PubMed Health⌕ Search

Biomedical subjects

M Higashihara

Publications and source records attributed to M Higashihara.

At least 91 records · Page 5Linked to original sources
PubMed1985

The platelet protein phosphorylation induced by a monoclonal antibody against human platelets (TP82).

In human platelets, a monoclonal anti-human platelet antibody (TP82) induced platelet aggregation and release of granules (i.e., serotonin, platelet factor 4, N-acetyl-beta-D-glucosaminidase). The release reaction occurred even in the absence of aggregation and was preceded by not only the protein phosphorylation, but the transient formation of endogenous diacylglycerol (DG). These results suggest that polyphosphoinositide breakdown plays an essential role in antibody-induced release of platelet granules.

Antibodies, Monoclonal↗
PubMed1985

The platelet activation induced by wheat germ agglutinin.

In human platelets, wheat germ agglutinin (WGA) induced serotonin release without cell agglutination. WGA induced the phosphorylation of both 40-kDa and 20-kDa proteins in a parallel manner, and at least, the phosphorylation of 40-kDa protein was preceded by transient formation of endogenous diacylglycerol (DG) accompanied by a decrease in phosphatidylinositol (PI). Both phosphorylation of these two proteins and serotonin release were inhibited by prior treatment of platelets with dibutyryl cyclic AMP, W-7, or TMB-8. These results suggest that both phosphatidylinositol turnover and Ca2+ mobilization play an essential role in WGA-induced platelet activation.

Aminoquinolines↗
PubMed1985

A novel leukocyte differentiation antigen: two monoclonal antibodies TM2 and TM3 define a 120-kd molecule present on neutrophils, monocytes, platelets, and activated lymphoblasts.

We produced two hybridomas by fusion of mouse myeloma cells with splenocytes from a mouse immunized with the THP-1 human monocytoid leukemia cell line. Two cloned hybridoma cell lines, designated as TM2 and TM3, were obtained. They secreted antibodies against a unique cell surface antigen expressed on all normal peripheral blood monocytes, neutrophilic granulocytes, platelets, and mitogen-induced lymphoblasts, some cells from patients with immature-type lymphoid leukemias. However, the antibodies reacted neither with large numbers of peripheral blood lymphocytes nor with red cells. Cross-blocking studies showed that these monoclonal antibodies recognized the same or a nearly positioned antigen epitope. Immunoprecipitation of THP-1 cell extract with TM2 or TM3 under reducing and nonreducing conditions yielded a specific band of mol wt equal to 120,000 daltons. This determinant appeared to be involved in granulocyte chemotaxis, since neutrophilic granulocytes exposed to TM2 or TM3 showed a significant decrease in chemotaxis toward endotoxin-activated serum. These two monoclonal antibodies did not affect O2- release or luminol-dependent chemiluminescence of neutrophils. Moreover, they did not alter platelet aggregation induced by thrombin. TM2 and TM3 will provide a new reagent in defining the linkage between lymphoid and myeloid differentiation and intermyeloid development.

Acute Disease↗
PubMed1985

A monoclonal anti-human platelet antibody: a new platelet aggregating substance.

A monoclonal anti-human platelet antibody, TP82, is described, which caused irreversible aggregation of platelets in association with the release of adenosine triphosphate or [14C] serotonin, and which inhibited ristocetin-induced agglutination. Immunofluorescence assay showed that the antibody binds to platelets, megakaryocytes, and common acute lymphoblastic leukemia cells. The antibody (IgG1) immunoprecipitated a polypeptide of 23,000 daltons with an isoelectric point of about 7.0. The aggregation induced by the purified antibody and/or F(ab')2 fragments occurred in platelet-rich plasma and with washed platelets, but not with formalin-fixed washed platelets. TP82-induced aggregation was completely inhibited by disodium ethylendiaminotetraacetate, diltiazem, W-7, PGE1, and several metabolic inhibitors. At a concentration of apyrase or CP/CPK, which inhibited adenosine 5-diphosphate-induced aggregation. TP82-induced aggregation was only partially affected. Thrombin was not required for the antibody-mediated effects, since two thrombin inhibitors failed to block the reaction. The antibody, at least at a high concentration, induced platelet aggregation by a mechanism almost independent of thromboxane A2 formation, since cyclooxygenase inhibitors had little inhibitory effect on aggregation. TP82 monoclonal antibody is a new platelet-aggregating substance that interacts with a low-molecular-weight binding site on the platelet membrane.

Adenosine Triphosphate↗
PubMed1984

Interaction of Solanum tuberosum agglutinin with human platelets.

Solanum tuberosum agglutinin (STA) binds to the surface of human platelets and leads to their agglutination. Lectin staining shows that 125I-STA most intensely labels a major platelet membrane glycoprotein identified as GPIIIa followed by GPIV . STA does not induce release reaction, TXB2 formation or platelet protein phosphorylation. Since STA-induced agglutination is independent of intracellular metabolism of platelets, STA may prove to be a useful tool to explore the clinical condition in which the composition of platelet membrane protein is altered.

Blood Platelets↗
PubMed1984

Purification and hemagglutinating properties of egg drop syndrome 1976 virus.

We purified three populations of virus particles, F7, F9 and F17, with buoyant densities of 1.34, 1.33 and 1.29 g/ml, respectively, in CsCl equilibrium density gradients from cultures of chick embryo liver cells infected with the H-162 strain of the virus of egg drop syndrome 1976. F9 particles were infectious complete virions and most F17 particles were empty particles. F7 particles were less infectious, and had little capacity of hemagglutination (HA). HA titers were the same at 4 degrees and 37 degrees C and maximal between pH 6.4 and 8.4 and ionic strength from 0.14 to 0.54 M of NaCl. HA titer was inversely proportional to erythrocyte concentration. Potassium periodate destroyed markedly the infectivity of the virus and partially its HA activity at 37 degrees C. HA activity was stable at 56 degrees C or lower temperatures and destroyed at 80 degrees C. Trypsin, alpha-chymotrypsin, papain, ficin and neuraminidase had no effect on HA activity. Alpha-chymotrypsin destroyed the receptor for the virus on chicken erythrocytes, whereas trypsin and neuraminidase did not affect the receptor.

Adenoviridae↗
PubMed1984

A case of tuberculous epididymitis associated with Addison's disease.

A 68-year-old man was admitted to the hospital because of loss of appetite, easy fatigability, and skin pigmentation. Physical examination revealed that the bilateral epididymides were enlarged and hard without tenderness. At 7 a.m., the basal cortisol level in the plasma was 22.4 ng/ml and ACTH 318 pg/ml. The clinical diagnosis was Addison's disease. Biopsy of the right epididymis revealed evidence of active tuberculosis. Hydrocortisone (18 mg/day) and anti-tuberculous drugs were administered, and the patient became well and regained his appetite in a week. In this case, laparotomy was not performed, but all clinical findings and the course indicated that adrenal tuberculosis was the most likely cause of Addison's disease. CT scanning of the adrenal region demonstrated large, bilateral, homogeneous, low density, and non-enhancing mass. This is the first report dealing with CT findings of Addison's disease with tuberculous epididymitis.

Addison Disease↗
PubMed1984

Protection by vaccination against bovine leukemia virus infection in sheep.

Four preparations were tested as potential vaccines to protect sheep against bovine leukemia virus (BLV) infection. Purified glycoprotein (gp) 51 and protein (p) 24 antigens from the virus and glutaraldehyde-fixed fetal lamb kidney (FLK) cells chronically infected with BLV or sheep fibroblasts transformed with BLV (SF-28 cells) were used to inoculate 12 sheep. Each vaccine was given 3 times 2 and 4 weeks apart to 3 sheep. Six sheep vaccinated with gp51 antigen or fixed FLK cells developed complement-fixing antibody against gp51; the titers ranged from 1:8 to 1:128 at the time of virus challenge exposure at postinoculation week 9. Although the 6 sheep inoculated with p24 antigen or fixed SF-28 cells developed antibody against the respective inoculum, none of these sheep had gp51 antibody at the time of challenge exposure. All 12 vaccinated and 2 control sheep were challenge exposed with BLV-infected lymphocytes, and cells from the sheep subsequently were tested for infection by syncytium assay. Sheep inoculated with gp51 antigen or FLK cells were protected, but sheep inoculated with p24 antigen or SF-28 cells became infected. The cytotoxic activity of lymphocytes from protected and nonprotected sheep was not different from that of normal sheep. Seemingly, purified gp51 antigen or fixed FLK cells were capable of preventing BLV infection in sheep. Humoral immune responses to gp51 appears to have an important role in protection against BLV infection, whereas cytotoxic activity of lymphocytes does not.

Animals↗