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Biomedical subjects

N Matsui

Publications and source records attributed to N Matsui.

At least 199 records · Page 11Linked to original sources

Serial DST, TRH test, and TRH-like immunoreactivity measurements in major affective disorders.

Neuroendocrine functions in depressed patients with major affective disorders were serially investigated by the Dexamethasone Suppression Test (DST), the thyrotropin-releasing hormone (TRH) stimulation test, and the plasma TRH-like immunoreactivity (TRH-LI) measurement. Prior to antidepressant therapy, the sensitivity for nonsuppression to the DST was 36.0%, whereas that for blunted thyroid-stimulating hormone (TSH) response to TRH was 28.0%. Both DST nonsuppression and TSH blunting appeared to be state-related markers for depressed patients. Specifically, a significant increase of maximum TSH response to TRH after 4 weeks of antidepressant therapy was associated with clinical improvement. Plasma TRH-LI in depressed patients was significantly lower than that of healthy controls. It is possible that the lower plasma TRH-LI level is related to the pathophysiology of some depressed patients with major affective disorders.

Adult↗

Thyroid hormone inhibits fibronectin synthesis by cultured human skin fibroblasts.

Fibronectin (Fn) is a glycoprotein composed of two different subunits, each with a mol wt of approximately 230K. Fn is important for cell adhesion and for maintaining normal cell morphology. Recent in vivo studies suggested that thyroid hormone affects the plasma Fn level in man. The aim of this study was to determine whether T3 regulates the synthesis of Fn in cultured human skin fibroblasts. Skin fibroblasts obtained from seven normal subjects were grown in Minimum Essential Medium supplemented with 10% fetal calf serum. After reaching confluence, the cells were exposed for 3 days to the same medium in which fetal calf serum was replaced by 10% thyroidectomized bovine serum without or with added T3. At the end of this period, the cultures were incubated with [35S]methionine (95 microCi/dish) for 4 h before harvesting. Cell lysates and corresponding media were combined, and 35S incorporation into total protein and Fn was determined by trichloroacetic acid precipitation and immunoprecipitation with antihuman Fn immunoglobulin, respectively. Analysis of the immunoprecipitated material by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that most of the 35S activity migrated as a 230K band which was displaced by excess unlabeled Fn. Addition of T3 did not affect trichloroacetic acid-precipitable 35S activity but decreased the 35S activity precipitated with anti-Fn in a dose-dependent manner. While addition of 10(-10) M T3 to the medium had no effect, 35S incorporation into Fn was inhibited by 22.5 +/- 7.4% (mean +/- SD) with 10(-9) M T3 (free T3, 6 X 10(-12) M) and by 31.3 +/- 5.8% with 10(-7) M T3. To assess whether the inhibition of Fn accumulation by T3 was due to suppression of Fn synthesis or enhanced Fn degradation, cells were labeled for 4 h with [35S]methionine and chased for another 4 h with excess unlabeled methionine. T3 had no effect on the rate of decline of [35S]Fn during the chase. We conclude that physiologic T3 concentrations inhibit the synthesis of Fn in normal human fibroblasts. This effect provides a new method to study the action of thyroid hormone which may prove useful in the tissue diagnosis of resistance to thyroid hormone.

Adult↗

Pathophysiological role of thyroid blocking antibody in patients with primary hypothyroidism.

The pathophysiological role of thyroid blocking antibody (TBAb) in patients with adult primary hypothyroidism and the mechanism of TBAb action were studied. A sensitive bioassay for TBAb, which inhibits the TSH-induced cAMP accumulation, was established using normal human thyroid cells in culture. Thirty-four patients with primary hypothyroidism consisting of 17 goitrous and 17 non-goitrous patients were examined. Two out of 17 goitrous patients (11.8%) and three out of 17 non-goitrous patients (17.6%) were TBAb positive. There were no significant differences between TBAb positive and negative patients in terms of the severity of hypothyroidism or the titers of MCHA or TGHA. Four out of the five TBAb-positive IgGs had strongly positive thyrotropin binding inhibitor immunoglobulin activities. All five TBAb-positive IgGs inhibited the cAMP increase induced by Graves' IgG, but did not affect the action of either prostaglandin E1 or cholera toxin. However, three TBAb positive IgG also inhibited the cAMP increase induced by forskolin. These findings indicate: 1) TBAb is present in hypothyroid patients with autoimmune thyroiditis and TBAb may play a role in the pathophysiology of these patients. 2) TBAb may inhibit the action of TSH not only at the level of the TSH receptor, but also at a different site from the TSH receptor.

Adolescent↗

The influence of transcortin on adrenocorticotropin-stimulated corticosterone production in monolayer cultured rat adrenal cells.

To verify the influence of the protein binding status of steroids adjacent to adrenal cells on steroidogenesis, the effect of transcortin, a specific binding protein of cortisol or corticosterone, on adrenocorticotropin (ACTH)-stimulated corticosterone production in monolayer cultured rat adrenal cells was studied. The transcortin in concentration of 5 x 10(-7) M was loaded with 0, 2.5, 5 and 10 pg/ml ACTH-(1-24), and the cells were incubated for 2 and 4 hours. Since molar concentrations of corticosterone produced in the medium were below the transcortin concentration at all levels of stimulation, protein-unbound corticosterone in the medium may have been largely reduced by the addition of transcortin. However, the total corticosterone production was not influenced by the transcortin added to the medium. It was speculated that protein-unbound steroid within the concentration range modulated by transcortin in the area surrounding the adrenal cells may not affect adrenal steroidogenesis.

Adrenal Glands↗

[Mitral valve disease and atrial natriuretic polypeptide].

We compared plasma ANP concentration and atrial content of ANP as well as plasma concentrations of other fluid regulating hormones and renal function between the MVR group (n = 12) and the non MVR group (n = 14) during open heart surgery. Preoperatively there was no significant difference in plasma ADH and ACTH between two groups, however plasma ANP was significantly higher in the MVR group (96.9 +/- 16.2 pg/ml) than in the non MVR group (22.8 +/- 8.6 pg/ml) (p less than 0.01). During extracorporeal circulation ANP was at a low level because of aortic clamping. Tissue concentration of ANP in right appendages was higher (p less than 0.02) in the MVR group (61.8 +/- 11.8 nmol/g wet weight) (n = 6) than that in the non MVR group (14.9 +/- 3.1 nmol/g wel weight) (n = 15). Also, concentration in left appendages of the MVR group (50.0 +/- 10.4 nmol/g wet weight) (n = 4) was higher than that in right appendages of the non MVR group (p less than 0.05). From these results it may be concluded that increased secretion of ANP is elicited by left atrial load and probably playing an important role on circulating blood volume regulation.

Aldosterone↗

[Hyponatremia with high plasma ANP level--report of two cases with emphasis on the pathophysiology of cerebral salt wasting].

Two cases of hyponatremia with intracranial lesions are reported with emphasis on diagnostic value of measurement of antidiuretic hormone (ADH) and atrial natriuretic polypeptide (ANP). Case 1. A 77-year-old female was transferred to our hospital for further care of vegetative state after subarachnoid bleeding on May 23, 1986. She was operated by neck clipping of rt-IC bifurcation aneurysm and lt-internal carotid-posterior communicating aneurysm at another hospital. On admission, computed tomography showed diffuse low density at bilateral thalamus and centrum semiovale. Biochemical analysis revealed hyponatremia (120 mEq/t) with increased natriuresis. Endocrinological date revealed normal plasma ADH and high plasma ANP levels. Patient was treated with infusion of 1% NaCl. Case 2. A 65-year-old male was admitted to our department because of gradual impairment of consciousness and generalized convulsion. Computed tomography showed small low density area at rt-thalamus and lt-cerebellar hemisphere. Biochemical date revealed severe hyponatremia (91 mEq/t) with normal plasma level of ADH and high plasma ANP. He was treated with infusion of 3% NaCl and hyponatremia was improved. The hyponatremia is frequently associated with intracranial disorders such as brain tumor, subarachnoid hemorrhage and head injury. Originally, hyponatremia with natriuresis was thought to be caused by salt wasting. This syndrome was defined as the inability to prevent salt loss in the urine due to undefined natriuretic factor in the brain. However, since 1957, because of introduction of concept of SIADH, it has generally become accepted that patients with natriuresis had SIADH. (ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Seadragon VI: a 7-day dry saturation dive at 31 ATA. III. Alterations in basal and circadian endocrinology.

Four male divers were exposed to an environment of 1 ATA air for 7 d, followed by 7 d of 31 ATA He-O2, and following decompression to a postdive 1 ATA air environment for 3 d. Urine and blood were collected for hormonal measurements. Divided 24-h urine collections were obtained during 3 consecutive d at predive 1 ATA conditions, and at 31 ATA conditions. Two consecutive day collections were obtained at early decompression (31-25 ATA), at late decompression (14-8 ATA), and at postdive 1 ATA. Two blood samples were obtained, at predive 1 ATA, at 31 ATA, and at postdive 1 ATA. Plasma antidiuretic hormone (ADH) concentration decreased about 45% (P less than 0.005), while plasma aldosterone concentration and urinary aldosterone excretion were doubled (P less than 0.005) after the subjects were at 31 ATA. Plasma cortisol concentration and plasma parathyroid hormone concentration were not significantly affected by hyperbaria. Urinary excretion of aldosterone was not significantly different between day (0700-1900) and night (1900-0700) at any time, and both day and night excretion rates were increased at 31 ATA through late decompression (P less than 0.005). Urinary ADH excretion was greater during daytime at predive 1 ATA (P less than 0.005), but not thereafter. Both daytime and nighttime ADH excretion rates were decreased from 31 ATA through late decompression (P less than 0.005). It is concluded that hyperbaria eliminates the circadian release pattern of ADH and that the overall reduction of ADH may contribute to the increased free water clearance observed at hyperbaria. Also, increased parathyroid hormone was not associated with the phosphaturia observed at hyperbaria, but increased aldosterone coexisted with the increased kaliuresis observed.

Adult↗

Seadragon VI: a 7-day dry saturation dive at 31 ATA. VI. Hyperbaria enhances renin but eliminates ADH responses to head-up tilt.

Three male subjects were passively tilted from a supine to a 90 degree head-up standing position on 2 d each at 1 and 31 ATA, then on 1 d of the postdive period. On each day the subjects were tilted once in the morning (0800-1000) and once in the evening (2000-2200). Before each tilt experiment, the subjects were first intravenously cannulated for blood sampling, then assumed the supine position. A blood sample was taken after 10 min in the supine position, and another sample was taken after 15 min of motionless, supported standing. The plasma was analyzed for antidiuretic hormone (ADH), plasma renin activity (PRA), plasma cortisol, and aldosterone. ADH, PRA, and cortisol were significantly increased by tilt, but the responses varied with time of day or atmospheric pressure. Cortisol increased only in the morning tilt (P less than 0.005) and was not affected by pressure. At 1 ATA, PRA was elevated in the morning tilt experiment (P less than 0.005) and not the evening tilt, but the overall response to tilt was greater at 31 ATA than at 1 ATA (P less than 0.005). The ADH response to tilt (P less than 0.025) was unaffected by time of day, but was eliminated at 31 ATA. The basal levels of ADH were also lower at 31 ATA (P less than 0.005). The mechanism of these responses remains unclear, but the eliminated postural stimulation of ADH may account for the eliminated circadian excretory pattern of the hormones. The altered responses to body fluid shifts possibly contribute to the increased aldosterone and decreased ADH frequently observed at hyperbaria.

Adult↗

Seadragon VI: a 7-day dry saturation dive at 31 ATA. II. Characteristics of diuresis and nocturia.

Four male divers were exposed to a dry, 31 ATA, He-O2 environment for 7 d (Seadragon VI). Urine was collected diurnally (0700-2200 h) and nocturnally (2200-0700 h) before (predive 1 ATA air), during, and after (decompression and postdive 1 ATA air) exposure to 31 ATA. A typical hyperbaric diuresis associated with a reduction in urine osmolality was observed in the face of a constant creatinine clearance. A significant increase (P less than 0.05) in osmolal clearance (COSM) was observed with concomitant decrease (P less than 0.05) in negative free water clearance, indicating that the diuresis has both osmotic and free water components. Although urine flow increased at pressure during both day and night, its magnitude was twofold greater at night as compared to daytime. Moreover, the diurnal diuresis was entirely due to an increase in free water excretion, whereas the nocturnal diuresis was largely due to an increased COSM. These results indicate that hyperbaric diuresis is induced by inhibition of tubular reabsorption of free water during daytime and of certain solutes during the night. Approximately 80% of the nocturnal increase in the excretion of osmotic substances was accounted for by Na, K, Cl, and urea.

Adult↗

Effect of estrogen on prolactin mRNA in the rat pituitary. Analysis by in situ hybridization and immunohistochemistry.

The effect of estrogen on prolactin (PRL) synthesis at a single-cell level was studied by in situ hybridization and immunohistochemistry. Long-term estrogen treatment increased PRL-containing cells from 10-20% of total cell population to 80-90%, as revealed by immunohistochemistry. PRL mRNA containing cells also increased in a similar fashion. Moreover, cytoplasmic PRL mRNA expressed as the number of silver grains per cell increased 4- to 5-fold by estrogen. These results suggest that long-term estrogen treatment causes not only PRL cell proliferation but also an increase in PRL mRNA in a single cell.

Animals↗

Ontogenesis of pituitary prolactin in the human fetus.

To study the ontogenesis of PRL synthesis and secretion in the human fetus, PRL mRNA was measured in 12 pituitaries from fetuses of 16-27 weeks of gestation by hybridization of cytosol RNA with 125I-labeled single stranded complementary DNA (cDNA). Pituitary PRL content and serum PRL concentration were assessed by RIA. Pituitary weight increased with fetal age, ranging from 12 mg at 16 weeks of gestation to 41 mg at 27 weeks. The increased weight was due to an increase in cell number. PRL mRNA content did not change during weeks 16-20 of gestation. However, it increased rapidly after 21 weeks, reaching 11.5 times the 16-20 week value at 27 weeks. Pituitary PRL content was constant at a low level until 21 weeks, but thereafter it increased markedly. The increase was greater than that in PRL mRNA, and therefore, the PRL to PRL mRNA ratio was 10-fold greater at 27 weeks of gestation. Serum PRL concentrations also gradually increased after 21 weeks of gestation. These results indicate that marked increases in fetal pituitary PRL synthesis and release occur after 21 weeks of gestation.

Base Sequence↗

Comparative study of primates' transcortin: immunoreactivity and steroid-binding activity.

To investigate the phylogenic aspect of transcortin (corticosteroid-binding globulin, CBG), the immunoreactivity of transcortin with anti-human transcortin antiserum was studied in primates. The anti-human transcortin antibody was recognized by plasma proteins obtained from Catarrhini, taxonomically the most evolved monkey group. The immunoreactivity was not observed in plasma obtained from Platyrrhini and Prosimiae, classified as less evolved monkey groups than Catarrhini. Though comparison of immunoreactivity among different classes of Catarrhini was difficult because of non-parallelism of their displacement curves, displacement of 125I-labelled human transcortin from the antiserum by 1:10 and 1:100 diluted plasma was highest in human followed by Pongidae, Cercopithecoidea. The immunoreactivity of thyroxine-binding globulin (TBG) with anti-human TBG antiserum was also examined. The anti-human TBG antibody was only recognized in plasma from Pan (anthropoid ape) among Pongidae, highly evolved monkeys among Catarrhini. The existence of immunoreactive transcortin and TBG to respective human protein antibody in the highly evolved ape agreed well with the cladogenetic division of primate species delineated by Goodman and Moore (1971). Cortisol-binding activity of transcortin was detected in all monkeys except three, tafted capuchin monkey, night monkey and cotton-headed tamarin, which belong to Platyrrhini. The absence of cortisol-binding activity in these animals might be attributed to high levels of endogenous cortisol and low cortisol-binding capacity of transcortin. It is speculated that the structure of the immunoreactive site in transcortin could be modified by evolution without affecting the biologically important site, the site for cortisol binding.

Animals↗

The effects of furosemide on adenosine 3':5'-cyclic monophosphate, guanosine 3':5'-cyclic monophosphate and corticosterone production stimulated by adrenocorticotropin in monolayer cultured rat adrenal cells.

Furosemide has been reported to have a suppressive effect on ADH-, PTH- and adrenaline-stimulated adenosine 3':5'-cyclic monophosphate (cAMP) production, but the effect on adrenocorticotropin (ACTH) action has not yet been elucidated. In the present study, therefore, the effects of furosemide on cAMP and also on guanosine 3':5'-cyclic monophosphate (cGMP) and corticosterone, stimulated by ACTH in monolayer cultured rat adrenal cells, were investigated. The intra- and extracellular cAMP stimulated by ACTH was dose-dependently suppressed by furosemide within the concentration range of 10(-3) M to 3 X 10(-3) M, and the suppressive effect of the drug was accompanied with decreased corticosterone production. However, non-stimulated basal corticosterone production was not influenced by the drug even at 3 X 10(-3) M. A similar suppressive effect of dibutyryl cAMP-stimulated corticosterone production by 3 X 10(-3) M furosemide was observed. The intracellular cAMP bound to its binding protein in sonicated adrenal cell extract was also suppressed in a very similar dose-dependent manner to total cAMP. However, though the effect on corticosterone production was also observed when the calcium concentration in the loading medium was changed, the magnitude of the effectiveness (percent of control) was relatively constant at each calcium concentration, suggesting that furosemide may not affect the site(s) at which calcium acts. Intracellular cGMP, on the other hand, was increased by 10(-3) M to 3 X 10(-3) M of furosemide, suggesting an intensifying effect of furosemide on guanylate cyclase activity. Dibutyryl cGMP-stimulated corticosterone production was also increased at the same concentration range. These results indicated that furosemide may act not only on adenylate cyclase but also on the additional step(s) to suppress the resultant corticosterone production. In contrast to the effects of furosemide on such cAMP-mediated processes, this drug treatment appeared to enhance cGMP-mediated corticosterone production.

Adrenal Glands↗

Role of sex-hormone-binding globulin and free sex steroid hormones in hyperandrogenic anovulation.

To clarify the mechanism of hyperandrogenic anovulation, the binding capacity of sex-hormone-binding globulin (SHBG-BC), the levels of free steroid hormones, and the levels of basal serum testosterone (T), estradiol (E2), estrone (E1) and gonadotropins were determined in 42 hyperandrogenic anovulatory women. The mean levels of basal T (0.74 +/- 0.04 ng/ml, p less than 0.001), free T (3.07 +/- 0.51 ng/dl, p less than 0.01) and free E2 (2.26 +/- 0.27 pg/ml, p less than 0.05), basal luteinizing hormone (LH) (33.4 +/- 2.7 mIU/ml, p less than 0.001), responsiveness of LH (180.7 +/- 21.5 mIU/ml, p less than 0.001) after luteinizing hormone releasing hormone (LHRH) administration, and the basal LH/basal follicle stimulating hormone (FSH) ratio (3.42 +/- 0.25, p less than 0.001) in the patients were significantly higher, the SHBG-BC level (1.76 +/- 0.33 micrograms DHT bound/dl, p less than 0.05) significantly reduced, and basal levels of E2 (38.0 +/- 3.2 pg/ml) and E1 (110 +/- 13 pg/ml) unchanged compared to the controls. These findings suggest that increased T in hyperandrogenic anovulatory women results in decreased SHBG-BC and increased free T and E2 which might be the cause of inappropriate gonadotropin secretion followed by chronic anovulation.

Acne Vulgaris↗

Measurement of human prolactin messenger RNA in decidual tissues using complementary DNA probe cloned in M13mp9 bacteriophage.

A human prolactin (PRL) cDNA clone was digested with restriction enzyme Pst I and the resultant fragments were cloned into bacteriophage M13mp9. Single stranded recombinant DNAs having a coding strand of the PRL cDNA were selected by hybridization with 125I-labeled PRL mRNA obtained from human prolactinoma tissue. One of the single stranded recombinant DNAs was purified by agarose gel electrophoresis and labeled with 125I to a specific activity of 1.4 X 10(8) cpm per microgram of DNA. The probe could be successfully used in RNA dot hybridization. Analysis of poly (A) RNAs from prolactinoma, liver and placental tissues revealed that this probe was specific to PRL mRNA sequence. Hybridization of poly (A) RNA from decidual tissue to this probe revealed the presence of PRL mRNA sequence. However, PRL mRNA in decidua was at least 20,000 times less than that in pituitary prolactinoma.

Cloning, Molecular↗