case of POEMS syndrome with high concentrations of interleukin-6 in pericardial fluid.

The POEMS syndrome (plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy of various forms, monoclonal gammopathy, skin changes) is a rare multisystem disorder of unknown pathogenesis. Overexpression of proinflammatory cytokines has been implicated in the pathogenesis of POEMS syndrome, however, it is not known whether there is an association between abnormalities in cytokines and pericardial fluid. We present a case of POEMS syndrome with high concentrations of interleukin-6 (IL-6) in pericardial fluid. In our patient, pericarditis developed into cardiac tamponade, and the concentration of IL-6 in pericardial fluid was remarkably elevated compared with that in serum (1760 vs. 6.57 pg mL(-1)). We suggest that IL-6 is associated with the progression or maintenance of pericarditis as a result of POEMS syndrome.

Adult↗
PubMed2001

Fulminant Mycoplasma pneumoniae pneumonia.

A 64-year-old woman, who was previously in good health was admitted because of progressive respiratory distress. Her chest radiograph revealed bilateral widespread alveolar infiltrates. She was given a diagnosis of pneumonia caused by Mycoplasma pneumoniae serologically, acute respiratory distress syndrome, and disseminated intravascular coagulation. She died of multiple organ failure despite intensive therapy with mechanical ventilation, intravenous erythromycin and corticosteroids, continuous hemodiafiltration, and plasma exchange. Although Mycoplasma pneumoniae infection is usually a benign self-limited disease, this case emphasizes its potentially serious nature even in normal healthy individuals.

Adrenal Cortex Hormones↗
PubMed2001

Diabetic ketoacidosis associated with recurrent pulmonary edema and rhabdomyolysis in a patient with Turner's syndrome.

Turner's syndrome is a condition involving total or partial absence of one X chromosome and has been associated with a number of diseases including non insulin dependent diabetes mellitus, abnormalities of glucose metabolism and hypothreosis. There have been many case reports in which Turner's syndrome is associated with type 2 diabetes, but the association with type 1 diabetes and/or life threatening complications is very rare. We present an unusual case of a patient with Turner's syndrome who has type 1 diabetes and is complicated with ketoacidosis, severe acute and recurrent pulmonary edema and rhabdomyolysis.

Acidosis↗
PubMed2000

Growth hormone secreting adenoma with unusual extension: coexisting pituitary cyst and its clinical significance.

A 58 year old man showed acromegalic features. The serum growth hormone (GH) level was 7.3 ng/ml and SMC (somatomedin-C) 637 U/ml. Triple stimulation test showed abnormal response compatible with a GH secreting tumour. The conventional enhanced MRI revealed a less enhanced hemisphere-shaped lesion at the right corner of the sella turcica. In addition, dynamic MRI demonstrated an elongated lesion extending to the left beyond the midline. The patient underwent transsphenoidal surgery. Besides the soft and suckable tumour at the right corner, we entered into a small cavity loosely filled with the tumour, which was subsequently also removed. The operative finding corresponded to the lesion shown in dynamic MRI. Postoperative GH and SMC levels became 2.3 ng/ml and 326 U/ml respectively. Incidental pituitary cystic lesions in autopsied cases have been reported to be 6-33%. This case had a GH secreting adenoma with coexisting pituitary cyst. The coexisting pituitary cyst supposedly influenced the unusual shape and extension of the pituitary adenoma. Coexistence of such lesion should be kept in mind for microadenoma on neuroradiological evaluation and on intraoperative inspection surrounding the tumour.

Adenoma↗
PubMed2000

[A case of pseudo-Bartter's syndrome with marked nephrocarcinosis].

A 38-year-old woman was admitted to our hospital on October 21, 1996 for evaluation of thirst, bilateral backache and a feeling of abdominal fullness. She had hypokalemia, normotension, hyperreninemia, hyperaldostronism and hyperplasia of the juxtaglomerular apparatus on renal biopsy. Ultrasonography, intravenous pyelography and computed tomography showed marked bilateral renal calcification. Considering her history of persistent soft stool caused by chronic laxative abuse for 15 to 16 years and past diuretic abuse for several years since 1986, we diagnosed her as pseudo-Bartter's syndrome with nephrocarcinosis. The value of urinary Ca excretion was in the normal range, and acidification disturbance in NH4Cl loading test was revealed. In addition, she had taken analgesics for 2 to 3 years and interstitial nephritis on renal biopsy was seen. It is thus suggested that the cause of nephrocarcinosis in this case was the reduction of Ca solubility in the tubular cavity induced by incomplete renal tubular acidosis associated with analgesic nephropathy or interstitial nephritis caused by hypokalemia.

Acidosis, Renal Tubular↗
PubMed1999

Eicosapentaenoic acid and docosahexaenoic acid inhibit vascular smooth muscle cell proliferation by inhibiting phosphorylation of Cdk2-cyclinE complex.

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in the form of triacylglycerol (TG) were dose dependently incorporated into phospholipid fraction of vascular smooth muscle cells (VSMC) and suppressed the proliferation of VSMC. Flow cytometric analysis demonstrated both EPA and DHA inhibited G1/S progression. EPA and DHA inhibited the phosphorylation of Cdk2 protein and Cdk2 kinase activity without altering the amount of cyclin E and p27(kip1) proteins and cyclin dependent kinase activating kinase activity by growth stimulation. This mechanisms remained to be clarified but this is the first report of a novel mechanisms of inhibition of DNA synthesis by EPA and DHA.

Animals↗
PubMed1999

Bilateral pleuritis caused by Legionella micdadei.

A 58-year-old woman was hospitalized because of progressive respiratory distress. She had a history of myasthenia gravis and invasive thymoma. After thymectomy, she had been administered oral prednisolone and intrathoracic anti-cancer drugs postoperatively. Her chest radiograph revealed bilateral pleural effusions. Legionella micdadei (L. micdadei) was isolated from the pleural effusions, and she was diagnosed as pleuritis caused by L. micdadei. She died despite intensive therapy with mechanical ventilation, drainage tube in the chest and intravenous erythromycin. Although only two cases of Legionellosis caused by L. micdadei have been reported in Japan, clinicians should be aware of L. micdadei as one of the candidates for infection in immunosuppressed hosts.

Combined Modality Therapy↗
PubMed1999

[Neurophysin].

Explore the source record for details and available documents.

Humans↗
PubMed1998

Geranylgeranylpyrophosphate plays a key role for the G1 to S transition in vascular smooth muscle cells.

Pravastatin, a HMG-CoA reductase inhibitor was found to inhibit DNA synthesis of vascular smooth muscle cells (VSMC) in a dose-dependent manner. Flow cytometric analysis demonstrated that pravastatin induced G1 arrest. Mevalonate restored the inhibitory effect of pravastatin on DNA synthesis and on cell cycle progression, suggesting the importance of mevalonate itself and/or its metabolites in VSMC proliferation. The major intermediate metabolites of mevalonate, geranylgeranyl-pyrophosphate (GGPP), farnesyl pyrophosphate (FPP) and IPP (isopentenyl pyrophosphate) were prepared in the form of liposomes, and the effects of GGPP, FPP and IPP on pravastatin induced inhibition of VSMC proliferation and G1 arrest were examined. Only GGPP restored the pravastatin-induced inhibition of DNA synthesis and G1 arrest. Pravastatin inhibited translocation of Rho small GTPase from cytosol to membrane. By the addition of GGPP, Rho small GTPase are geranylgeranylated and translocated to membranes during G1/S transition. These data suggest that GGPP, rather than FPP or IPP, is an essential metabolite among mevalonic acid metabolites for VSMC proliferation and the G1/S transition.

Animals↗
PubMed1997

Geranylgeranylated rho small GTPase(s) are essential for the degradation of p27Kip1 and facilitate the progression from G1 to S phase in growth-stimulated rat FRTL-5 cells.

Cyclin-dependent kinase (Cdk) enzymes are activated for entry into the S phase of the cell cycle. Elimination of Cdk inhibitor protein p27Kip1 during the G1 to S phase is required for the activation process. An inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase prevents its elimination and leads to G1 arrest. Mevalonate and its metabolite, geranylgeranyl pyrophosphate, but not farnesyl pyrophosphate, restore the inhibitory effect of pravastatin on the degradation of p27 and allow Cdk2 activation. By the addition of geranylgeranyl pyrophosphate, Rho small GTPase(s) are geranylgeranylated and translocated to membranes during G1/S progression. The restoring effect of geranylgeranyl pyrophosphate is abolished with botulinum C3 exoenzyme, which specifically inactivates Rho. These results indicate (i) among mevalonate metabolites, geranylgeranyl pyrophosphate is absolutely required for the elimination of p27 followed by Cdk2 activation; (ii) geranylgeranylated Rho small GTPase(s) promote the degradation of p27 during G1/S transition in FRTL-5 cells.

Animals↗
PubMed1997

Mechanisms of enhanced production of PGI2 in cultured rat vascular smooth muscle cells enriched with eicosapentaenoic acid.

The present investigation was performed to clarify the effect of EPA on PGI2 production in vitro using cultured rat vascular smooth muscle cells (VSMC). To simulate in vivo conditions, a triacylglycerol (TG) emulsified form of EPA was used. An increase in EPA content was achieved without alteration of arachidonic acid concentration. These experiments clearly demonstrated that co-incubation of EPA-TG increased PGI2 production by cultured VSMC in a dose dependent fashion. Among polyunsaturated fatty acid TG examined (docosahexaenoic acid, linoleic acid, oleic acid and EPA), only EPA-TG was effective. Cyclooxygenase (COX) was activated, but neither phospholipase A2 nor PGI2 synthase activity was changed. EPA treatment did not alter the amount of COX-1 and COX-2 protein in VSMC. Addition of antioxidants, such as butylated hydroxytoluene or vitamin E, decreased MDA levels in the medium and cells and reversed the enhanced PGI2 production in EPA rich-VSMC. Therefore, the high polyunsaturation of EPA could generate low levels of lipid peroxides and thereby lead to activation of COX and an increased PGI2 production. Although EPA increased PGI2 production, only a negligible amount of PGI3 was produced by rat aortic tissues. Enhanced production of PGI2 might contribute to the anti-atherogenic effect of EPA.

Animals↗
PubMed1997

Complexes of apoA-1 with phosphatidylcholine suppress dysregulation of arterial tone by oxidized LDL.

The aim of this study was to determine whether apolipoprotein A-1 (apoA-1) may suppress the vasomotor dysregulation by oxidized low-density lipoprotein (ox-LDL), which is known to be an atherogenic lipoprotein. The isolated porcine coronary arterial rings and the cultured endothelial cells from the porcine coronary arteries were exposed to ox-LDL in the presence or absence of complexes of apoA-1 with dimyristoylphosphatidylcholine (DMPC/apoA-1), apoA-1 alone, or DMPC alone. DMPC/apoA-1 but not apoA-1 alone or DMPC alone was found to suppress both impairment of endothelium-dependent arterial relaxation and vasocontraction caused by ox-LDL in the isolated porcine coronary arterial rings suspended in organ chambers. DMPC/apoA-1 absorbed lysophosphatidylcholine (LPC) from ox-LDL and decreased the transfer of LPC from ox-LDL to the surface membrane of the cultured endothelial cells, but apoA-1 alone and DMPC alone had no effect. High-density lipoprotein exerted the protective actions mimicking those observed in DMPC/apoA-1. Thus DMPC/apoA-1 decreased the transfer of LPC from ox-LDL to surface membrane by absorbing LPC, leading to the suppression of ox-LDL-induced dysregulation of endothelium-dependent arterial tone. Therefore, apoA-1 appears to require formation of the complexes with phospholipids to prevent the endothelial dysfunction caused by ox-LDL.

Analysis of Variance↗