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Y Fuse

Publications and source records attributed to Y Fuse.

At least 73 records · Page 4Linked to original sources

Distribution of thyrotropin-releasing hormone (TRH) and precursor peptide (TRH-Gly) in adult rat tissues.

TRH (pGlu-His-Pro-NH2) arises from the post-translational processing of a larger precursor peptide containing multiple copies of the TRH progenitor sequence, Gln-His-Pro-Gly. Concentrations of TRH and its precursor peptide (TRH-Gly) were determined in serum and a variety of tissues of the rat using specific RIA systems. TRH and TRH-Gly immunoreactivities were detectable in almost all tissues studied. TRH was distributed mainly in neural tissues, with the highest mean concentration (126 pg/mg tissue) in hypothalamus. In extra-neural tissues, mean TRH levels ranged from 0.6-4.8 pg/mg tissue; the mean serum concentration was 12.4 pg/ml. In contrast to the distribution of TRH, relatively higher mean TRH-Gly concentrations were observed in serum (76.5 pg/ml) and in extraneural tissues, including prostate (83.3 pg/mg tissue), spleen (19.0 pg/mg), adrenal (16.2 pg/mg), kidney (13.3 pg/mg), and gastrointestinal tract (6.3-19.8 pg/mg). Among brain tissues, the TRH-Gly concentration was highest in pituitary gland (13.1 pg/mg). The mean ratio of TRH-Gly/TRH concentrations was less than 1 in neural tissues and pancreas. The lowest ratio (0.04) was observed in hypothalamus, and the highest ratio (66) in prostate gland. Assuming that tissue TRH-Gly levels reflect TRH synthesis, these results suggest that 1) the processing of TRH-Gly to TRH varies among tissues, 2) TRH-Gly to TRH conversion occurs most efficiently in neural tissues, and 3) TRH-Gly to TRH conversion may be a rate-limiting step in TRH biosynthesis.

Animals↗

Thickness of Brunner's glands and its clinical significance in duodenal ulcer disease.

The thickness of Brunner's glands was measured with an ocular micrometer in 75 cases of surgically resected duodenal ulcer and in 75 autopsy cases (control group). Endoscopic findings before operation were also studied. Maximum mean thickness of Brunner's glands in the control group was 1.54 +/- 0.38 mm (mean +/- SD), and no regional difference in thickness was noted. The thickness of Brunner's glands in the duodenal ulcer group was widely distributed, from 0.5 mm to 5.0 mm, and the average value was 3.0 +/- 1.0 mm, with a statistically significant difference from that of the control group. In most duodenal ulcer cases Brunner's glands were thickest within 1 cm from the center of an ulcer. Only six cases of duodenal ulcer (8.0%) showed a diffusely thin layer of Brunner's glands, less than 1.5 mm thick. These results show that the Brunner's glands become hyperplastic in duodenal ulcer patients, especially near the ulcer. In the healed ulcer Brunner's glands were thin at the center of an ulcer scar, and the average thickness was 0.42 +/- 0.26 mm. This histologic finding corresponded to the depressed scarred area observed endoscopically, suggesting a decreased mucosal resistance at this area.

Adolescent↗

Maturation of feedback control of thyrotropin in premature infants.

Serum thyrotropin (TSH), free T4 and free T3 concentrations were measured longitudinally in 26 preterm infants for 14 weeks after birth, using highly sensitive immunoradiometric assays. Serum TSH values on days 4-5 were positively correlated with gestational age and birth weight. In the premature infants of 25 weeks mean gestation, the mean TSH concentrations increased from a very low value of 0.84 microU/ml at 5 days to a peak value of 6.1 microU/ml by 5 weeks of age, then slightly decreased and remained stable. Serum free T4 and free T3 concentrations increased in parallel and free T3 level reached the range of term infants by 6 weeks. Serum free T4/TSH and free T3/TSH ratios began to increase at the 6th week of age. The results suggest that: (i) the thyroid hormone feedback control of pituitary TSH release in the extremely premature infants begins to mature after 6 weeks of postnatal age, (ii) the maturation pattern of the hypothalamic-pituitary-thyroid system in premature infants is similar to that of the intrauterine fetus.

Birth Weight↗

[Myelofibrosis associated with immunological abnormalities].

A 74-year-old man was admitted to the National Defense Medical College Hospital because of purpura on the extremities. The blood hemoglobin level was 11.5 g/dl, the white blood cell count 7. 3 x 10(9)/l with 3% blastic cells, and the platelet count 4.0 x 10(9)/l. There was leukoerythroblastosis with only mild teardrop appearance of erythrocytes. The blastic cells consisted of two types, megakaryoblast-like cells and myeloblast-like cells. There was a very mild hepatosplenomegaly, but no lymphadenopathies. The bone marrow aspirations yielded dry taps. The marrow biopsy specimen revealed myelofibrosis associated with trilineage hyperplasia, but no apparent infiltration of leukemic cells. Platelet-associated IgG (PAIgG) had a high titer and the response to platelet transfusions was poor. On prednisolone and colchicine, the blastic cells in the peripheral blood disappeared and the platelet count increased. He died of pneumonia. The autopsy showed myelofibrosis with hyperplasia of myeloid and erythroid lineage in the bone marrow. Megakaryocytes were relatively few and there was no infiltration of leukemic cells.

Aged↗

Thickness of Brunner's glands and its clinical significance in peptic ulcer diseases.

The thickness of Brunner's glands was measured using an ocular micrometer in 297 cases of surgically resected peptic ulcer and in 120 autopsy cases (control group). The mean maximum thickness of Brunner's glands in the control group was 1.55 +/- 0.37mm (mean +/- SD) and no difference in thickness was noted for each decade of age. The mean maximum thickness of Brunner's glands in patients with gastric ulcer, duodenal ulcer and gastroduodenal ulcer was 2.34 +/- 1.06, 3.18 +/- 1.07 and 3.24 +/- 1.05mm, respectively. When an ulcer is within the duodenum, Brunner's glands near the ulcer were thicker than those contralateral to it. In patients with gastric ulcer, Brunner's glands were the thickest in the pyloric ulcer group and negative correlation was noted between the thickness of Brunner's glands and the distance to the ulcer from the pyloric ring. Since gastric acidity is supposed to be lower when an ulcer is located more proximally, these results suggest that Brunner's glands become hyperplastic not only with the presence of an ulcer in the duodenum but also by acid hypersecretion of the stomach.

Adult↗

A case of leiomyosarcoma associated with humoral hypercalcemia of malignancy: demonstration of biological and immunological activities of parathyroid hormone-related protein in the tumor extract.

Hypercalcemia occurred in a patient with leiomyosarcoma when multiple lung metastases developed. Despite normal plasma parathyroid hormone (PTH) levels and low 1,25-dihydroxyvitamin D, this hypercalcemic patient had a marked hypercalciuria and phosphaturia associated with an increased excretion of nephrogenous cyclic AMP (NcAMP). Administration of cisplatin ameliorated both the hypercalcemia and hypercalciuria without any reduction in tumor size of NcAMP excretion. Terminally, acute pancreatitis occurred producing a profound hypocalcemia. In the extract of tumor tissue obtained post mortem, bioactivity stimulating the generation of cyclic AMP in osteogenic cells was demonstrated along with the immunoreactive PTH-related protein (PTH-rP). the first report of a solid non-epithelial malignancy producing PTH-rP and associated with humoral hypercalcemia of malignancy. The hypercalcemia in this case caused acute pancreatitis, which led to a profound hypocalcemia.

Calcium↗

Healing process of experimental esophageal ulcers induced by acetic acid in rats.

We studied the healing of acetic acid-induced esophageal ulcers in rats with respect to the cellular kinetics. Esophageal ulcers were induced by topical application of acetic acid to the serosal surface. Well-demarcated circular or elliptical ulcers had developed by day 3 after the acid treatment. These ulcers began to decrease in size from day 7 and had healed by day 14. Histological and cellular kinetic findings, with bromodeoxyuridine (BrdU), were degeneration of the esophageal mucosa on day 1 and ulcer formation on day 3, with an increase in the number of BrdU-labeled cells in the esophageal mucosa around the ulcer. On day 7, regenerated epithelium was found to extend towards the ulcer base and the regenerated epithelium had become thicker, with papilla formation, by day 10. On day 14, the ulcer base was covered with thickened regenerated mucosa, with a decrease in the number of BrdU-labeled cells. Marked proliferative activity of the regenerated mucosa and thickening of the esophageal mucosa, with papilla formation, were observed during the healing process.

Acetates↗

Possible mechanisms of diethyldithiocarbamate-induced gastro-duodenal mucosal damage in rats.

A single s.c. injection of diethyldithiocarbamate (DDC, 1 g/kg) induced not only gastric but also duodenal mucosal damage in rats. DDC induced marked decreases in gastric acid output, gastro-duodenal mucosal blood flow and transmucosal potential difference prior to the development of mucosal lesions. Superoxide dismutase activity in the gastro-duodenal mucosa was also inhibited, while catalase and glutathione peroxidase activities gradually increased after the administration of DDC. These results suggest that a decrease in mucosal defensive mechanisms plays an important role in the development of DDC-induced gastro-duodenal mucosal damage and that oxygen-derived free radicals may also participate in the development of this mucosal damage.

Animals↗

[Possible mechanisms of diethyldithiocarbamate-induced duodenal mucosal damage in rats].

Diethyldithiocarbamate (DDC), which markedly lowers activity of Cu, Zn-superoxide dismutase (SOD), induces not only gastric but also duodenal mucosal damage in rats. In this experiment, we studied on the mechanisms of DDC-induced duodenal mucosal damage with special reference to aggressive and defensive factors. Possible importance of oxygen-derived free radicals was also investigated. Male Wistar rats weighing about 200 g received a single subcutaneous injection of DDC at a dose of 1 g/kg. Mucosal lesions such as edema, shortness of villi and shallow erosion developed from 3 hours after DDC injection. The ulcer index reached at its maximum 12 hours later. Gastric acid output was markedly inhibited from 87.7 +/- 8.7 to 14.0 +/- 2.6 microEq/kg/h (m +/- SE) 30 minutes after the administration of DDC (p less than 0.01), which gradually recovered thereafter. Duodenal mucosal blood flow before DDC injection was 144.7 +/- 12.7 ml/min/100 g, which decreased to 83.3 +/- 5.1 (p less than 0.01) 1 hour later. Transmucosal potential difference of the duodenum before DDC injection was -9.5 +/- 1.0 mV, which decreased to -3.8 +/- 1.3 (p less than 0.05) 30 minutes later. Duodenal alkaline secretion before DDC injection was 15.6 +/- 0.8 microEq/kg/h, which decreased to 5.0 +/- 0.9 microEq/kg/h (p less than 0.01) 90 minutes later. PAS-stained mucus of Brunner's glands remained unchanged by the administration of DDC. SOD activity was markedly inhibited from 57.7 +/- 4.0 to 15.7 +/- 0.9 u/mg protein 3 hours after the administration of DDC (p less than 0.01), then recovered 24 hours later.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Autoradiographic study on healing process of cysteamine-induced duodenal ulcer in rat. Possible importance of Brunner's glands in ulcer healing.

The healing process of cysteamine-induced duodenal ulcer was studied by [3H]thymidine autoradiography. After the development of ulcer in the duodenum, cell proliferation was markedly activated not only in the crypts but also in the Brunner's glands near the ulcer. In the initial stages of ulcer healing, they both contributed to form the surface covering regenerating epithelium. Granulation tissue also proliferated at the base of the ulcer. In later stages of ulcer healing, new crypts were formed in the floor of the ulcer. New villi regenerated from these crypts and Brunner's glands regenerated by proliferation in situ. The ulcer base then was completely covered with new villi and granulation tissue was replaced by dense fibrous connective tissue. The present study suggested that the Brunner's glands, together with the crypts of Lieberkühn, play an important role in the healing process of cysteamine-induced duodenal ulcer.

Animals↗