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Biomedical subjects

N Konno

Publications and source records attributed to N Konno.

At least 91 records · Page 5Linked to original sources
PubMed1980

[Normality of serum thyroid hormones, thyroxine binding globulin and thyroid stimulating hormone concentrations in normal adult men (author's transl)].

The normality of serum thyroxine (T4), triiodothyronine (T3), reverse T3, thyroxine binding globulin (TBG) and thyroid stimulating hormone (TSH) concentrations were investigated by using normal probability paper. 107 healthy adult men (age 35-48) were carefully selected; their healthiness was evaluated by physical, biochemical and roentogenologic examinations as well as by intensive interview on their past history. All assays were simultaneously carried out. When each cumulative distribution was plotted on normal probability paper, the straight line was obtained in T4, T3 and TBG but in rT3 and TSH, the lineality was seen only when logarithmic normal probability paper was used. The normal ranges by conventional statistical calculation, i.e., mean +/-2 S.D. was compared with those obtained on normal probability paper. The normal ranges of T4, T3 and TBG agreed well each other, whereas in rT3 and TSH, normal ranges obtained on the probability paper shifted toward higher levels than those by statistical calculations. Thus, it is suggested that the normal ranges of rT3 and TSH should be defined either by statistical calculation of each result after logarithmic transformation or by using logarithmic probability paper.

Adult↗
PubMed1979

Accumulation of Phosvel in adipose tissue of hens.

Phosvel, an organophosphorus pesticide, was stored in the adipose tissue of hens after they were given daily a single oral dose. The concentration of Phosvel in fat was related to the size of the daily dose.

Adipose Tissue↗
PubMed1978

Comparison between the thyrotropin response to thyrotropin-releasing hormone in summer and that in winter in normal subjects.

A comparison was made between the thyrotropin (TSH) response to 500 microgram thyrotropin-releasing hormone (TRH) in summer and that in winter in ten healthy normal adults living in Supporo. The serum resin triiodothyronine (T3) uptake (RT3U), thyroxine (T4) and T3 levels were also measured. While the TSH response to TRH in summer was similar to that in winter, serum T3 concentration and free T3 index were significantly higher in winter than in summer, associated with the similar values in RT3U and T4 levels in serum. Independently measured 86 specimens (43 in summer and 43 in winter) from normal adults living in the same district also showed a significant increase in serum free T3 index as well as a slight elevation of serum T3 concentration in winter but not in serum T4 level. These results indicate that the primary change in cold winter would be the stimulation of peripheral conversion of T4 to T3 rather than the activation of hypothalamo-pituitary-thyroid axis. The relevance of this interpretation was discussed.

Adult↗
PubMed1977

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familial thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3.4 +/- 0.9 microgram/dl, mean +/- SD. vs. 9.0 +/- 1.5 microgram/dl, p less than 0.01 and 87 +/- 27 ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs. 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 muU/ml) and the maximum TSH increments following TRH 500 microgram iv were 8.9 +/- 2.0 muU/ml and of no significant difference from the normal control (10.2 +/- 4.5 muU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗
PubMed1976

[The relationship between the timing of the Korotokoff sound (QKd) and the serum thyroid hormone concentrations].

The interval between the onsets of the QRS complex and of the brachial Korotokoff sounds at the diastolic pressure was termed QKd and it was already known that QKd was shortend in hyperthyroidism and prolongad in hypothyroidism distinctly. In the present study, simultaneous measurements of QKd, serum thyroxine (T4) and triiodothyronine (T3) concentrations, free T4 index (FT4I) and free T3 index (FT3I) were undertaken and attempts were made to examine the possible correlation of QKd to these parameters of thyroid function in sera. The QKd values of 24 euthyroid subjects had a normal range of 190 to 230 msec., 10 patients with hypertyroidism had Qkd values ranging from 145 to 180 msec. and 9 hypothyroid patients had QKd values ranging from 230 to 305 msec. Plots of QKd agaist serum T4 and T3 concentrations denoted statistically significant inverse relations in the T4 and T3 concentrations denoted statistically significant inverse relation in the T4 and T3 concentrations approximately less than 20 mug/dl and 400 ng/dl respectively (4 = 0.59 and -0.62 respectively) and above these concentrations of T4 and T3, QKd was nearly constant at the level of 165 msec irrepective of T4 and T3 concentrations. The statistically significant inverse relations were also observed between QKd and FT4I and FT3I in the FT4I and FT3I values less than 18 and 280 respectively (r= -0.80 and -0.74 respectively) and above these values of FT4I and FT3I, QKd was remained constant. In 18 hyperthyroid subjects receiving antithyroid medication, QKd, FT4I and FT3I were measured. QKd values from the patients whose FT4I and/or FT3I were above normal were significantly shorter than the QKd from the patients with normal FT4I and ft3i (183 +/- 9.8 msec vs 211 +/- 19 msec, p less than 0.01). In 16 patients with primary hypothyroidism receiving L-thyroxine for replacement therapy more than 6 months of period, QKd, FT4I and FT3I were measured and TRH-test was performed. FT4I and FT3I in these patients were all in normal range and 8 out of 16 patients had normal response to TRH-test and others were of no response to TRH-test. No difference in QKd values was obtained between patients with normal response and with no response to TRH-Test. These results indicate that QKd is more closely related to serum free T4 and free T3 concentrations and the extent of prolongation of QKd in hypothyroidism reflects the decreased serum thyroid hormone concentrations, whereas the shortend QKd in hyperthyroidism does not parallel the increased serum thyroid hormone concentrations. QKd is useful index not only for the rapid assessment of thyroid function as proposed by previous investigaters, but also for the rpaid evaluation of efficacy of antithyroid drugs administered in hyperthyroidism.

Auscultation↗
PubMed1976

Serum thyrotropin response to thyrotropin-releasing hormone and free thyroid hormone indices in patients with familiar thyroxine-binding globulin deficiency.

The response in serum thyrotropin (TSH) to synthetic thyrotropin-releasing hormone (TRH) as well as serum free thyroxine index (FT4I) and free triiodothyronine index (FT3I) was investigated in six patients with familial thyroxine-binding-globulin (TBG) deficiency. The total serum thyroxine (T4) and triiodothyronine (T3) concentrations were significantly decreased, compared with those of normal subjects (3,4 +/- 0.9 microng/dl, mean +/- S.D. vs. 9.0 +/- 1.5 microng/dl, p less than 0.01 and 87 +/- ng/dl vs. 153 +/- 37 ng/dl, p less than 0.01, respectively). FT4I was lower than the normal range in all but one (5.3 +/- 1.5 vs. 8.9 +/- 1.6, p less than 0.01), whereas FT3I was all in the normal range and of no significant difference from the normal control (132 +/- 22 vs 148 +/- 25). Serum TSH concentrations in TBG deficiency were all in the normal range (1.0-4.2 micronM/ml) and the maximum TSH increments following TRH 500 microng iv were 8.9 +/- 2.0 micronU/ml and of no significant difference from the normal control (10.2 +/- 4.5 micronU/ml). These results indicate that the euthyroid state in familial TBG deficiency is more clearly defined by TRH-test and the normal response to TRH in familial TBG deficiency is presumably under the control of the serum free T3 level rather than the serum free T4 level.

Adult↗