Search PubMed⌕ Search

Biomedical subjects

Y Uchida

Publications and source records attributed to Y Uchida.

At least 235 records · Page 13Linked to original sources
PubMed1997

Iodothyronine deiodinases in a mammalian hibernator, the chipmunk (Tamias asiaticus).

We examined the activities of iodothyronine deiodinase, a key enzyme for thyroid hormone metabolism, in selected tissues of the chipmunk (Tamias asiaticus), a mammalian hibernator, of both sexes in the summer season. Reverse T3 5'-deiodinase (5'-D) activity was the highest in the liver followed by the kidney; T4 5'-D activity was the highest in brown adipose tissue (BAT) and T3 5'-deiodinase (5-D) activity was the highest in the testes followed by the brain. Distributions of three types of deiodinase activities in liver kidney BAT, and brain were comparable to other mammals reported, except that the type III deiodinase was unique in testes. The 5'-D activity of liver and kidney of chipmunks was 52% and 24%, respectively, of male rats and the 5-D activity of brain and testes of chipmunks was 227% and 567%, respectively of male rats. In addition, the cold exposure increased BAT 5'-D activity in chipmunks as reported in the ground squirrels. Our results indicated that tissue distribution of deiodinases and response to cold exposure in BAT in hibernators are similar to nonhibernators. However, there was a quantitative difference of rT3 5'-D and T3 5-D activities in some tissues between chipmunks and rats, indicating different local thyroid hormone metabolisms in hibernators and nonhibernators.

Adipose Tissue, Brown↗
PubMed1997

Developmental immunohistochemistry of growth inhibitory factor in normal brains and brains of patients with Down syndrome.

Growth inhibitory factor, a new metallothioneinlike protein, was investigated at postmortem examination in the brains of 18 patients with Down syndrome ranging in age from 18 weeks gestation to 50 years of age and in 20 age-matched normal controls by developmental immunohistochemistry. In the frontal cortex of both Down syndrome patients and controls, growth inhibitory factor immunoreactivity was localized in the cell bodies and processes of protoplasmic astrocytes from 18 weeks gestation, and these immunoreactive processes formed so dense a meshwork in the gray matter that they outlined neuronal perikarya as negative contours in the brain at age more than 16 years. The number of growth inhibitory factor-immunoreactive astrocytes exhibited a greater increase in layer 3 than in layer 2 in controls from 37 weeks gestation to 7 months of age, although there was no difference in the growth inhibitory factor-positive cell number between layers 2 and 3 in young Down syndrome patients. Therefore, growth inhibitory factor in astrocytes may be correlated with dendritic maturation of neurons. On the other hand, growth inhibitory factor-immunoreactive astrocytes in layer 2, where senile plaques are abundant, were smaller than those in layer 3 in adult Down syndrome patients from age 32 years. When senile plaques began to immunoreact with the amyloid precursor protein, the number of growth inhibitory factor-immunoreactive astrocytes decreased around senile plaques in elderly Down syndrome brains with the Alzheimer type of dementia. On the contrary, the number of glial fibrillary acidic protein-immunoreactive astrocytes around senile plaques increased. This loss of growth inhibitory factor around senile plaques may be correlated with neuronal loss or degeneration and lead to sprouting responses which may be involved in the formation of senile plaques.

Adolescent↗
PubMed1997

Relationship between the response to the angiotensin converting enzyme inhibitor imidapril and the angiotensin converting enzyme genotype.

Insertion (I)/deletion (D) polymorphism of the angiotensin converting enzyme (ACE) gene has been reported to be involved in various cardiovascular diseases. We investigated prospectively whether the response to the ACE inhibitor imidapril varied according to the ACE genotype or plasma ACE activity in Japanese hypertensive patients. The study population consisted of 57 hypertensive patients. After a 4-week observation period, imidapril was administered at a dose of 5 mg/day and blood pressure was measured every 2 weeks for 6 weeks. The plasma ACE activity in patients with the DD or ID genotype was significantly higher than that in patients with the II genotype. Neither the reduction nor the percent reduction in systolic blood pressure was significantly different between patients with either the DD or ID genotype and patients with the II genotype (DD or ID v II, 18.8 +/- 2.4 v 20.2 +/- 3.3 mm Hg; P = NS, 10.9 +/- 1.4 v 11.7 +/- 1.9%; P = NS, respectively). However, both the reduction and the percent reduction in diastolic blood pressure tended to be higher in patients with the II genotype (DD or ID v II, 7.9 +/- 1.2 v 12.4 +/- 2.2 mm Hg; P = .0669, 8.1 +/- 1.2 v 12.4 +/- 2.2%; P = .0569, respectively). The reduction in diastolic blood pressure was inversely correlated with plasma ACE activity (r = 0.301, P = .0253). In conclusion, the response to imidapril in hypertensive patients is determined at least in part by the ACE genotype.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Magnetic resonance galactography for a patient with nipple discharge.

A new method of galactography using magnetic resonance imaging for a patient with nipple discharge is developed. The method is as follows; coronal T1-weight images are obtained after an injection of contrast medium of 1 mmol/L Gd-DTPA directly into the discharge duct, before and after rapid intravenous infusion of Gd-DTPA. A case of a 29-year-old woman with ductal carcinoma in situ with minimal invasion is reported, in which all portions of the entire discharge duct system is clearly shown as viewed from the surface and the surrounding area is enhanced with Gd-DTPA. The enhanced area is coincidental with the extent of the disease. This magnetic resonance galactography for patients with nipple discharge may be used to supplement conventional mammography and/or galactography especially for the evaluation of the extent of disease, although it is somewhat inferior to mammographic galactography in terms of differential diagnosis of ductal disease.

Adult↗
PubMed1997

Adjunctive Therapy with an Antithrombotic Drug Can Prevent Reocclusion and Induce Residual Thrombus Reduction After Percutaneous Transcatheter Angioplasty of the Thrombotic Lesions.

Acute reocclusion after successful angioplasty is a severe complication. The preventive effects of heparin, the synthetic antithrombin, argtroban, and the defibrinogenating agent batroxobin on reocclusion after balloon angioplasty of thrombotic occlusions were evaluated in canine iliac arteries. After the 2-hour-old thrombus was evaluated by angiography and angioscopy, percutaneous transcatheter angioplasty (PTA) was performed on the thrombotic stenosis. We used one of the three agents, heparin (100 U/kg), the antithrombin argatroban (0.3 mg/kg), or the defibrinogenating agent batroxobin (0.3 U/kg). Then angioscopy and angiography were performed before, just after, and 2 hours after PTA. After PTA, angiography revealed a marked reduction in percent stenosis in all groups (from 88 +/- 8% to 24 +/- 4% in the heparin group, from 79 +/- 7% to 26 + 11% in the argatroban group and from 89 +/- 12% to 32 +/- 7% in the batroxobin group). At 2 hours after PTA, angiography demonstrated a greater reduction in percent stenosis with argatroban (from 26 +/- 11% to 9 +/- 3%) and batroxobin (from 32 +/- 7% to 10 +/- 8%), and maintenance of percent stenosis reduced by PTA with heparin (from 24 +/- 5% to 28 +/- 9%) when compared with the significant reversal of percent obstruction in the control side. Angioscopic visualization also demonstrated a similar trend. These results show that these antithrombotic drugs have a preventive effect on reocclusion after balloon angioplasty for thrombotic obstruction.

Journal Article↗
PubMed1997

Arthrobacter ureafaciens sialidase isoenzymes, L, M1 and M2, cleave fucosyl GM1.

Among bacterial, fungal and viral sialidases, the sialidase from Arthrobacter ureafaciens has the unique property of cleaving sialic acids linked to the internal galactose of gangliotetraose. In this study, we examined the ability to cleave the internal sialic acids of GM1 and fucosyl GM1 of sialidases from several bacterial and fungal origins, including Clostridium perfringens and Vibrio cholerae. We found that A. ureafaciens sialidase could liberate the sialic acid of GM1 at the highest rate, and was the only enzyme which could cleave fucosyl GM1 among the sialidases examined. The affinity-purified sialidase derived from the culture medium of A. ureafaciens was comprised of four isoenzymes with different molecular weights and isoelectric points, the isoenzymes that cleaved fucosyl GM1 being L (88 kDa, pl 5.0), M1 (66 kDa, pl 6.2) and M2 (66 kDa, pl 5.5), but not S (52 kDa, pl 6.2) which showed the highest specific activity toward colominic acid among the four isoenzymes.

Animals↗
PubMed1997

Defective stimulation of thyroxine 5'-deiodinase activity by cold exposure and norepinephrine in brown adipose tissue of monosodium glutamate-obese mice.

In order to examine the possible change in the thyroid hormone metabolism in the monosodium glutamate (MSG)-obese mice, we determined the iodothyronine deiodinase activity of brown adipose tissue (BAT), liver and kidney of male and female mice. There was no significant difference in the type II thyroxine 5'-deiodinase (T4 5'DII) activity in BAT between MSG-obese and control mice when they were kept at the ambient temperature of 22 degrees C. T4 5'DII activity in BAT of control mice increased markedly after exposure to cold (4 degrees C) for 4 h; however, the extent of cold-induced increase in T4 5'DII activity in BAT of MSG-obese mice was greatly reduced. Injection of norepinephrine (NE) (0.8 mg/kg, s.c.) 4 h previously increased T4 5'DII activity in BAT of control mice, but NE-induced increase in T4 5'DII activity was also markedly reduced in BAT of MSG-obese mice. Both cold- and NE-induced increase in T4 5'DII activity was greater in female, although similar tendency was obtained in male mice. Type I 3,3',5'-triiodothyronine deiodinase (rT3 5'DI) activity of liver and kidney, and serum thyroxine (T4) and 3,5,3'-triiodothyronine (T3) levels in MSG-obese mice were essentially the same as those of the control male and female mice irrespective of cold exposure. These results suggest that defective stimulation of T4 5'DII activity of BAT by cold in the MSG-obese mice is due to deficient sympathetic input to BAT and/or to diminished response of BAT to NE, and may contribute to a possible cause of inability of MSG-obese mice to maintain body temperature under cold exposure.

Adipose Tissue, Brown↗
PubMed1997

Intracellular calcium increase in gerbil taste cell by amino acid sweeteners.

Gustatory transduction mechanisms for sucrose and amino acid sweeteners in gerbil taste cells were studied with Ca2+ imaging and whole cell recording techniques. A 100 mM sucrose stimulus with Ca2+ increased the intracellular Ca2+ concentration ([Ca2+]i) in sweet-sensitive taste cells of the taste bud, but the sucrose stimulus without Ca2+ did not change the [Ca2+]i. A 10 mM D-phenylalanine sweet stimulus with or without Ca2+ similarly increased the [Ca2+]i in the taste bud. The addition of 5 microM ionomysin, a Ca(2+)-ionophore, without Ca2+ greatly increased the [Ca2+]i in the taste bud. The application of 10 mM D-phenylalanine stimulus without Ca2+ enhanced the outward K+ current in isolated taste cells. These results suggest that a sugar sweetener such as sucrose induces a depolarization in gerbil taste cells which activates voltage-dependent Ca2+ channels and that a non-sugar sweetener such as D-phenylalanine releases Ca2+ from the internal stores without a depolarization.

Animals↗
PubMed1997

Changes in outward K+ currents in response to two types of sweeteners in sweet taste transduction of gerbil taste cells.

Using the whole cell patch clamp technique, we measured changes in outward K+ currents of gerbil taste cells in response to different kinds of sweeteners. Outward K+ currents of the taste cell induced by depolarizing pulses were suppressed by sweet stimuli such as 10 mM Na-saccharin. The membrane-permeable analog of cAMP, cpt-cAMP, also decreased outward K+ currents. On the other hand, the K+ currents were enhanced by amino acid sweeteners such as 10 mM D-tryptophan. The outward K+ current was enhanced by external application of Ca(2+)-transporting ionophore, 5 microM ionomycin, and intracellular application of 5 microM inositol-1,4,5-trisphosphate (IP3). The outward K+ currents were no longer suppressed by 10 mM Na-saccharin containing 20 microM gurmarin, but were still enhanced by 10 mM D-tryptophan containing 20 microM gurmarin. These results suggest that sweet taste transduction for one group of sweeteners such as Na-saccharin in gerbils is concerned with an increase of the intracellular cAMP level, and that the transduction for the other group of sweeteners such as D-tryptophan is concerned with an increase of the intracellular IP3 level which releases Ca2+ from the internal stores.

Animals↗
PubMed1997

Life-threatening dysphagia following prolonged neuroleptic therapy.

We report the cases of two patients with complaints of dysphagia following long-term neuroleptic therapy. Esophageal contrast radiography revealed that one patient suffered disruption of the normal swallowing activity of the pharyngoesophagus due to tardive dyskinesia. Her dysphagia disappeared following changes in her neuroleptic medications and the administration of clonazepam. The other patient demonstrated severe rabbit syndrome involving the glossopharynx. This 3-Hz rhythmic movement disorder resolved following injection of an anticholinergic agent. Thereafter, the addition of oral trihexyphenidyl to her medication regimen improved her dysphagia. It should be emphasized that the differential diagnosis of neuroleptic-associated dysphagia subtypes is important because therapeutic strategies differ depending on the subtype of this life-threatening illness.

Antipsychotic Agents↗
PubMed1997

Transient and intermittent oral dyskinesia appearing in a young woman ten days after neuroleptic treatment.

A 22-year-old woman was admitted to our hospital because she showed psychomotor excitement and signs of schizophrenia following psychological stress. Nine days after neuroleptic medication, she could not eat and exhibited high fever, diaphoresis, excessive salivation, and severe extrapyramidal signs with cogwheel rigidity and resting tremor of the upper extremities. The next day, bucco-linguomasticatory dyskinesia, which is quite similar to tardive dyskinesia, appeared. The dyskinesia lasted intermittently for 6 days. The present case shows that buccolingual dyskinesia can occur even after early neuroleptic exposure in certain patients.

Adult↗
PubMed1997

Imaging assessment of the response of bone tumors to preoperative chemotherapy.

Assessment of the response of bone tumors to preoperative chemotherapy is of clinical importance. The authors determined the value of 3 imaging techniques (digital subtraction angiography, thallium scintigraphy, and dynamic magnetic resonance imaging) in guiding patient management by assessing the response of 17 bone sarcomas to preoperative chemotherapy compared with histologic evaluation of the resected specimens. Digital subtraction angiography showed a sensitivity of 87.5%, specificity of 57.1%, and accuracy of 73.3%. Thallium scintigraphy (sensitivity, 85.7%; specificity, 85.7%; accuracy, 85.7%) was superior to angiography in predicting tumor responses. The results of dynamic magnetic resonance imaging were analyzed on the basis of the value of slopes, which represents the percent increase in signal intensity per minute. The differences in slope before and after chemotherapy and the postchemotherapy slope values correlated with the histologic responses. The assessment by dynamic magnetic resonance imaging showed a sensitivity of 100%, specificity of 85.7%, and accuracy of 90.9%. Thallium scintigraphy and dynamic magnetic resonance imaging were considered noninvasive, reliable techniques that had about equal ability to assess the response of bone sarcomas to preoperative chemotherapy. Dynamic magnetic resonance imaging offers major advantages in the spatial resolution and can be more readily quantitated when compared with thallium scintigraphy.

Adolescent↗
PubMed1997

Intrinsically aged epidermis displays diminished UVB-induced alterations in barrier function associated with decreased proliferation.

Ultraviolet (UV) irradiation of the skin induces a variety of responses in the epidermis, including sunburn cell formation, epidermal hyperplasia, and a dose-dependent permeability barrier abnormality, an effect that appears to be dependent upon both UVB-induced hyperplasia and T-cell activation. Since intrinsically aged epidermis displays decreased epidermal turnover, diminished inflammatory response to various stimuli, including UVR, and impaired immune function, we investigated the effects of UVB on both epidermal barrier function and proliferation in hairless mice of increasing chronologic age (27, 61, and 90 wk). After a single UVB exposure (0.15 J/cm2 7.5 MED), a barrier abnormality developed (i.e., increased transepidermal water loss; TEWL), after a delay of > or = 48 h, regardless of age. In young mice (27 wk old), TEWL levels peaked at 72-96 h (9.9-fold over untreated controls), whereas increased epidermal [3H]thymidine incorporation preceded the peak TEWL increase (i.e., approximately 570% increase over controls at 48 h). In contrast, the UVB-induced increased in both TEWL and DNA synthesis were significantly diminished, with decreased epidermal hyperplasia evident, in intrinsically aged versus young mouse epidermis. Baseline epidermal thickness decreased with animal age (i.e., 16.8 +/- 3.1 vs. 27.9 +/- 0.7 microm for 90- vs. 27-wk-old animals, respectively; p < 0.02), suggesting that the diminished barrier response with aging reflects an attenuation of events subsequent to initial UVB exposure, rather than an increase in the UV dose delivered. These results demonstrate that (i) murine epidermis becomes less sensitive to UVB-induced barrier alterations with age and (ii) decreased DNA synthesis after UVB correlates with the age-related decrease in barrier dysfunction.

Animals↗
PubMed1997

UVB-induced alterations in permeability barrier function: roles for epidermal hyperproliferation and thymocyte-mediated response.

UV irradiation induces a variety of cutaneous responses, including disruption of epidermal permeability barrier function, the basis for which is not known. Herein, we investigated the separate roles of hyperproliferation and inflammation in the pathogenesis of UVB-induced barrier disruption. Adult hairless mice were exposed to increasing doses of UVB (1.5-7.5 MED), and transepidermal water loss (TEWL) was monitored daily for up to 7 d. The extent of TEWL increase was dependent on the UVB dose, but with all doses, the increase began after > or =48 h and peaked at 96 h, decreasing by 120 h. Epidermal [(3)H]thymidine incorporation increased at 24 h and peaked at 48 h (570%), preceding the maximal increase in TEWL. Cyclosporin A, methotrexate, 5-fluorouracil, or arabinosylcytosine significantly diminished the UVB-induced TEWL increase. Athymic nude mice also displayed a markedly diminished response to UVB, and DNA synthesis did not increased at 48 h. Transplantation of athymic mice with T-cell-enriched mixed immune cells significantly restored sensitivity to both the UVB-induced hyperproliferation and the barrier defect. Finally, although UVB exposure increased PGE2 levels in whole skin samples (2- to 3-fold within 1-3 h; p < 0.005), this increase was completely blocked by topical indomethacin, and neither topical indomethacin nor topical glucocorticoids blocked development of the barrier abnormality. These results show that (i) UVB produces delayed alteration in barrier function and (ii) both an epidermal proliferative response and thymocyte-mediated events (but not PGE2 production and nonspecific inflammation) appear to contribute to UVB-induced abrogation of the permeability barrier.

Adrenal Cortex Hormones↗
PubMed1997

Structural and biochemical basis for the UVB-induced alterations in epidermal barrier function.

Ultraviolet light (UVR) induces a myriad of cutaneous changes, including delayed disruption of the permeability barrier with higher doses. To investigate the basis for the UVB-induced barrier alteration, we assessed the epidermal lamellar body secretory system at various time points before and after barrier disruption with a single high dose of UVB (7.5 MED) to murine epidermis. Morphological data were correlated with changes in epidermal proliferation and lipid synthesis, indicative of lamellar body generation. Twenty-four hours following UVB, the stratum corneum (SC) is normal, but a layer of abnormal, vacuolated, and lamellar body (LB)-deficient cells is present, immediately beneath the stratum granulosum (SG)/SC interface. Immediately subjacent to this band of damaged cells, normal keratinocytes that contain intact LBs are present. By 72 h, concomitant with the appearance of a barrier abnormality, extensively damaged cells persist at the SC/SG interface, and abnormal lamellar membrane structures appear in the lower SC. Upper stratum spinosum (SS) and lower SG cells appear normal, with increased numbers of LBs. A barrier abnormality is still present at 96 h, in association with membrane abnormalities in the lower SC interstices, but up to four normal appearing, subjacent SG cell layers are present. By 120 h, accelerated LB formation and precocious LB extrusion occur throughout the thickened SG; normal lamellar membranes are present in the lower SC; and barrier recovery is almost complete. Whereas, epidermal synthesis of the major barrier lipid species (i.e., cholesterol, fatty acids, and ceramides, including acylceramides) is reduced or unchanged at 24 and 48 h, it increases significantly 72 h after exposure to UVB. Therefore, the delayed disruption of the permeability barrier following acute UVB exposure results from the arrival of a band of lamellar body-incompetent (i.e., damaged) cells at the SG/SC interface. The subsequent, rapid recovery of the barrier, in turn, results from compensatory hyperplasia of subjacent, undamaged SS/SG cells, generating increased numbers and contents of LB. These results underscore the critical role of the stratum compactum in mediating barrier function, and suggest that beneficial therapeutic effects of UV exposure may be due to enhanced lipid production and barrier regeneration.

Acyltransferases↗
PubMed1997

Inhibitory activities of quinolones against DNA gyrase and topoisomerase IV purified from Staphylococcus aureus.

In order to clarify the mechanism of action of quinolones against Staphylococcus aureus, GrlA and GrlB proteins of topoisomerase IV encoded by genes with or without mutations were purified separately as fusion proteins with maltose-binding protein in Escherichia coli. The reconstituted enzymes showed ATP-dependent decatenation and relaxing activities but had no supercoiling activity. The inhibitory effects of quinolones on the decatenation activity of topoisomerase IV were determined by quantitative electrophoresis with kinetoplast DNA as a substrate. The 50% inhibitory concentrations (IC50s) of levofloxacin, DR-3354, DU-6859a, DV-7751a, ciprofloxacin, sparfloxacin, and tosufloxacin against topoisomerase IV of S. aureus FDA 209-P were 2.3, 97, 0.45, 1.5, 2.5, 7.4, and 1.8 microg/ml, respectively, and were correlated well with their MICs. The IC50s of these drugs were from 2 to 20 times lower than those for the DNA gyrase. These results support genetic evidence that the primary target of new quinolones is topoisomerase IV in quinolone-susceptible strains of S. aureus. Three altered proteins of topoisomerase IV containing Ser-->Phe changes at codon 80 or Glu-->Lys changes at codon 84 of grlA, or both, were also purified. The inhibitory activities of quinolones against the topoisomerase IV which contained a single amino acid change were from 8 to 95 times weaker than those against the nonaltered enzyme. These results suggest that the mutations in the corresponding genes confer quinolone resistance.

DNA Topoisomerase IV↗
PubMed1997

Retrovirus in salivary glands from patients with Sjögren's syndrome.

AIMS: To investigate the possibility of an immune response to retroviral antigens or of detecting retrovirus in Sjögren's syndrome. METHODS: Retroviruses were sought in labial salivary glands and peripheral blood mononuclear cells from patients with Sjögren's syndrome by immunoblotting assay, immunohistochemical assay, polymerase chain reaction (PCR), reverse transcriptase (RT) activity assay, and transmission electron microscopy. RESULTS: Sera from five of 15 patients with Sjögren's syndrome (33%) reacted against p24 group specific antigen (gag) of human immunodeficiency virus (HIV). Labial salivary gland biopsy specimens from seven of the 15 patients with Sjögren's syndrome (47%) contained an epithelial cytoplasmic protein reactive with a monoclonal antibody to p24 of HIV. PCR was performed to detect HIV and human T lymphotropic virus type I (HTLV-I) genes from salivary gland tissues and peripheral blood mononuclear cells from patients with Sjögren's syndrome. Mn2+ dependent, Mg2+ independent RT activity was detected in the salivary gland tissues in three of 10 patients. A-type-like retroviral particles were observed in epithelial cells of salivary glands by transmission electron microscopy. Target genes for HIV and HTLV-I were not found in any of the salivary gland tissues or peripheral blood mononuclear cells from Sjögren's syndrome patients. CONCLUSIONS: The data suggest the presence of an unknown retrovirus similar to HIV in the salivary gland which might be involved in the pathogenesis of a subpopulation in Sjögren's syndrome.

Adult↗