[Origins, processing, and qualities of crude drugs (1). Preventive effects of a Chinese crude drug, Zhu, on experimental stomach ulcer and its pharmacological evaluation. 1].
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Biomedical subjects
Publications and source records attributed to M Kubo.
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The present data describe the mechanism of the inhibitory effects of human plasma apolipoproteins A-I and A-II on hydrolysis of triglyceride catalyzed by hepatic triglyceride lipase using a substrate of triolein particles stabilized with gum arabic in vitro. The experimental data could well be described by a model in which apolipoproteins bound to the surface of lipid substrate particles inhibited the enzyme reaction. The values of Km obtained were similar with or without inhibitors and the calculated saturation levels of apolipoprotein binding to the lipid were in good agreement with those obtained in independent binding experiments.
To evaluate the effect of PRL on the male pituitary-gonadal system, serum concentrations of PRL, testosterone, LH and FSH were determined in healthy young men daily before, during, and after 3-day oral administration of bromocriptine, metoclopramide or sulpiride. Bromocriptine (2.5 mg as a single dose) caused, concurrently with a marked suppression of serum PRL, a significant increase of serum testosterone and a transient decrease of serum LH. The changes of PRL and testosterone were negatively correlated. With metoclopramide (10 mg q.i.d.) serum PRL was increased and testosterone inversely decreased. There was no change in LH and FSH. Sulpiride (50 mg q.i.d.) evoked the elevation of serum PRL and LH, but no change in testosterone. A significant increase in serum concentration of testosterone was also observed in a patient with PRL-producing pituitary tumour and four out of seven patients with acromegaly during bromocriptine treatment. These results suggest an inhibitory effect of PRL on testosterone secretion at the gonadal level, or direct dopaminergic stimulatory control of testosterone secretion.
A male infant with partial DiGeorge syndrome responded to weekly administration of levamisole (2.5 mg/kg of body weight) with an increase of circulating E-rosette-forming T cells. Thymic hormone activity in plasma appeared to be elevated to a near-normal level of 11.6 ng thymopoietin equivalent/ml after levamisole administration. The in vitro incubation studies indicated that levamisole by itself had no E-rosette-promoting ability, but a dialysable and relatively heat-stable plasma factor induced by levamisole both in the patient and in healthy individuals had E-rosette-promoting activity for the patient's lymphocytes. Such a plasma factor, however, could not be induced in all four thymectomized myasthenic subjects examined, suggesting a thymus-dependent nature of the plasma factor. These results suggest that levamisole might mediate an increased secretion of humoral factor(s) with E-rosette-promoting activity, even from such a rudimentary thymus as in the partial DiGeorge syndrome.
In 15 pigs affected with cerebrospinal angiopathy accompanied by demyelination and malacia, the main symptoms were diarrhea and subsequent circling, spasms, sudden forward movements, ataxia, and inability to hold the head straight. Escherichia coli was isolated in a pure culture from the small intestine of pigs with diarrhea. The only gross change was a slight increase in cerebrospinal fluid. Histologic examination showed vascular lesions, demyelination, and malacia, most commonly located in the medulla oblongata, pons, and midbrain. The vascular lesions were degenerative and there were necrotic changes of the vessel walls and formation of periodic acid-Schiff positive perivascular eosinophilic droplets. Ultrastructurally, the swollen astrocytes around the vessels had many osmiophilic bodies in their cytoplasm with no limiting membrane. Demyelination and malacia, as well as vascular lesions, were considered to be the characteristic changes of cerebrospinal angiopathy. Our study suggests that E. coli may be a cause of cerebrospinal angiopathy.
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One- to 21-day-old mice were examined pathologically after inoculated intracerebrally or subcutaneously with the Kakegawa strain of bovine coronavirus. In 1- to 4-day-old mice inoculated intracerebrally, the brain contained a small number of neutrophils and lymphocytes having infiltrated diffusely and perivascularly and some degenerative neurons. In mice inoculated intracerebrally at 7 to 21 days of age, severe necrosis of pyramidal cells was shown in Ammon's horn. Perivascular infiltrations of neutrophils and lymphocytes were moderate to severe. Some neurons were degenerative in the cerebral cortex, thalamus and midbrain. Degeneration of some neurons and mild infiltration of neutrophils and lymphocytes were observed in the brain of mice inoculated subcutaneously at 1 to 7 days of age. Perivascular infiltration of neutrophils and lymphocytes was prominent in the cerebral cortex of mice inoculated subcutaneously at 14 days of age. Cellular infiltration was also seen in the thalamus, Ammon's horn, midbrain, cerebellum and medulla oblongata. All the mice, except one, inoculated subcutaneously at 21 days of age were free from neural changes. Electron-microscopically, virus particles were observed in and outside of the degenerative neurons. They had a core 70 nm in diameter and an envelope with spikes.
Sulfur granules produced by Staphylococcus aureus and Corynebacterium pyogenes were studied by light and electron microscopy. They consisted of bacteria and electron-dense amorphous substance which formed clubs in the periphery of each granule. In those produced by Staph. aureus, cocci were seen at the center of each granule. They were round or pleomorphic. Binary fission was frequently observed. In those produced by Coryn. pyogenes, degenerative bacteria were present at the center of each club. Bacteria found just beneath the club had a thick, electron-less-dense cell wall and electron-dense cytoplasm. Those present at the center of the granule were very long and had a cell wall thin and sometimes undulant, containing ribosomes. The electron-dense amorphous substance surrounded these bacteria and faced the neutrophils or epithelioid cells in the periphery of the granule both species of organisms. They might have been produced by bacteria. Cellular reactions of neutrophils, epithelioid cells, fibroblasts and plasma cells were seen around the sulfur granules produced by both species of organisms.
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Two cases of red cell aldolase deficiency associated with congenital nonspherocytic hemolytic anemia are reported. The proband is a fourteen-month-old Japanese boy. Consanguineous marriage was not proven but probable in this family, as the parents were born in the same small island. The proband had moderate to mild anemia aggravated by upper respiratory infections, 1 cm hepatomegaly and 2.5 cm splenomegaly, but was unremarkable in other respects and has thus far not shown mental or growth retardation. He did not have dysmorphic features. The red cell aldolase activity was 6% of the normal mean. The enzyme was unstable with respect to heat, and Km for fructose 1,6-diphosphate (F-1,6-DP) was high. The parents and other heterozygotes showed intermediate activity between that of the proband and that of normal subjects. Red cell F-1,6-DP concentration in this case was remarkably increased. Red cell glucose consumption, and lactate formation, as well as hexose monophosphate shunt activity, were decreased as compared with a comparable reticulocyte-rich hereditary spherocytosis patient. Hexose monophosphate dehydrogenase by a high concentration of F-1,6-DP in his red cells. As a result of family study, another homozygous aldolase deficiency case associated with hemolytic anemia was found. He is 13 years old and a nephew of the proband's paternal grandmother. His hemolytic anemia also is moderate to mild and aggravated by upper respiratory infections. He does not seem to have mental or growth retardation, nor does he possess dysmorphic features.
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