The penetration and metabolism of H3-dimethoate in insects.
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Biomedical subjects
Publications and source records attributed to T Uchida.
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Hepatic amyloid, when identified, is usually located in the sinusoids, portal tracts, and arterioles. We report 14 cases of hepatic amyloidosis where eosinophilic globules having the histochemical and electron microscopic features of classic amyloid were found. The globules were round to oval, 5 to 40 micrometer in diameter, and were found within the space of Disse as well as aggregated within the portal tracts. There were no distinctive clinical or laboratory features distinguishing this type of amyloidosis from classic hepatic amyloidosis. However, there were no cases of multiple myeloma and only one of benign monoclonal gammopathy. All seven patients who were studied at postmortem examination had systemic (nonglobular) amyloidosis. This form of hepatic amyloidosis is probably not an early form of the disease but is an original but rare presentation of hepatic amyloid deposition.
A sequential study was performed to investigate the occurrence and localization of duck hepatitis B virus in the liver of domestic ducks utilizing the indirect immunoperoxidase method and electron microscopy. Seventeen ducklings were injected intravenously with duck hepatitis B virus-positive serum within 24 hr after hatching and were subsequently sacrificed on the 2nd, 3rd, 4th, 5th, 27th and 44th day after injection. Nine ducklings were not injected and were used as a negative control. Duck hepatitis B virus DNA by spot hybridization using a [3P]-labeled probe occurred in trace amounts on the 2nd day and in large amounts on the 4th day after inoculation. Immunoreactivity for DHBV was seen in the hepatocytes, sporadically on the 2nd day and diffusely on the 4th day, and also in the biliary epithelial cells on the 27th day. Both kinds of cells revealed staining in the cytoplasm but not in the nucleus. Virus particles were recognized by electron microscopy in the hepatocytes beginning on the 4th day. The hepatocytes had many incomplete virus particles, 40 to 61 nm in diameter, and a few complete virus particles, 40 nm in diameter, in the cisternae of the rough and smooth endoplasmic reticula. Such particles and the endoplasmic reticulum showed reaction products for duck hepatitis B virus by immunoelectron microscopy. There were clusters of core particles, 27 nm in diameter, in the hyaloplasm around peroxisomes where an assembly of cores appeared to occur. No conspicuous virus particles were recognized in the biliary epithelial cells. The similarities and differences in virus localization between duck hepatitis B virus and hepatitis B virus are discussed.
An attempt was made to infect primary duck hepatocyte cultures with duck hepatitis B virus in vitro in order to clarify the biology of hepatitis B virus. Livers of ducklings, 0 to 17 days posthatch, without viremia were digested ex situ by perfusion of collagenase solution through the portal or hepatic vein. Homogeneous hepatocyte suspensions were seeded into plastic dishes in L-15 medium containing 10(-8) M insulin, 2 X 10(-8) M glucagon and 10(-8) M dexamethasone and were subsequently inoculated with sufficient numbers of duck hepatitis B virus. As a result, duck hepatitis B virus multiplication started weakly on Day 2, gradually increased and reached the maximum level approximately on Day 10 postinoculation. Viral replication was revealed by duck hepatitis B virus DNA in the cell pellet and in the culture medium and duck hepatitis B virus DNA-specific transcripts in the cell pellet. Immunostaining demonstrated duck hepatitis B virus core antigen in approximately 10% of cultured hepatocytes, and an increase in numbers of positive cells was not observed with time for up to 18 days of culture. Viral particles were found within the endoplasmic reticulum, and the inoculation of culture medium provoked viremia in the ducklings. The age of ducklings did not influence the numbers of cells infected. The in vitro infection system was similar to the in vivo one; however, the former seemed to be age-independent and to allow replication of duck hepatitis B virus in the limited number of hepatocytes.
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Absorption, distribution, metabolism and excretion of [125I]-rhIL-11 (recombinant human interleukin-11) after subcutaneous administration in rats were investigated. After a single administration, the concentration of radioactivity in the tissues was 2-6-fold higher in the liver and kidneys, and slightly higher in the gastrointestinal tract as compared to the plasma concentration. However, since the concentration in the other tissues was lower than the plasma concentration, the transport of rhIL-11 into tissues appeared to be low. Tissue radioactivity rapidly diminished, thus accumulation of rhIL-11 in tissues was thought to be low. Excretion of radioactivity into urine and feces was almost complete 72 h after administration, with 88.5% of the dosed radioactivity being found in urine and 7.9% in feces. When [125I]-rhIL-11 was administered to bile-duct cannulated rats, 44.4% of the dosed radioactivity was excreted into bile up to 48 h after administration. Most radioactivity in bile and urine was found in the TCA supernatant and low molecular weight fraction by HPLC analysis, indicating that rhIL-11 was eliminated from the body by metabolism.
Placental transfer and excretion into milk of [125I]-rhIL-11 (recombinant human interleukin-11) after subcutaneous administration in female rats were investigated. After administration of [125I]-rhIL-11 to rats on the 14th day of gestation, radioactivity in the kidney was the highest among excised tissues, being 3 times higher than that in the plasma at 1.5 h. Radioactivity in other tissues, including the mammary gland, ovary, uterus, placenta and amniotic fluid, was lower than that in the plasma. Although radioactivity in fetuses was detected 6 h after administration, the level was only 2% of the plasma concentration in dams, and the radioactivity was not found in fetal-derived TCA precipitates. These results indicate that rhIL-11 does not readily pass through the placenta into the fetus. After subcutaneous administration of [125I]-rhIL-11 to lactating rats 14 days after delivery, radioactivity in milk was 1.1-1.6 times that in the plasma of dams. Radioactivity in clotted milk in the stomachs of suckling infants was almost equal to that in the dam's milk; however, only a small amount of radioactivity was detected in infant kidneys.
A 93-year-old patient with hypoplastic acute monocytic leukemia (AMoL) achieved a complete remission after macrophage colony-stimulating factor (M-CSF) therapy. Initially, the patient was treated with a low dose of cytarabine, but this treatment proved ineffective. M-CSF was administered for 14 days by drip intravenous infusion, 800 x 10(4) units per day. After a gradual decrease in the number of leukemic cells, a rapid increase in neutrophils was observed in the peripheral blood, and a bone marrow examination 22 days after discontinuation of M-CSF medication revealed a complete remission. These findings suggest that M-CSF may be useful in treating some elderly patients who have hypoplastic AMoL.
Morphometric analysis was performed after histochemical staining on 12 biopsied muscles of the affected limbs from 12 patients with arthrogryposis multiplex congenita. Except for one muscle, samples demonstrated variation in fiber size associated with abnormal fiber type distribution suggesting abnormal innervation: large groups of atrophic fibers in one muscle, either type 1 or 2 fiber predominance with occasional fiber type grouping in five, a complete lack of type 2 fibers in one, type one fiber atrophy in one, both type 2A and 2B fiber atrophy in two, and increased number of type 2C fibers in four. In most patients with arthrogryposis multiplex congenita, a defect in neural influence on the developing muscles may be responsible for the absence or maldevelopment of some muscle groups. Underdeveloped muscles are then assumed to induce imbalance of agonists and antagonists resulting in permanent contractures.
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Tau protein kinases (TPK) I and II were isolated as candidate enzymes responsible for the hyperphosphorylation observed in PHF-tau. Four phosphorylation sites of tau were identified for each kinase, accounting for most, but not all, of the major phosphorylation sites of PHF-tau. Immunostaining with anti-TPKI antibody indicated that this kinase is up-regulated in AD brain. Such up-regulation of TPKI and phosphorylatioin of tau were reproduced by treating cultured hippocampal cells with amyloid beta (Abeta) protein. In addition, we found that TPKI can phosphorylate and inactivate pyruvate dehydrogenase (PDH), which is expected to result in depletion of acetyl-CoA, a key substrate of acetyl choline synthesis. Indeed, when septum cells were treated with Abeta, the level of acetyl choline decreased dramatically.
It has been suggested that progressive pathophysiologic modifications of endothelium are associated with aging. Aging has been shown to influence some specific functions at the cellular level. In the present study, the effects of aging on levels of prostacyclin (PGI2) production were examined in cultured rat aortic endothelial cells from young (six-week-old) and old (100-week-old) Wistar rats. The level of PGI2 production from rat aortic endothelial cells decreased significantly with increasing age, suggesting decreased function of the endothelial cells. The production of PGI2 stimulated by thrombin was decreased in old rat aortic endothelial cells compared to young rat aortic endothelial cells, whereas there was no difference in the rate of intracellular calcium mobilization caused by thrombin. These data indicate that aging nonuniformly affects both basal and agonist-induced levels of PGI2 production in rat aortic endothelial cells, and that this diminution in PGI2 production may be related to the age-related potentiation of various thrombotic events.