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Biomedical subjects

K Fujieda

Publications and source records attributed to K Fujieda.

At least 91 records · Page 5Linked to original sources
PubMed1989

The prediction of thyroid function in infants born to mothers with chronic thyroiditis.

To elucidate the relationship between the mother's TSH-receptor antibody activities and the status of thyroid dysfunction in their offspring, blood was taken from 5 mothers with chronic thyroiditis with potent thyrotropin (TSH)-receptor blocking activity, and the potency of TBII and TSBAb activity was assayed more quantitatively. In those mothers whose infants suffered from neonatal hypothyroidism, the 50% inhibition of binding of labeled TSH to its receptors was obtained at more than 30 to 50-fold dilution, while in those mothers whose infants had transiently increased TSH or were euthyroid, the titers were of less than 30-fold dilution. Similarly, in those mother whose infants suffered from neonatal hypothyroidism, the 50% inhibition of TSH-induced cAMP accumulation was obtained at approximately 400 to 3000-fold dilution, while in those mothers whose infants had transiently increased TSH or were euthyroid, the titers were of less than 50-fold dilution. On the other hand TBII activity was much less potent in serum from patients with Graves' disease. These results suggested that the titration of serum with dilution to obtain 50% inhibition of labelled TSH binding to its receptor may be the simplest way to predict thyroid dysfunction of the newborn infants born to mothers with chronic thyroiditis.

Adolescent↗
PubMed1989

Measurement of plasma free and total growth hormone concentrations in patients with growth hormone antibodies developed in response to therapy.

Recombinant human growth hormone is more antigenic than pituitary preparations. Since GH antibodies interfere with radioimmunoassay of GH, we measured plasma free and total GH in patients with pituitary dwarfism with GH antibodies during treatment with a recombinant methionyl GH preparation. Plasma free GH was measured in the supernatant after polyethylene glycol precipitation. Total GH was measured after extracting plasma with acid-ethanol. In normal subjects, both free and total GH levels were similar to those measured in plasma by a direct conventional RIA. Peak free GH levels after administration of 4 IU methionyl GH to 3 normal subjects were 38.0, 30.7 and 13.2 micrograms/1, values similar to those measured in most of the patients with GH antibodies. All values were undetectable in one patient with a very high antibody titre. Total GH levels were similar to free GH levels in normal subjects. In patients with GH antibodies, total GH levels were high compared with their free levels, but similar to those assayed by conventional RIA. The patient with the highest antibody titre had total GH levels which were the lowest of those observed in the patients with GH antibodies in spite of having the highest GH levels measured by conventional RIA. The antibody in this particular case may have a high capacity and a high affinity. A relatively poor growth rate in this patient may be associated with the finding of undetectable free GH levels. Measurement of plasma free and total GH may be of value in examining GH dynamics and their relation to the clinical effectiveness of GH treatment in patients with GH antibodies.

Adolescent↗
PubMed1989

[A case of localized pleural tuberculosis exacerbated during antituberculous chemotherapy].

A 24 year-old male with pulmonary tuberculosis in right upper lobe developed two lesions of extrapulmonary pleural tuberculoma during the course of antituberculous therapy. He had no history of lung tuberculosis nor pleurisy. However, the chest X-ray film on first admission showed scattered nodular shadows in right upper lung field. He had no subjective symptoms and no abnormalities of laboratory findings except mild iron deficiency anemia, from which he recovered completely without specific therapy. Three months after starting the antituberculous therapy including SM, INH, and RFP, a new round homogeneous opacity appeared in the right lower lung field (S4). Chest CT scan revealed the lesions in S10 as well as in S4. Microscopic examination of the specimen obtained by ultrasound-guided needle aspiration biopsy disclosed positive acid-fast bacilli. Because of the lack of effect of drug therapy on pleural lesions, surgical treatment was performed. The visceral pleura was found adherent fibrously to parietal pleura, which was easily separated by hand. However, at the site of lesions, the adhesion was so tight that extrapleural resection was needed. Because lung tissue and tumor were connected tightly, the lung had to be partially resected. Most content of tumors were caseous necrosis. Although main lesion was located outside of the lung, intrapulmonary invasion was also noticed. Double lesions of this kind of disease seem to be very rare. There is no evidence of relapse until eight months after surgery.

Adult↗
PubMed1988

Complex glycerol kinase deficiency: molecular-genetic, cytogenetic, and clinical studies of five Japanese patients.

Five male Japanese patients with complex glycerol kinase deficiency (CGKD) and their relatives were studied clinically, cytogenetically, and molecular-genetically. All patients had muscular dystrophy or muscle weakness, mental retardation, congenital adrenal hypoplasia, and glycerol kinase deficiency. High-resolution GTG-banded chromosomes showed a microdeletion in the Xp21 region in all four patients examined and in all five mothers. Southern hybridizations, after digestions by restriction endonucleases, with various cloned DNAs (D2, 99-6, B24, C7, L1-4, cDMD13-14, J66-HI, P20, J-Bir, ERT87-30, ERT87-15, ERT87-8, ERT87-1, XJ-1.1, 754, cx5.7, and OTC-1) that are located around Xp21 also showed a deletion in the genome of all patients and mothers. Although the deletion differed in size among patients, a segment commonly absent was located between the genomic sequences corresponding to L1-4 and cDMD13-14. This finding indicated that the gene coding for glycerol kinase (GK) is located within this segment. A comparison of the clinical manifestations of the present five patients and reported CGKD or Duchenne muscular dystrophy (DMD) patients with DNA deletion suggests the existence of a certain gene responsible for gonadotropin deficiency (GTD). The result of the present study and results of previous studies suggest that genes for ornithine transcarbamylase (OTC), DMD, and GK and putative genes responsible for congenital adrenal hypoplasia (AHC) and GTD are arranged from telomere to centromere as pter--GTD--AHC--GK--DMD--OTC--cen.

Adolescent↗
PubMed1988

Suppression of delayed-type hypersensitivity in mice pretreated with diethylstilbesterol: involvement of sex hormones in immunomodulation.

Delayed-type hypersensitivity (DTH) responses were suppressed in female mice treated with diethylstilbesterol (DES), a synthetic nonsteroidal compound possessing estrogenic activity, but not in male mice. Upon analysis of this DTH-suppression in DES-treated female mice by use of the macrophage migration inhibition (MI) assay, an in vitro correlate of DTH, suppressor adherent cells (i.e., macrophages) in the peritoneal cavity were found to play an important role in this DTH suppression. On the other hand, DES-induced suppression was observed in surgically castrated male mice with depressed plasma testosterone (TS) levels, but not in TS-treated female mice or in castrated male mice, which suggests that TS inhibited the DES suppression. These results provide evidence that DTH response may be modulated by sex hormones.

Adjuvants, Immunologic↗
PubMed1988

[Antiemetic treatment with metoclopramide and high-dose lorazepam and additional long-term treatment with lorazepam during CDDP administration].

We studied the antiemetic effects of a combination therapy consisting of metoclopramide (MCP) and high-dose lorazepam (HiLor; 3-4.5 mg/day) in patients with lung cancer who were being treated with cis-diamminedichloroplatinum (CDDP). This study was designed in order to compare the antiemetic efficacy of two different-term treatments. In the short-term treatment, MCP and HiLor were given for three days after the beginning of the CDDP regimen (group 1). In the long-term treatment (group 2), the same dose of MCP and a decreased dose of HiLor (1.5-3 mg/day) were administered for another three days (eventually for 6 days). Thirty-one trials were evaluated in eighteen patients for 8 days after the CDDP treatments initiated. The frequency of episodes of vomiting was less than two times in 70% and 82% of trails, in group 1 and group 2, respectively. This finding indicates that the combination therapy of MCP and HiLor for a long period would be the same or more effective than that of MCP and steroid agents. Furthermore, in group 2, the frequency and severity of late emesis were significantly less than in group 1, and appetite recovery was observed significantly earlier than in group 1. There was no side effect related to the administration of MCP and HiLor during this study. These findings suggested that the combination treatment of MCP and HiLor with a decreased dose of HiLor for a long period was markedly effective for antiemesis in patients treated with CDDP, especially for the prophylaxis of CDDP-induced late emesis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Worldwide experience in newborn screening for classical congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

The need for a reliable screening test for classical congenital adrenal hyperplasia prompted development of newborn screening programs. Worldwide incidence of classical congenital adrenal hyperplasia in this report was taken from newborn screening programs in France, Italy, Japan, New Zealand, Scotland, and the United States. Two populations in which the occurrence of congenital adrenal hyperplasia among live births has been reported with greater than usual frequency are the Yupik Eskimos of southwestern Alaska (1:282) and the people of La Reunion, France (1:2,141). Aside from these populations, 1,093,310 newborns were screened between 1980 and 1988, of whom 77 had congenital adrenal hyperplasia. Thus, worldwide incidence of this disorder was estimated at 1:14,199 live births for homozygous patients, 1:60 for heterozygous subjects, with a gene frequency of 0.0083. Incidence of congenital adrenal hyperplasia among whites was estimated to be 1:11,909 (41:488,279) for homozygous patients, 1:55 for heterozygous subjects with a gene frequency of 0.0091. Incidence for the salt-wasting form of congenital adrenal hyperplasia was 1:18,850 (58:1,093,310) compared with 1:57,543 (19:1,093,310) for congenital adrenal hyperplasia in the simple virilizing form. Thus, salt-wasting congenital adrenal hyperplasia was three times more common than simple virilizing congenital adrenal hyperplasia. Estimated incidence of congenital adrenal hyperplasia in white populations in Italy and France (1:10,866) was higher than in Scotland (1:17,098), New Zealand (1:14,500). The incidence in an Asian population (Japan) (1:15,800) did not differ significantly from that of the white population. In four of five populations, overall incidence was higher than previously reported, as was the frequency of the salt-wasting form (75% v 50% to 66%), suggesting improved case detection by newborn screening.(ABSTRACT TRUNCATED AT 250 WORDS)

17-alpha-Hydroxyprogesterone↗
PubMed1987

[Neonatal screening for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 4. Development of enzyme-linked immunosorbent assay for dried blood cortisol and its application to neonatal screening for congenital adrenal hyperplasia due to 21-hydroxylase deficiency].

An enzyme-linked immunosorbent assay (ELISA) for Cortisol in dried blood collected on filter paper has been developed. The ELISA method is very simple and rapid and has sensitivity, accuracy and precision. The detection limit of the ELISA is 10 ng/ml blood. The intra- and interassay coefficients of variation are 11.5-13.5% and 15.7-16.7, respectively. Using the ELISA for Cortisol and 17-hydroxyprogesterone (17-OHP) previously reported, dried blood from normal newborns including premature infants (n = 1583) and 21-hydroxylase deficiency (21-OHD) patient (n = 9) were analyzed. 17-OHP, Cortisol and 17-OHP/Cortisol ratio of normal newborns are 12.5 +/- 7.5 ng/ml (1.0-140 ng/ml), 89.0 +/- 64.3 ng/ml (10-1580 ng/ml) and 0.16 +/- 0.08 (0.01-0.86), respectively. In 21-OHD patients, 17-OHP is 109-1361 ng/ml, Cortisol is 35.1-146.7 ng/ml and 17-OHP/cortisol ratio is 1.84-12.2. It made recall rate less to measure Cortisol in addition to 17-OHP and to take 17-OHP/Cortisol ratio. Therefore, additional measurement of Cortisol to the primary 17-OHP screening test is advantaged in differentiating the normal newborns from the 21-OHD patients.

Adrenal Hyperplasia, Congenital↗
PubMed1987

[Neonatal screening for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 2. Analysis of steroids with high-performance liquid chromatography for diagnosis of congenital adrenal hyperplasia].

A quantitative analysis of steroids in serum, dried blood samples on filter paper and amniotic fluid with high-performance liquid chromatography has been developed and applied to the diagnosis of risk infants on neonatal screening for congenital adrenal hyperplasia. The present method is simple, rapid and accurate. The detection limits of cortisol and 17 alpha-hydroxyprogesterone are 0.2 ng and 0.3 ng, respectively. The twenty-two steroids can be analysed within 60 minutes using the isogradient mobile phase. The method is highly correlated with radioimmunoassay and enzymeimmunoassay. In 4 patients with the salt-losing form, 17 alpha-hydroxyprogesterone was higher and cortisol lower than in 4 patients with the simple-virilizing form. This method seems suitable for the routine clinical elucidation of congenital adrenal hyperplasia.

17-alpha-Hydroxyprogesterone↗
PubMed1987

[Neonatal screening for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 3. An enzyme-linked immunosorbent assay for dried blood 17 alpha-hydroxyprogesterone].

An enzyme-linked immunosorbent assay (ELISA) for 17 alpha-hydroxyprogesterone (17-OHP) in dried blood collected on filter paper has been developed. The ELISA method is very easy and rapid and has sensitivity, accuracy and precision. The detection limit of the ELISA method is 0.5 ng/ml blood. Intra- and interassay coefficients of variation are 7.0 approximately 8.3% and 6.7 approximately 10.5%, respectively. Correlation between the ELISA method and previously reported enzyme immunoassay is good (r = 0.961). 17-OHP values of neonates with congenital adrenal hyperplasia (CAH) are extremely high compared with normal neonates (11.0 +/- 5.9 ng/ml blood). The present study demonstrates that the ELISA method for 17-OHP is applicable to neonatal screening for CAH.

17-alpha-Hydroxyprogesterone↗
PubMed1986

[Neonatal screening for congenital adrenal hyperplasia due to 21-hydroxylase deficiency. 1. Enzyme immunoassay of dried blood 17 alpha-hydroxyprogesterone and its application to neonatal screening for congenital adrenal hyperplasia].

An enzyme immunoassay for measuring 17 alpha-hydroxyprogesterone (17-OHP) in dried blood collected on filter paper has been developed. The method is easy and rapid and has specificity, accuracy and precision. 17-OHP values of neonates with congenital adrenal hyperplasia (CAH, 40 ng/ml) were extremely high compared with normal neonates (1.1 +/- 0.7 ng/ml). There was a negative correlation between the 17-OHP value and birth weight. The method has been applied to neonatal screening for CAH due to 21-hydroxylase deficiency. During 38 months, 67,392 neonates were screened. The recall rate and the medical evaluation rate were 1.16% and 0.09%, respectively. A third of recalled neonates were low birth weight infants. 5 neonates were proven to have CAH, and its incidence was 1:13,478. The present study demonstrates the feasibility of a neonatal screening for CAH and indicates that the frequency of CAH may be greater than previously reported by case assessment method in Japan.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Depression of delayed-type hypersensitivity in mice with hypothalamic lesion induced by monosodium glutamate: involvement of neuroendocrine system in immunomodulation.

Delayed-type hypersensitivity (DTH) was depressed in mice that had been treated with monosodium glutamate (MSG) in their suckling period. Analysis of the DTH depression by use of the macrophage migration inhibition assay showed dysfunction of DTH effector T cells. The neuronal loss of nuclei in the hypothalamus, which elaborates the corticotropin-releasing factor and the hypersecretion of adrenocorticotrophic hormone, was observed in the MSG-treated mice. Therefore, DTH response may be modulated by the neuroendocrine system.

Adrenocorticotropic Hormone↗