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Biomedical subjects

T Yamamura

Publications and source records attributed to T Yamamura.

At least 343 records · Page 19Linked to original sources
PubMed1987

Subcortical vascular encephalopathy in a normotensive, young adult with premature baldness and spondylitis deformans. A clinicopathological study and review of the literature.

Progressive subcortical vascular encephalopathy (PSVE) usually occurs in elderly individuals, suffering from hypertension. We here describe a male, born of consanguineous parents, who first showed signs of PSVE at the age of 30. Despite the absence of hypertension or known metabolic causes, the degenerative cerebral vascular disease developed progressively. Several cases, surprisingly identical to the one reported here, were traced using Japanese medical records. They are clinically characterized by: early onset of PSVE (at age 25-30), absence of persistent hypertension, diffuse alopecia since youth, spondylitis deformans with early onset, often so severe as to necessitate surgery, and the possible existence of an autosomal recessive transmission. Cases with these features appear to constitute a distinct clinical entity, possibly a new form of premature aging syndrome.

Adult↗
PubMed1987

Lectin histochemistry of malignant fibrohistiocytic tumors.

The staining pattern by Ricinus communis agglutinin (RCA), a lectin used as a good marker for histiocytes, in 24 cases with malignant fibrous histiocytoma (MFH) was studied and compared with that of 12 cases of fibrosarcoma (FS). In 20 (83%) of 24 cases of MFH, varying degrees of RCA binding were observed, whereas only four (33%) of 12 cases of FS were positive. RCA-positive FS included three cases with infantile FS and one adult case with post-radiation FS. Eight adult patients with FS were entirely negative. This positivity rate of RCA binding in MFH was much higher than those of antisera against lysozyme, alpha-1-antitrypsin, and alpha-1-antichymotrypsin previously reported. Seven MFH patients with focal aggregation of RCA-positive benign-appearing (reactive) histiocytes died earlier than the other patients with only scattered RCA-positive histiocytes; 5-year survival rates were 32% and 69%, respectively (p less than 0.05). These findings suggest that RCA reactivity can be used as a potential diagnostic and prognostic marker for MFH.

Adult↗
PubMed1987

Recovery mechanisms from experimental allergic encephalomyelitis in rats: analyses by using encephalitogenic T cell line.

The recovery mechanism of acute experimental allergic encephalomyelitis (EAE) in Lewis rats was studied by using an encephalitogenic T cell line specific for myelin basic protein. Antigen-activated line cells were highly encephalitogenic, but unstimulated line cells were not encephalitogenic. The activated line cells returned to the unstimulated state in a few days in culture medium without antigen. This decline of proliferative and encephalitogenic activities of the activated line cells was also observed even if the activated line cells were continuously stimulated with the antigen. In addition, rats during the convalescent stage from acute EAE showed only mild clinical signs of EAE even by transfer of almost a lethal dose of activated line cells. Thus, self-limiting capacity of autoaggressive cells and attenuation of effector cell function during the convalescent stage seem to be involved in the recovery mechanism of EAE.

Acute Disease↗
PubMed1987

Morphological changes of intercellular junctions in the rat submandibular gland treated by long-term repeated administration of isoproterenol.

Long-term repeated administration of isoproterenol (IPR) 2 mg/100 g bw, once daily for ten days, resulted in morphological changes in the intercellular junctions of rat submandibular glands, which were investigated by means of the freeze-fracture technique. A significantly increased number of tight-junctional strands was present. These junctional strands extended much deeper toward the basal membrane than those in normal acinar cells. The basal frontier strands that branched from the networks of tight junctions were elongated and had either free-endings or terminal loops, which were more frequently observed in the IPR-treated acinar cells than in untreated acinar cells. Some of the strands of tight junctions were connected to small gap junctions. The diameters of gap junctions were not significantly different from those of control acinar cells. However, smooth areas devoid of particles were found intermingling with the usual packed particles in irregularly shaped small gap junctions. There was no significant difference between the desmosomes of IPR-treated and untreated acinar cells, in terms of either morphology or distribution. These changes in junctional morphology in the IPR-treated acinar cells resemble those seen in salivary glands during development, and in some experimental conditions including tumorous changes.

Animals↗
PubMed1987

[Gastrointestinal polyposis and hereditary large bowel cancer].

Hereditary large bowel cancer is roughly divided into the hereditary gastrointestinal polyposis (HGIP) that is including adenomatosis coli (AC), Peutz-Jeghers syndrome and juvenile polyposis, and non-polyposis familial large bowel cancer (NPF) which is including cancer family syndrome and its related conditions. In the HGIP, AC is most frequent and of highest risk of large bowel cancer, and epidemiological method of approach to patients has been well studied. NPF, however, has been insufficiently studied because of lacking of distinctive marker as seen in the polyposis in spite of that it may be actually present much more frequently than AC. In order to extract NPF from the general large bowel cancer group, the marker or criteria for it has been studied. The factors besides family history presently considered to be useful for detecting NPF are multiple cancers, proximal cancer, association of multiple adenoma and young (50 years or younger) onset of the disease.

Adenoma↗
PubMed1986

DM-20, a proteolipid apoprotein, is an encephalitogen of acute and relapsing autoimmune encephalomyelitis in mice.

Experimental allergic encephalomyelitis (EAE) was successfully induced in BALB/c mice with DM-20, a protein component of proteolipid apoprotein. DM-20 was separated by ion exchange column chromatography with CM-Trisacryl from proteolipid apoprotein obtained from bovine spinal cords. Its purity was ascertained by SDS-polyacrylamide gel electrophoresis, a dot immunobinding procedure, and amino acid analysis. Nine of 15 animals with a single injection of 100 micrograms of DM-20 and five of seven animals with a booster injection developed hind leg paralysis or axial rotatory movement 16 to 27 days after sensitization (mean 21.3 days). Five of the 14 animals relapsed 2 to 6 wk after the first attack. Histological examination revealed inflammatory lesion, with significant demyelination in the central nervous system. Antibody levels to DM-20 were not related to the clinical signs. Five of 11 BALB/c nude mice reconstituted with T cells developed similar clinical and pathologic signs. This DM-20-induced EAE in mice may provide a valuable model because it is similar to multiple sclerosis and because it can be induced in inbred mice in which immune mechanisms can be easily studied.

Acute Disease↗
PubMed1986

Immunohistochemical and ultrastructural studies on disseminated skin lesions of midline malignant reticulosis.

Midline malignant reticulosis (MMR), a disease included in the lethal midline granuloma, is histologically characterized by a mixture of lymphoid cells and atypical reticulum cells. Recent investigations of the nature of proliferating cells in MMR have suggested different conclusions, i.e., that the lesion is a true histiocytic, B- or T-cell. Two cases of MMR are presented, on which extensive laboratory studies were carried out. The results showed that the atypical reticulum cells were negative when stained immunohistochemically with monoclonal antibodies for T- or B-cells, diffusely stained by reactions for acid phosphatase and alpha-naphthyl acetate esterase, positively stained with human lysozyme and alpha-1-antitrypsin, and possess abundant cytoplasm containing primary lysosomes, polylysosomes and residual bodies. These findings indicate the true histiocytic nature of the proliferating cells in MMR.

Adult↗
PubMed1986

Effects of probucol on xanthomata regression in familial hypercholesterolemia.

Fifty-one patients with familial hypercholesterolemia were treated for 2 to 4 years with probucol, cholestyramine, clofibrate and compactin in various combinations. Mean baseline serum cholesterol was 359 +/- 10 mg/dl in the heterozygote, and 582 +/- 52 mg/dl in the homozygote patients. We found that a combination of probucol, cholestyramine and compactin decreased serum cholesterol to normal or near normal in most of the heterozygote patients. In 3 severely affected heterozygote and all 8 homozygote patients, adequate cholesterol reduction was only possible with plasmapheresis plus a hypolipidemic agent. Measurement of the Achilles tendon after 12 to 16 months of treatment showed that reductions in thickness occurred in all patients taking probucol, even in a single-drug regimen, in those undergoing plasmapheresis, especially if probucol was used and in those receiving a combination of cholestyramine and compactin. Probucol was most effective in patients who experienced the greatest decreases in high density lipoprotein (HDL) levels, whereas the cholestyramine-compactin combination worked without decreasing HDL concentrations. Combined clofibrate-cholestyramine therapy, by contrast, led to increased tendon thickness in all but 1 patient. It is believed that probucol exerts its positive effect on xanthomata regression by reducing the size of HDL particles, as was shown in this study. It has already been reported that smaller HDL particles are more active in reverse cholesterol transport. The direct peripheral action of probucol may have aided regression as well.

Achilles Tendon↗
PubMed1986

Cholecystokinin octapeptide-evoked [3H]acetylcholine release from guinea pig gallbladder.

Cholecystokinin-octapeptide (CCK-OP) produced a contractile response in isolated guinea pig gallbladder; the response consisted of scopolamine-sensitive and scopolamine-insensitive components, neither of which were affected by tetrodotoxin or hexamethonium. In the presence of tetrodotoxin, CCK-OP evoked [3H]acetylcholine (ACh) release from strips of gallbladder in a concentration-dependent manner. These results suggest that CCK-OP acts at two sites in the guinea pig gallbladder, viz. the smooth muscle cell and the postganglionic cholinergic nerve terminal.

Acetylcholine↗
PubMed1986

Comparison of apolipoprotein C-II-deficient triacylglycerol-rich lipoproteins and trioleoylglycerol/phosphatidylcholine-stabilized particles as substrates for lipoprotein lipase.

The effect of apolipoproteins C-II and C-III on the lipoprotein lipase-catalyzed hydrolysis of apolipoprotein C-II-deficient triacylglycerol-rich lipoproteins and particles of trioleoylglycerol stabilized with a phosphatidylcholine monolayer was investigated. For both triacylglycerol-rich lipoproteins and artificial lipid particles, maximal lipoprotein lipase activity occurred at a constant apolipoprotein C-II/phospholipid mol ratio of 2.0 X 10(-4) and was independent of particle size, indicating that the amount of apolipoprotein C-II bound to the surface of the substrate is important for enzyme activation. The effect of apolipoprotein C-II on lipoprotein lipase activity with apolipoprotein C-II-deficient lipoproteins as substrate was to decrease the apparent Michaelis constant (Kmapp) from 7.1 to 1.0 mM with minor changes on the apparent maximal velocity (Vmax) (22.2 mmol free fatty acid released/h per mg enzyme). In contrast, apolipoprotein C-II increased the apparent Vmax from 2.4 to 20.0 mmol free fatty acid/h per mg enzyme for the lipoprotein lipase-catalyzed hydrolysis of trioleoylglycerol/phospholipid particles with little change in Kmapp (1.0 mM). Addition of apolipoprotein C-II-deficient triacylglycerol-rich lipoproteins or high-density lipoproteins to trioleoylglycerol/phospholipid particles in the presence of apolipoprotein C-II inhibited lipoprotein lipase activity. Lipoprotein lipase activity was also inhibited by the addition of a large excess of lipid-free apolipoprotein C-III to the artificial particles. The decrease in lipoprotein lipase activity correlated with the amount of bound apolipoprotein C-II. We suggest that the reported discrepancies on the effect of apolipoproteins C-II and C-III on lipoprotein lipase catalysis is related to differences in substrates and to the amount of added apolipoproteins.

Apolipoprotein C-II↗
PubMed1986

Effects of cholecystokinin-octapeptide on the human gallbladder both in vivo and in vitro.

To determine the sites and mechanisms of action of cholecystokinin-octapeptide (CCK-OP) on the human gallbladder, effects of atropine sulfate on CCK-OP-evoked contractions were studied in both in vivo and in vitro experiments. In vivo studies performed by means of real time ultrasonography in six healthy volunteers showed remarkable contractions of the gallbladder after intramuscular injection of CCK-OP (0.07 microgram/kg), which was nearly abolished by premedication of atropine sulfate (0.015 mg/kg). Atropine sulfate (10(-6) M) slightly but significantly reduced CCK-OP (10(-11) M-3 X 10(-7) M) induced contractions and the dose-response curve for CCK-OP was shifted to the right of the muscle strips of the human gallbladders. It is suggested that CCK-OP acts mainly on cholinergic neurons in vivo. On the contrary, the most sensitive sites of action of CCK-OP might be smooth muscles rather than cholinergic neurons in vitro.

Adult↗
PubMed1986

Probucol prevents lipid storage in macrophages.

Effects of probucol on lipid storage in macrophages in vitro in the presence of acetylated low density lipoprotein (acetyl-LDL) were observed using macrophage-like cells (UE-12) established from a human histiocytic lymphoma cell line (U-937). Under ordinary light microscopy as well as under electron microscopy we found that probucol added to the medium, either in ethanolic solution or bound to LDL, markedly prevented the development of macrophages into foam cells. Microscale enzymatic assay of cholesterol also showed that the intracellular accumulation of esterified cholesterol caused by acetyl-LDL was markedly decreased by the addition of probucol. The concentration of probucol added to the medium was almost comparable to the plasma concentration of the drug usually obtained in patients under treatment with probucol. The possibility that probucol interferes with the binding of acetyl-LDL to the receptors on the cell surface was suggested. The results of the present investigation coincide with the clinical findings that probucol causes a more marked regression of xanthomas than would be expected from the extent of lowering of LDL cholesterol.

Cell Line↗