An experimental study on the biochemical consequences of hydrofluoric acid burns.
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Biomedical subjects
Publications and source records attributed to A Harada.
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A 1-year controlled trial was performed to confirm the effects of 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) in chronic hemodialysis patients. Initially, a daily dose of 2 micrograms of 1 alpha-OH-D3 was given orally to 24 patients and its placebo to another 24 patients during the first 3 months. For the following 9 months the dose of 1 alpha-OH-D3 or its placebo was reduced to 1 microgram per day in the individual groups. Serum calcium was significantly increased to the normal level after 1 month of treatment and sustained at this level for 1 year. Serum parathyroid hormone was significantly decreased at 3 months. Serum alkaline phosphatase was decreased to the normal level at the 5th month and thereafter. At 2 months serum phosphorus was significantly increased in the 1 alpha-OH-D3 group. None of the patients on 1 alpha-OH-D3 showed increased subperiosteal resorption on X-rays, whereas 8 out of 20 patients on placebo did (p less than 0.002). No adverse effects were seen apart from 3 patients with the 'red eye' of scleral calcification.
The present study described 3 patients with idiopathic membranous glomerulonephritis associated with diabetes mellitus. Clinical characteristics of the 3 patients contrasted with diabetic glomerulosclerosis in the following manner: absence of diabetic retinopathy and neuropathy, and presence of nephrotic syndrome associated with relatively short duration of diabetes mellitus. Renal histology showed the characteristic changes of membranous glomerulonephritis along with those of diabetic glomerulosclerosis. Immunofluorescent studies demonstrated a granular pattern of IgG and C3 deposits along the glomerular capillary wall. Electron microscopic study also demonstrated thickening of glomerular basement membrane and increase of mesangial matrix as well as the presence of electron-dense deposits primarily in the subepithelial and mesangial areas.
The characteristics of the motion corrector system attached to LFOV gamma-camera (Searle) was evaluated using a T-shaped plane source and point sources. The random movement without rotation of a T-shaped plane source was successfully corrected. However, rotating motion of the plane source was not corrected. When a point source placed on a rotating table, ring images were obtained. When motion corrector was used, the radius of ring images was increased with the increase of rotating speed and it was decreased with the increase of radioactivity of the source. Line images were obtained when point sources were placed on a shaker, which caused linear periodic motion of the sources. The use of the motion corrector reduced the length of line images.
In our nuclear medicine laboratory the quality control (QC) of radioimmunoassay (RIA) has been performed along the line of WHO program for standardization and quality control of RIA. The QC procedure was automated using a minicomputer in order to avoid tedious and time-consuming hand processing. The program was written with BASIC language. The counts of radioactivity measured in autowell counters are regarded in PTR, through which the data are read into a minicomputer (Scintipac 200). After informations on the concentrations of standards are registered through keyboard of CRT, the data processing is performed including curve fitting, dose calculation and quality control. As the indicators for QC response error relationship (RER), standard curve, precision profile and QC chart are displayed on CRT. On the basis of rejection criteria using these indicators, bad assays are identified to be omitted from reporting. The subroutine installed in the minicomputer system is used for the storage of data on QC samples in each assay, which are used for construction of QC charts. The use of a minicomputer enables implementation of QC of RIA on routine basis with ease and speed.
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Bovine thyrotropin (bTSH) was administered to 17 patients who had thyroid carcinoma. Anti-bTSH antibodies in the patients' sera were detected by three methods: 1) cross-reaction of sera in a homologous bTSH RIA, 2) [125I]bTSH binding to the patients' sera using charcoal to separate bound from free fractions, and 3) gel filtraton to detect [125I]bTSH bound to anti-bTSH in patients' sera. Immunoreactive anti-bTSH antibodies were thus demonstrated in 14 patients. These patients showed specific binding of their sera to [125I]bTSH with the charcoal separation of free from bound hormone. A high titer of antiserum (1:10,000) was found in those patients whose sera reacted strongly in the bTSH RIA (greater than 50 mu U/ml). The binding capacity of the serum of 1 patient was estimated as 2,600 mu U/ml serum. Ten of the patients' sera which showed immunoreactivity to bTSH neutralized bTSH activity in the McKenzie mouse bioassay but did not neutralize the activity of human TSH in this bioassay. Repeated administration of bTSH to 14 patients resulted in development of immunoreactive and neutralizing anti-bTSH antibodies. Development of immunological resistance to bTSH appears inevitable in patients who receive repeated injections of this hormone. Because of the loss of effectiveness of bTSH by antibody formation, the repeated diagnostic and therapeutic use of bTSH is not recommended.
Six patients on conventional acetate hemodialysis who had a marked decrease in total peripheral resistance index (TPRI) and hypotension after dialysis were selected for study. Systemic hemodynamic factors such as cardiac output, blood pressure, hematocrit and heart rate were measured, and the values were compared to those found after bicarbonate hemodialysis (Bi-HD) or ultrafiltration without simultaneous dialysis (UF) in the same patients. After Bi-HD and UF, the hemodynamic indices remained stable. Hematocrit level was significantly elevated after Bi-HD (+2.7%, P less than 0.05). Heart rate was insignificantly increased after each procedure. We concluded that Bi-HD can prevent unpleasant side effects induced by the decrease in TPRI with acetate hemodialysis. The stability of TPRI resulting from the increase in hematocrit level during Bi-HD may contribute to the prevention of cardiovascular instability.
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To clarify the role of various thyroid stimulators in normal human pregnancy, we measured serum TSH, chorionic TSH (hCT), hCG, bioassayable thyroid-stimulating activity, T4, T3, T3 uptake, free T4 and free T3 indexes, free T4, and free T3 by dialysis in 339 serum samples from pregnant women at various intervals of pregnancy and in 40 normal female controls. Serum T4 and T3 and free T4 and free T3 indexes were significantly elevated throughout pregnancy in comparison with controls. Free T4 concentration was elevated after 10 weeks of pregnancy and free T3 concentration was elevated at 13--20 weeks. Bioassayable thyroid-stimulating activity was elevated from 9--16 weeks when serum hCG concentrations were highest. Serum TSH levels were significantly lower at 9--12 weeks compared with the rest of pregnancy. hCT was detected in only 35% of sera tested; the mean detectable value was 0.60 +/- 0.04 (SE) microU/ml; only 15% of the detectable values exceeded 1 microU/ml. The level of hCG correlated with bioassayable thyroid-stimulating activity (P less than 0.01). The data indicate that hCT is not a significant thyroid stimulator. We propose that hCG, as a weak thyroid stimulator, causes a modest rise in free thyroid hormone levels early in pregnancy which in turn causes a modest reduction in pituitary TSH secretion.
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In an attempt to study the site and mechanism of action of estrogen in producing positive feedback control, porcine anterior pituitary slices were incubated in vitro in the presence of estradiol benzoate (EB). EB elevated pituitary cyclic AMP concentration within 5 min and augmented pituitary release of luteinizing hormone (LH). The magnitude of increase of cyclic AMP and LH release was related to the doses of EB used. Also, luteinizing hormone releasing hormone (LH-RH) elevated pituitary cyclic AMP concentration and stimulated pituitary release of LH. The magnitude of increase of cyclic AMP and LH release was inversely related to the doses of LH-RH used. EB and LH-RH were additive in increasing cyclic AMP. Progesterone and clomiphene citrate interfered with an increase of pituitary cyclic AMP produced by EB, but did not significantly affect the basal level of pituitary cyclic AMP. Testosterone propionate, human chorionic gonadotropin and hexestrol were without effect on either basal or stimulated level of pituitary cyclic AMP. Since cyclic AMP and dibutyryl cyclic AMP (DBC) stimulated LH release, it is suggested that EB directly stimulates the release of LH by augmenting cyclic AMP synthesis in the anterior pituitary.
We extracted human placentas by three methods to obtain chorionic TSH (hCT). The extracts were assayed by a sensitive homologous RIA for bovine TSH with an antibody which had veen used previously for assay of hCT. Based on the RIA for hCT, the yield of hCT was only 0.68 +/- 0.15 (SE) mU/100 g placenta by the Bates method, 2.01 +/- 0.35 mU/100 g by the Reisfeld method, and 4 mU/100 g by a Concanavalin A-Sepharose technique. Thyrotropic activity was detected by bioassay only in one Reisfeld extract; this biological activity could be attributed to hCG in this fraction. In TSH bioassays of other extracts, the responses were less than the sensitivity of the assay; some extracts were lethal to the bioassay mice. The low yield of hCT, about one-tenth to one-hundredth of that reported previously, casts doubt on the validity of the previous observations.
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In an attempt to study the functional relation between pituitary cyclic AMP and TSH secretion in response to thyrotropin releasing hormone (TRH) or thyroid hormone administration, pituitary concentration of cyclic AMP was measured by protein binding assay after in vivo and in vitro administration of test materials (TRH, thyroxine, triiodothyronine, actinomycin D, puromycin and cycloheximide singly or in combination). Small dose of TRH apparently augmented TSH secretion as evidenced by a marked increase of intrathyroidal colloid droplet, but failed to elevate the pituitary concentration of cyclic AMP. Triiodothyronine (T3) and thyroxine (T4) blocked an increase of TSH secretion produced by TRH, but they elevated pituitary concentration of cyclic AMP in vivo and in vitro. Actinomycin D (Act D), puromycin and cycloheximide elevated pituitary cyclic AMP concentration without stimulating TSH secretion. From the data accumulated, it appears that the measurement of total anterior pituitary concentration of cyclic AMP is not useful to evaluate the activity of TSH cells in response to thyroid hormone, TRH and TRH plus thyroid hormone.
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