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Biomedical subjects

M Kaji

Publications and source records attributed to M Kaji.

At least 199 records · Page 11Linked to original sources

Hypothalamic-pituitary function in growth hormone-deficient patients with pituitary stalk transection.

We compared 1.5 T magnetic resonance (MR) image findings with hypothalamic-pituitary function in 11 patients with idiopathic pituitary dwarfism, each of whom had a history of perinatal abnormalities, and 1 patient with posttraumatic pituitary dwarfism. MR imaging revealed transection of the pituitary stalk in all patients and the formation of an ectopic posterior lobe at the proximal stump in 9 patients, none of whom had polydipsia or polyuria. Three patients without an ectopic posterior lobe had diabetes insipidus. The 5 patients who had small pituitary glands (less than 2 mm in height) had hypothyroidism with low serum TSH concentrations and low serum cortisol responses to insulin-induced hypoglycemia; however, 7 patients with normal-sized pituitary glands had normal thyroid and adrenal function. The serum GH response to GHRH did not correlate with the size of the pituitary gland. The patients with small pituitary glands had delayed or prolonged serum TSH responses to TRH and impaired serum LH and FSH responses to GnRH; 4 of the patients with normal-sized pituitary glands had normal serum TSH, LH, and FSH responses. Only 2 patients had high basal serum PRL concentrations. The endocrinological data suggest that reestablishment of the hypothalamo-hypophyseal portal circulation, which cannot be seen by MR imaging, may occur. We suggest that the primary cause of idiopathic pituitary dwarfism in many patients is injury to the pituitary stalk at birth.

Adolescent↗

An outbreak of influenza A (H3N2) in a hospital for the elderly with emphasis on pulmonary complications.

From Dec 1, 1985 to Jan 18, 1986, 133 of 379 (35.1%) mainly elderly in-patients at a hospital in Fukuoka City were infected with influenza virus A (H3N2). In 32 of the 133 (24.1%) infected with the virus, pneumonia occurred. The occurrence was significantly higher in man (33.1%) than in women (17.1%) (p less than 0.05), and the same occurrence was found to be higher in bed-ridden patients (32.7%) than in ambulatory patients (17.3%) (p less than 0.05). It was also higher in those age 70 or older (25.4%) than in those 69 years or younger (17.4%), but with no statistical difference. Seven men and one woman, all 70 years old or older, infected with the virus died of pneumonia. The overall case-fatality ratio was 6.0%. Thus, male bed-ridden patients aged 70 years or older are highly vulnerable to pneumonia in case of infection with influenza virus A.

Aged↗

Purification and characterization of a Ca2+-dependent membrane peptidase involved in the signaling of mating pheromone in Rhodosporidium toruloides.

A mating-type-specific, membrane thiol peptidase (referred to as trigger peptidase) that seems to play a key role in the transmembrane signaling of the lipopeptidyl mating pheromone rhodotorucine A at the cell surface of mating type a cells of Rhodosporidium toruloides (T. Miyakawa, M. Kaji, T. Yasutake, Y.K. Jeong, E. Tsuchiya, and S. Fukui, J. Bacteriol. 162:294-299, 1985) was purified to homogeneity and characterized. The following lines of evidence support the contention that the enzyme we purified was the trigger peptidase: the identical specificity of hydrolysis at the Arg-Asn sequence of rhodotorucine A and the sensitivity of the reaction to sulfhydryl-blocking reagents; the identical specificity for the substrate, with a strict requirement for the presence of the lipid moiety; and the absence of the corresponding activity in the pheromone-producing strain (mating type A) and in a sterile mutant strain, M-39 (type a), that lacks trigger peptidase activity in vivo. The apparent molecular weight of trigger peptidase was estimated to be 68,000 by Sepharose 6B gel filtration in the presence of octylglucoside and 63,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Trigger peptidase alone was inactive but exhibited enzymatic activity with the simultaneous addition of Ca2+, membrane phospholipids, and a nonionic detergent such as octylglucoside. The concentration of Ca2+ required for maximum activation was approximately 1 mM. Only Mn2+ could replace Ca2+ at comparable concentrations. Among the phospholipids tested, only phosphatidylserine and phosphatidylethanolamine supported trigger peptidase activation. Solubilized trigger peptidase was strongly inhibited by antipain and phosphoramidon.

Basidiomycota↗

Failure to induce puberty in a man with X-linked congenital adrenal hypoplasia and hypogonadotropic hypogonadism by pulsatile administration of low-dose gonadotropin-releasing hormone.

To elucidate the mechanism of hypogonadotropic hypogonadism in a patient with X-linked congenital adrenal hypoplasia, we studied the effects on serum LH and FSH of repeated iv administration of GnRH (400 micrograms, over 2 h, once a day, for 14 consecutive days), pulsatile sc administration of GnRH (5 micrograms every 90 min during days 1 approximately 56, 10 micrograms every 90 min during days 57 approximately 91) and an iv bolus injection of 10 mg of naloxone. The repeated administration of GnRH restored the hyporesponsiveness of serum FSH and increased serum testosterone level from less than 1.0 to 1.7 nmol/l, but the impaired LH response to the standard GnRH test was not improved. The pulsatile administration of GnRH for 91 consecutive days did not induce a clinical or a biochemical change of puberty. Serum testosterone remained undetectable less than 1.0 nmol/l, the hyporesponsiveness of serum LH was not improved, but basal FSH level was significantly increased and the impaired FSH response to the standard GnRH test was slightly improved. Naloxone had no effect on serum LH or FSH before or during the pulsatile administration. We conclude that hypogonadotropic hypogonadism in our patient is due to the pituitary dysfunction and that the endogenous opioid peptides may not play a role in the mechanism of inhibited gonadotropin secretions.

Adolescent↗

Age-specific prevalence of hepatitis B e antigen (HBeAg) and antibody to HBeAg (anti-HBe) among asymptomatic hepatitis B surface antigen (HBsAg) carriers in Okinawa and Kyushu, Japan.

A total of 1,741 asymptomatic hepatitis B surface antigen (HBsAg) carriers in two areas (Okinawa and Kyushu) in Japan were surveyed for the presence of hepatitis B e antigen (HBeAg) and the corresponding antibody (anti-HBe) to determine the age-specific prevalence of these markers and the mean age of carriers with HBeAg. Prevalence of HBeAg was significantly higher in Kyushu (36.4% of 755 carriers) than in Okinawa (20.0% of 986 carriers) (P less than 0.001). The mean age of carriers with HBeAg was 25.5 years in Kyushu and 16.1 years in Okinawa, suggesting that HBeAg converted to anti-HBe earlier in Okinawa than in Kyushu. In contrast, the prevalence of anti-HBe was significantly higher in Okinawa (74.6% of 986) than in Kyushu (56.3% of 755) (P less than 0.001). The prevalence of HBeAg decreased with age up to 40-49 years of age and then increased in both areas. Prevalence of anti-HBe was inversely related to the prevalence of HBeAg in both areas. These data suggest that HBeAg and anti-HBe are chronological markers of chronic hepatitis B virus infection and that the duration of HBeAg persistence can be different in different area, even in the same country.

Age Factors↗