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Biomedical subjects

N Matsui

Publications and source records attributed to N Matsui.

At least 217 records · Page 12Linked to original sources
PubMed1986

Indium-111 leukocyte imaging in patients with rheumatoid arthritis.

This study evaluates the usefulness of labeled leukocyte imaging in patients with rheumatoid arthritis. In 33 patients, the incidence of pain and swelling in 66 wrist joints and 66 knee joints was compared with the accumulation of [111In]leukocytes. No accumulation of [111In]leukocytes was seen in any of the patients' wrists (0/12) or knee joints (0/14) when both pain and swelling were absent. In contrast, 93% (25/27) of wrist joints and 80% (24/30) of knee joints with both pain and swelling were positive by [111In]leukocyte scintigraphy. There was little correlation between the stage of the disease, as determined by radiography, and [111In]leukocyte accumulation. This study suggests that [111In]leukocyte imaging may be a reliable procedure for monitoring the activity of rheumatoid arthritis, especially for confirming the lack of an ongoing inflammatory response.

Adult↗
PubMed1986

[Penetration of cefotaxime into human bone marrow blood].

Concentrations of cefotaxime (CTX) in bone marrow blood and venous blood were examined with the passage of time in 21 cases which received operations of bone and joint. Concentrations of CTX in bone marrow blood at 30 minutes of a single intravenous administration 2 g each of CTX were found to be 85.2 +/- 24.5 micrograms/ml. Concentration ratio of CTX in bone marrow blood to that in venous blood was reached the peak at 120 minutes after administration. Concentrations of CTX observed were higher than the MIC of CTX against major pathogens responsible for the postoperative infections in orthopaedic field. The CTX, therefore, is expected to have an effective antibiotic in prophylaxis.

Adolescent↗
PubMed1985

[Thyroid stimulating immunoglobulin bioassay using cultured normal human thyroid cells].

It is currently believed that the thyroid stimulating immunoglobulin (TSI) of Graves' disease is involved in the pathogenesis of hyperthyroidism through the stimulation of the adenylate cyclase-cyclic AMP system. To evaluate this mechanism, TSI in the serum of patients with Graves' disease was determined by its ability to generate cyclic AMP (cAMP) in monolayer cells prepared from a normal thyroid gland. The thyroid tissue was digested with collagenase, and the liberated follicles were collected from the supernatant and cultured for 7 days. One gram of thyroid tissue yielded more than 1 X 10(7) monolayer cells which were stored in aliquots at -80C. Cells (1 approximately 2 X 10(4)/0.28 cm2 microtiter well) were incubated for 4 hours in 0.2 ml Hanks solution poor in NaCl, with various amounts of bovine TSH (bTSH) or 1.5 mg/ml Graves' serum IgG extracted by polyethylene glycol. cAMP accumulated in medium and cells was measured by RIA. Total cAMP (both medium and cells) was about 4 times higher when NaCl was deleted from Hanks solution. Moreover, as more than 90% of the cAMP was released into the medium, it was possible to omit the measurement of cellular cAMP, which requires extraction. The increase in medium cAMP concentration was dependent upon the number of cells, incubation time, and dose of bTSH. Time course and dose response curves in medium cAMP stimulated by IgG from 3 Graves' patients paralleled those of bTSH equivalent units. Accordingly, TSI activity could be expressed in bTSH equivalent units (bTSH microUeq). The assay could detect 1.0 or 3.3 microU/ml of bTSH and was highly reproducible. TSI activity in all of 16 IgGs from normal subjects was under 3.3 bTSH microUeq/ml, while it was greater than 3.3 bTSH microUeq/ml in IgGs from 33 of 37 (89%) untreated patients with Graves disease. Of the 13 patients followed for 2 to 7 months while on antithyroid drugs, 12 had greater than 3.3 bTSH microUeq/ml and, with the exception of one, all showed a decrease in their TSI activity. Moreover, 5 of 12 patients treated continuously for more than 1 year were TSI negative (less than 3.3 bTSH microUeq/ml), and except for one case, all had TSI values below 8 bTSH microUeq/ml (a value found in only 25% of untreated patients). This in vitro bioassay for TSI is simple and sensitive. It detects the presence of TSI in virtually 90% of untreated patients with Graves' disease. TSI activity showed a clear decrease during the course of antithyroid drug therapy.

Biological Assay↗
PubMed1985

Rat renal cell monolayer culture: a sensitive method for investigating ADH and PTH actions on the kidney by determining adenosine 3' :5'-cyclic monophosphate.

The response of cAMP to antidiuretic hormone (ADH) was studied using rat renal medullary cells in a monolayer culture. In addition, cAMP response to parathyroid hormone (PTH) was studied in renal cortical cells. As the culture aged, an increase in basal cAMP content and a gradual decrease in the cAMP responsiveness to arginine vasopressin (AVP) were observed. After 2 days of culture, AVP and hPTH-(1-34) produced a rapid increase in intracellular cAMP with single peaks, after 10 min and 5 min, respectively. Extracellular cAMP was increased linearly by both AVP and hPTH-(1-34). The response of cAMP to AVP was markedly greater in the medulla than in the cortex, while the response to hPTH-(1-34) was remarkable only in the cortex. Outstanding sensitivity of cAMP responsiveness was observed in this system, i.e., 10(-12) M AVP (1 pg/ml) and 2.43 X 10(-10) M hPTH-(1-34) (1 ng/ml) provoked significant increases in cAMP from the basal level of 0.31 +/- 0.04 and 0.59 +/- 0.05 pmol/dish to 0.79 +/- 0.03 and 1.07 +/- 0.13 pmol/dish, respectively (P less than 0.001). In the medulla, potencies of lysine vasopressin (LVP), DDAVP and oxytocin at a concentration of 10(-9) M were 76.1%, 154.2% and 8.1% of that of AVP, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1985

Development of enzyme-linked immunospecific assay (ELISA) for the detection of monoclonal antibody: application to detection of monoclonal anti-TBG.

An enzyme-linked immunospecific assay (ELISA) was developed to screen monoclonal antibody to human thyroxine-binding globulin (TBG). The assay is based on the absorption of TBG from human pooled serum by rabbit polyclonal anti-TBG antibody coated on a microtiter plate and subsequent binding of monoclonal antibody to the absorbed antigen. Monoclonal antibody which binds TBG can be detected by peroxidase labeled anti-mouse IgG. From the examination with two different rabbit polyclonal anti-TBG antibodies, it was demonstrated that both purified IgG fraction and whole serum could be used as coating materials. It was not necessary to use purified TBG to react with anti-TBG antibody coated on the microtiter plate. When eight commercially available microtiter ELISA plates were tested in the assay, only 3 gave satisfactory results. The sensitivity of the assay was comparable with that of the conventional immunoprecipitation method using 125I-TBG and formalin fixed Staphylococcus aureus (Kowan strain) as an immunoabsorbent. The ELISA method could detect antibody activity in 0.032 microliter of medium obtained from a 3 day culture of confluent hybridoma cells. It is possible to store the antibody-antigen complexed microtiter plate for more than 2 weeks at 4 C. This makes possible rapid screening of monoclonal antibody.

Animals↗
PubMed1985

Human transcortin synthesis by a cell-free translation of hepatic mRNA.

To evaluate the site of synthesis and to characterize the translated transcortin, poly (A)-containing RNA (mRNA) from human liver was translated in a cell-free system derived from rabbit reticulocyte lysate. The in vitro synthesized product was identified as transcortin by immuno-precipitation with its specific antiserum. This translated transcortin could be displaced from the antibody by unlabeled purified transcortin obtained from plasma. Furthermore, when the translation mixture was applied to a cortisol-Sepharose column, the translated transcortin was bound to the matrix in a specific manner, indicating that this product binds to cortisol. The molecular weight of the translated transcortin was estimated to be 45,700 by its mobility in sodium dodecyl sulfate polyacrylamide gel electrophoresis, while that of plasma transcortin was 53,800. The difference in molecular weight between the translated transcortin and plasma transcortin was probably due to the presence of pre-sequence (signal peptide) in addition to the absence of carbohydrate moiety in the former. In conclusion, human liver mRNA directed the synthesis of transcortin, and the translated transcortin binds to cortisol in spite of the absence of carbohydrate moiety.

Animals↗
PubMed1985

[Alterations in urinary N-Acetyl-beta-D-glucosaminidase (NAG), beta 2-microglobulin (BMG) under acute exposure to simulated 6,000 m altitude].

The changes in NAG and BMG concentration in the urine during sudden exposure to a simulated 6,000 m altitude (354 mmHg) were studied. Subjects were 5 healthy male volunteers before a mountain climbing expedition (20-25 years old). Decompression was commenced at 11:00 and terminated at 17:00 (2-h ascent, 2-h sojourn, 2-h return) for 5 successive days. Urine was discarded at 9:00 and thereafter collected at 11:00 (group I), 14:00 (group II) 17:00 (group III), and 9:00 the next day (group IV) and urinary NAG and BMG was measured. The rate of NAG indicated elevation above 5.0 U/L in 2 cases in group III and elevation which was significantly different from that of the other 3 groups. In the other 3 cases, significant elevation was not observed, but for group III as a whole NAG excretion was significantly elevated compared of the other 3 groups. However, increased excretion of NAG was not observed on all 5 successive days. The change in BMG values was smaller than that of the NAG values and no significant elevation was observed in any of the 4 groups. Increasing urinary excretion of NAG by sudden exposure to a high altitude indicated excessive destroy of epithelium in the proximal tubules, but this change was reversible.

Acetylglucosaminidase↗
PubMed1985

Binding capacity of sex-hormone-binding globulin and free testosterone determination in evaluation of hirsute women.

To investigate the relation between free testosterone (T) and binding capacity of sex-hormone-binding globulin (SHBG-BC) and a degree of hirsutism, 34 women were classified into 3 groups according to the criteria of Ferriman and Gallway on the degree of the hirsutism; 11 patients with a total score of 1 to 3 (group 1), 8 patients with a total score of 4 to 10 (group 2), and 15 patients with a total score of 11 or more (group 3). Total plasma T, SHBG-BC, and free plasma T were measured in each group, and they were compared with those of controls. In groups 1 and 2, mean levels of total T were slightly higher than in controls but the differences were not significant. Total T levels were extremely elevated in group 3. Mean level of SHBG-BC in group 1 was slightly lower than in controls but was not statistically significant. SHBG-BC was drastically reduced in groups 2 and 3. The percent free T levels and free T concentrations were significantly higher than those of controls in groups 2 and 3, but not in group 1. The results suggested that decreased SHBG-BC and increased free T might be the cause of hirsutism in women with normal total T levels.

Amenorrhea↗
PubMed1985

[Changes in % free testosterone and sex-hormone binding globulin during danazol administration].

To clarify the androgen balance on the administration of danazol a study was conducted on the levels of % free testosterone (% free T) and sex-hormone-binding globulin (SHBG) during the therapy and the binding properties of danazol to SHBG and androgen receptor. It was found that danazol displaced testosterone (T) from SHBG and R1881 from androgen receptor, in vitro. During treatment with danazol, levels of % free T were increased about three fold, but in contrast the SHBG concentration were significantly decreased. Similar changes in % free T were observed by computer simulation. These data suggest that the androgenic effects of danazol were the results of increased free T levels by the T-displacing ability of danazol from SHBG. The concentration of SHBG might be reduced as a consequence of increased levels of free T. On the other hand, danazol binding to androgen receptor might partially inhibit the action of excess amounts of free T, because the androgenization during therapy was too weak to compare the levels of free T.

Computers↗
PubMed1984

Hormonal disturbances of fluid-electrolyte metabolism under altitude exposure in man.

Early alterations in fluid, electrolytes, and their regulating hormones were investigated in men exposed to 6,000 m simulated altitude (2 h-ascent, 2 h-sojourn, 2 h-return). Hematocrit and serum protein rose with elevated serum osmolality and reduced urine flow upon arrival at 6,000 m, suggesting decreased plasma volume probably due to hypotonic fluid shift to intracellular spaces. Serum K declined reflecting respiratory alkalosis. The exposure raised plasma antidiuretic hormone (ADH), plasma renin activity (PRA), serum cortisol and aldosterone. Increases both in ADH and aldosterone showed close correlations with that in cortisol, suggesting that ADH may be elevated by hypoxic stress in addition to elevated serum osmolality and decreased plasma volume, and that increased secretion of adrenocorticotropin may be the main cause of increased aldosterone, though PRA involvement cannot be excluded. These rises in ADH and aldosterone may act to retain body water, and the latter may exaggerate alkalosis; thus, these hormonal changes may be related to acute mountain sickness.

Adult↗
PubMed1984

Responses of salt- and water-regulating hormones during a saturation dive to 31 ATA (SEADRAGON IV).

Four Japanese male subjects were studied during 3 days at 1 ATA, 3 days of compression to 31 ATA (1000 fsw), 14 days at 31 ATA, 12 days of decompression, and 3 days of postdive control at 1 ATA. The chamber was maintained at thermoneutral temperatures. During the 31-ATA exposure, urine flow increased about 500 ml/day (P less than 0.05) accompanied by an approximate 500-ml/day increase in osmotic clearance (Cosm) (P less than 0.05). Both urine flow and Cosm increases were primarily attributable to an increase in the overnight flow rates (P less than 0.01). The negative free water (-CH2O)/Cosm decreased during exposure to 31 ATA, indicating that a reduction in tubular water reabsorption may also contribute to the diuresis. Urine flow, Cosm, and -CH2O/Cosm all returned to predive values during decompression to 1 ATA. The urinary excretion rate of aldosterone increased from 2.7 +/- 0.3 micrograms/day at 1 ATA to 4.3 +/- 0.0 micrograms/day (P less than 0.01) at 31 ATA, remaining at about 3.8 micrograms/day until decompression. Urinary antidiuretic hormone (ADH) decreased from 50 +/- 7 to 33 +/- 3 mU/day (P less than 0.01) upon compression to 31 ATA and continued to decrease throughout the decompression phase. Plasma renin activity was increased by twofold (P less than 0.01) and plasma aldosterone by about 37% (NS) during exposure to 31 ATA. It is concluded that the reduction in ADH does not contribute significantly to the hyperbaric diuresis, and that the increased activity of the renin-angiotensin-aldosterone is a result of other postulated mechanisms resulting in an increased Cosm.

Adult↗
PubMed1984

Hormonal response to acute diuresis--a comparative study of furosemide and azosemide.

We observed and compared the hormonal response to acute diuresis for 6 hours by orally administered furosemide 40 mg and azosemide 60 mg in normal male volunteers. The treatment resulted in significant urine volume increase with its peak during 1 to 2 and 2 to 3 hours after administration, and the 6-hour cumulative urine volume was 2488 +/- 163 ml in furosemide and 2930 +/- 109 ml in azosemide, respectively. The plasma noradrenalin concentration rose with the increase of urinary noradrenalin excretion, but plasma adrenalin remained unchanged in spite of its increased excretion. Serum aldosterone and plasma renin activity rose with resultant increase of urinary aldosterone excretion. Such a stimulation of the renin-angiotensin-aldosterone system was greater with azosemide than with furosemide. Plasma ADH and serum prolactin concentration was also increased. As compared with the furosemide responses, 1 to 2 hour delayed responses were observed in urinary adrenalin and noradrenalin, plasma renin activity, serum and urinary aldosterone, plasma ADH and serum prolactin. This was probably caused by delayed onset of the diuretic action in the case of azosemide. The findings suggested that the differences in the hormonal responses of the two drugs are mainly explained by the difference in their diuretic phase.

Adult↗