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Biomedical subjects

A Ito

Publications and source records attributed to A Ito.

At least 541 records · Page 30Linked to original sources
PubMed1993

Nephrotic syndrome with massive accumulation of type I and type III collagen in the glomeruli.

A 54-year-old woman with nephrotic syndrome underwent renal biopsy. By light microscopy, the glomerular capillary lumen was remarkably narrowed because of diffuse accumulation of Periodic acid Shiff (PAS) positive material along the glomerular capillary wall. By electron microscopy, collagenous fibers were observed in the mesangium and subendothelial area. The fibrous material reacted with antibodies against type I and III collagen but not with those against laminin or type IV collagen by an indirect immunofluorescence technique. This case seemed to be a case of collagenofibrotic glomerulonephropathy.

Collagen↗
PubMed1993

Human macrophage colony-stimulating factor induces the differentiation of trophoblast.

When human cytotrophoblastic cells in the early stage of pregnancy were cultured in a serum-free medium in the presence of human macrophage colony-stimulating factor (M-CSF), the cytotrophoblastic cells fused and formed a typical syncytiotrophoblast which had a dense distribution of microvilli revealed under an electron microscope. On the other hand, cytotrophoblasts incubated with anti-M-CSF antibody showed hardly any syncytiotrophoblast formation. Following this finding, we studied the differentiation of chorionic cells from the viewpoint of hormone secretion. When cytotrophoblasts were incubated in the presence of M-CSF, the supernatant of the culture showed an increase in human chorionic gonadotropin and human placental lactogen levels in proportion to the concentration of M-CSF added. When cytotrophoblasts were incubated in the presence of anti-M-CSF antibody or anti-fms antibody, human chorionic gonadotropin and human placental lactogen secretion were suppressed. Thus, M-CSF was morphologically and endocrinologically found to induce the differentiation of chorionic cells.

Cell Differentiation↗
PubMed1993

Differential serodiagnosis of alveolar and cystic hydatid disease in the People's Republic of China.

Western blot analysis was carried out using crude antigens of Echinococcus multilocularis and 33 serum samples from the People's Republic of China to differentiate patients with alveolar hydatid disease (AHD) with active lesions from those with inactive lesions, those with other parasitoses including cystic hydatid disease (CHD), and healthy persons. This analysis was based on the detection of antibody responses against two polypeptides, Em18 and Em16, which appeared to be species specific and good indices for the differentiation of AHD with active lesions from AHD with inactive lesions. Twenty-one of the 33 samples showed antibody responses against Em18 and/or Em16. Fifteen were antibody-positive for both Em18 and Em16, five were antibody-positive for Em18 only, and one was antibody-positive for Em16 only. Of the subjects from which the 33 samples were obtained, 12 patients had AHD with active lesions, two had AHD, but their lesions were resolved by surgical resections, 14 had CHD with active lesions, and five were apparently healthy people. Western blot analysis confirmed all 14 cases of AHD, three of the 14 cases of CHD, and showed that one of the five apparently healthy individuals had a positive serologic response for AHD. This apparently healthy person with a positive serologic response for AHD by Western blot analysis was found to be positive for the disease on re-examination. Thus, Western blot analysis based on the antibody responses against Em18 and Em16, especially against Em18, was extremely reliable for the detection of AHD with active lesions, although it failed to differentiate two of the 14 patients with CHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Possible involvement of c-kit receptor and its ligand in increase of mast cells in neurofibroma tissues.

Many mast cells are present in the tumor tissues of neurofibromatosis 1. We investigated the mechanism of the mast cell increase. Since the stem cell factor (SCF) induces development of mast cells and since the receptor of SCF is encoded by the c-kit gene, we examined the expression of SCF mRNA and c-kit mRNA in neurofibroma tissues. In situ hybridization demonstrated strong expression of c-kit messenger RNA in mast cells in the neurofibroma, but the expression of SCF mRNA was not demonstrable by in situ hybridization in either neurofibroma tissues or control normal skin tissues. When RNA extracted from neurofibroma tissues or normal skin tissues was reverse transcribed and then amplified by the polymerase chain reaction, the amount of SCF cDNA was greater in neurofibroma tissues than in normal skin tissues. The results suggest that SCF and the c-kit receptor are associated with the increase of mast cells in neurofibroma tissues.

Adolescent↗
PubMed1993

Expression of osteopontin messenger RNA by macrophages in atherosclerotic plaques. A possible association with calcification.

Calcification is a common complication in atherosclerosis. As osteopontin (OPN) and osteonectin (ON) are not only involved in the physiological but also the pathological calcification of tissues, we examined the expression of OPN and ON messenger (m)RNAs in normal and atherosclerotic human aortas. By Northern blotting, the OPN mRNA expression was related to the severity of the atherosclerosis. However, ON mRNA expression decreased with the development of atherosclerosis. By a combination of in situ hybridization and immunohistochemistry of serial sections, the macrophages surrounding the atheromatous plaques were identified as the OPN mRNA-expressing cells. The ON mRNA-expressing cells in aortas of a newborn baby and a 3-year-old boy were medial smooth muscle cells, but in aortas of adults, smooth muscle cells that had invaded the intima were found to express ON mRNA. As OPN mRNA-expressing macrophages surrounded the atheromatous plaques, and as the level of OPN mRNA expression increased as atherosclerosis advanced, it is possible that OPN plays a role in the calcification of atheromatous plaques.

Aged↗
PubMed1993

[The role for Helicobacter pylori infection in intractable and recurrent ulcer].

Patients with intractable peptic ulcer or recurrent peptic ulcer have high rate of Helicobacter pylori infection. To study the effect of H. pylori on the recurrence of peptic ulcer, we treated the patients, who had H. pylori infection, with antibiotics (amoxicillin, clarithromycin, fosfomycin). After one year, none of peptic ulcer patient in whom H. pylori was eradicated had a recurrence. Among patients who remained positive for H. pylori, the ulcer relapse rate was 61% (11 of 18). In patients who were successfully eradicated of H. pylori with antibiotics the rate of recurrence was reduced. Patients with both intractable peptic ulcer and H. pylori infection were treated with antibiotics. Eradication of H. pylori induced ulcer healing. These findings suggest an important role for H. pylori in intractable and recurrent peptic ulcer.

Aged↗
PubMed1993

[Evaluation of left ventricular early diastolic function by first pass radionuclide angiocardiography after dipyridamole infusion in patients with coronary artery disease--comparison with exercise test].

To evaluate the left ventricular early diastolic function after dipyridamole infusion or during exercise, the first pass radionuclide angiocardiography (FPRA) by a multicrystal gamma camera (SIM-400) was performed in 32 patients with coronary artery disease (CAD) and 14 normal subjects. Dipyridamole was administered intravenously (0.56 mg/kg in 4 min). The first third filling fraction (FF 1/3) and the first third mean filling rate (MFR 1/3) were calculated from the time-activity curve. FF 1/3 decreased and MFR 1/3 increased in both normal subjects and patients with CAD during exercise. After dipyridamole infusion, FF 1/3 and MFR 1/3 unchanged in normal subjects, in contrast, FF 1/3 and MFR 1/3 decreased in patients with CAD. Thus, dipyridamole infusion FPRA is more sensitive method to detect early diastolic dysfunction in patients with CAD than FPRA during exercise.

Aged↗
PubMed1992

252Cf relative biological effectiveness and inheritable effect of fission neutrons in mouse liver tumorigenesis.

To determine the relative biological effectiveness of 252Cf fission neutrons versus 60Co gamma-rays for inducing liver tumorigenesis, C57BL/6NCrj x C3H/NCrj F1, hereafter called B6C3F1, mice were irradiated once either with 252Cf or 60Co and the tumorigenicity of the two types of radiation was studied. Individual groups of B6C3F1 mice (about 30 mice/group) were irradiated once with 252Cf at doses of 0, 3, 6, 12.5, 50, and 200 cGy for males and 0, 12.5, 50, and 200 cGy for females or with 60Co at doses of 0, 12.5, 50, and 200 cGy for both sexes. The groups were observed for 13 months after irradiation. The incidence of hepatic tumors in nonirradiated controls was 3.8% in males and 3.2% in females. 252Cf irradiation increased the incidence dose dependently in males and females, but less efficiently in females. The mean number and size of hepatic tumors were well correlated with tumor incidence. In contrast, 60Co was less efficient at inducing tumors. The relative biological effectiveness of 252Cf compared to 60Co was quite high in the low-dose range. Overall, the average relative biological effectiveness of 252Cf versus 60Co was 15.2 in males and 2.5 in females. In another experiment, 7-week-old male C3H mice, which are known to be carriers of hepatic tumorinogens, and that were the fathers of the B6C3F1 mice, were irradiated with 0, 50, and 200 cGy of 252Cf, and 2 weeks later they were mated with nonirradiated female C57BL mice. The control mice had nonirradiated fathers. The incidence of hepatic tumors in the offspring of irradiated fathers was 43% in males and 1.7% in females, whereas in the offspring of control mice with nonirradiated fathers the incidence was 3.2% in males and 3.3% in females. The multiplicity of the hepatic tumors was similar to the tumor incidence. Thus our results indicated a strong hepatocarcinogenic potential for 252Cf neutrons compared to 60Co gamma-rays, and that the cancer-prone genetic trait activated by 252Cf irradiation was inherited by first-generation offspring, especially in males.

Animals↗
PubMed1992

Regulation of acetylcholine release in vivo from rat hippocampus by monoamines as revealed by novel column-switching HPLC with electrochemical detection.

To clarify monoaminergic regulation of acetylcholine (ACh) release in the rat hippocampus, the effects of administration of monoamines through a dialysis probe on extracellular ACh levels were examined using in vivo brain microdialysis combined with a novel column-switching HPLC system. Infusion of dopamine or 5-hydroxytryptamine, but not noradrenaline, increased ACh levels. The ACh levels also increased following infusion of apomorphine and 5-methoxy-N,N-dimethyltryptamine. These results demonstrate that hippocampal ACh release is regulated by dopamine and 5-hydroxytryptamine.

Acetylcholine↗
PubMed1992

Effects of interleukin-6 on the metabolism of connective tissue components in rheumatoid synovial fibroblasts.

OBJECTIVE: High levels of interleukin-6 (IL-6) have been found in the synovial fluid of patients with rheumatoid arthritis (RA). We undertook the present study to investigate the role of IL-6 in this disease. METHODS: We examined the effects of IL-6, in comparison with IL-1, on the biosynthesis of extracellular matrix macromolecules and of matrix-degrading proteinases in rheumatoid synovial fibroblasts. RESULTS: In rheumatoid synovial fibroblasts, IL-6 by itself enhanced the production of plasminogen activator, its inhibitor, and tissue inhibitor of metalloproteinases, whereas it did not modulate the biosynthesis of precursor of matrix metalloproteinase 1 (proMMP-1) (tissue collagenase), proMMP-3 (stromelysin), or connective tissue components. However, IL-1-induced production of proMMP-1 and proMMP-3 was preferentially augmented by IL-6. CONCLUSION: These results suggest that in RA, IL-6 may participate along with IL-1 in fine tuning of the catabolism of connective tissue components, by modulating the balance between connective tissue-degrading enzymes and their inhibitors.

Arthritis, Rheumatoid↗
PubMed1992

The carboxy-terminal 10 amino acid residues of cytochrome b5 are necessary for its targeting to the endoplasmic reticulum.

Cytochrome b5 is an integral membrane protein located on the outer surface of the endoplasmic reticulum (ER). This cytochrome is considered to be synthesized on free ribosomes and to be inserted post-translationally into the ER membrane, without participation of a signal recognition particle. To elucidate the signal responsible for targeting of cytochrome b5 to the ER membrane in vivo, DNAs encoding various derivatives of the cytochrome were constructed and introduced into cultured mammalian COS cells, and the subcellular distributions of the derivatives expressed in the cells were then analyzed. The deletion of more than 11 amino acid residues at the carboxy-terminal end of cytochrome b5 abolished the targeting and anchoring of the cytochrome to the ER membrane. Fusion proteins consisting of the carboxy-terminal 10 amino acid residues of cytochrome b5 and passenger proteins with the hydrophobic portion could be localized in the ER membrane. Thus, the last 10 amino acid residues of cytochrome b5 carry information necessary for the cytochrome to be targeted to the ER membrane.

Amino Acid Sequence↗
PubMed1992

Biochemical characterization of programmed cell death in NGF-deprived sympathetic neurons.

Young sympathetic neurons die when deprived of nerve growth factor (NGF). Under such circumstances, cell death is appropriate to the developing nervous system and requires RNA and protein synthesis. We have hypothesized the existence of an endogenous death program within neurons that is suppressed by trophic factors. The extent and timing of required changes in the synthetic events that comprise the death program are unknown. In an effort to characterize the biochemical events that mediate the death program further, we performed several experiments on embryonic rat sympathetic neurons in vitro. The death program was blocked with cycloheximide when total protein synthesis was inhibited > or = 80%. When protein synthesis was inhibited within 22 +/- 4 h of NGF deprivation, death was prevented in half the neurons. Hence, we define the commitment point for protein synthesis to be 22 +/- 4 h. Analogously, the commitment point for RNA synthesis was 26 +/- 4 h and that for NGF rescue, 24 +/- 4 h. We tested the ability of a wide variety of chemicals to interfere with the death program. Most compounds tested were unable to prevent neuronal death. Some treatments, however, did save NGF-deprived neurons and were subsequently characterized. These included ultraviolet light and agents that raise intracellular concentrations of cAMP. Finally, we looked for the neuronal expression in vitro and in vivo of genes that have been associated with programmed death in other cell types, including TRPM-2/SGP-2, polyubiquitin, TGF beta-1, c-fos, and c-myc. None of these genes showed significant activation associated with neuronal death.

Adenylate Kinase↗
PubMed1992

Characterization of nicotinic acetylcholine receptors on cultured bovine adrenal chromaffin cells using modified L-[3H]nicotine binding assay.

To characterize the properties of nicotinic acetylcholine receptors (nAChRs) in autonomic ganglia, we examined L-[3H]nicotine binding to membrane fraction prepared from cultured bovine adrenal chromaffin cells, using a modified filtration method. Binding of L-[3H]nicotine to non-treated glass fiber filters interfered with the detection of specific binding to the membrane fraction. Presoaking glass fiber filters in 3% or higher concentrations of polyethyleneimine (PEI) solution (sixty times higher than earlier used concentration) for at least 5 h could reduce the binding of L-[3H]nicotine to the filters to the background level. Specific L-[3H]nicotine binding to the membrane fraction was detected only when the membrane fraction was prepared in Ca(2+)-and Mg2+ (EDTA, EGTA and protease inhibitors were added) -free buffer. Specific binding of L-[3H]nicotine was saturable and reversible. Both computer program and Scatchard analysis revealed a single class of high affinity binding sites with an average Kd of 8.9 nM and a Bmax of 42.5 fmol/mg protein. The Hill coefficient was 0.98. In inhibition studies, both cholinergic agonists (carbachol and L-nicotine) and ganglionic agonists (lobeline and 1,1-dimethyl-4-phenylpiperazinium iodide) were much effective in inhibiting L-[3H]nicotine binding, whereas both neuromuscular blocking (alpha-bungarotoxin and d-tubocurarine) and ganglionic blocking agents were less effective. These results suggest that high affinity nicotinic binding sites on adrenal chromaffin cells are nAChRs of the ganglion-type, which have properties different from nAChRs on the neuromuscular junction but similar to nAChRs in the brain.

Animals↗