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Biomedical subjects

R Inoue

Publications and source records attributed to R Inoue.

At least 235 records · Page 13Linked to original sources
PubMed1987

The risk of a second primary cancer occurring in five-year survivors of an initial cancer.

Patients with a greater than five-year survival diagnosed with cancer of the stomach, colon, breast and uterus (included in situ) at the Kanagawa Cancer Center from 1963 to 1980 were studied for multiple primary cancers. They were followed up to December 31, 1985, for the occurrence of second primary cancers by means of a record linkage to the population-based cancer registry in Kanagawa Prefecture. The occurrence rate of total second primary cancers was 2.6% (76/2,977). Among the first primary cancer sites, the rate for cancer of the colon was highest: 5.3% (5/94), and the rate for women with cancer of the uterus lowest: 1.4% (16/1,146). The number of observed second primary cancers was compared with the expected number, which was calculated by the person-years method, to obtain an estimate of the risk. The relative risks (RR: observed: expected value) of women with cancer of the breast were significantly high for developing cancer of the colon (RR, 3.7), cancer of the opposite breast (RR, 3.9) and cancer of the ovary (RR, 5.8). Men with cancer of the stomach had a significant risk of developing cancer of the colon (RR, 3.3). It may be considered, at least in part, that some cancer patients, especially those with cancer of the breast, have a high risk of a second primary cancer occurring. These results may provide clues and information to the etiology of predisposition to and prevention of cancer.

Adult↗
PubMed1986

OKM1-positive T-cell leukemias. Relationships among morphologic features, phenotype, and functional activities.

The morphologic features, phenotype, and functions of OKM1+ leukemic T-cells were studied. The leukemic T-cells in two patients with chronic lymphocytic leukemia (CLL) had specific features of large granular lymphocytes (LGL), and those in two patients with acute lymphocytic leukemia (ALL) had L2 morphologic characteristics. The phenotype of the leukemic cells from one patient with CLL was OKM1+, ER+, OKT3+, OKT4+, OKT8-, OKIa1-, IgGFc receptor (EA gamma)+, Leu-7+, Leu-11b+, and anti-Tac-. The cells had antibody-dependent cell-mediated cytotoxicity (ADCC), but no natural killer (NK) activity. They had a definitive helper effect on pokeweed mitogen-induced normal B-cell differentiation. The leukemic cells from the other patient with CLL were Leu-7-, and Leu-11b-, and lacked both ADCC and NK activity. The leukemic cells in the two patients with ALL were ER+, OKM1+, Leu-7-, and Leu-11-, and did not have any cytotoxicity. One was EA gamma +, and the other was EA gamma -. These findings suggest that OKM1+ leukemic T-cells consist of at least two subgroups: (1) T-cells with the morphologic features of LGL; and (2) those with a lymphoblastic morphologic type. In either case, the phenotype is novel and suggests the emergence of a small, distinct lymphocyte subset.

Acid Phosphatase↗
PubMed1986

Actions of quinidine and apamin on after-hyperpolarization of the spike in circular smooth muscle cells of the guinea-pig ileum.

The effects of quinine and quinidine on membrane potential and action potential were investigated in circular smooth muscle of the guinea-pig ileum and the findings compared with the actions of apamin. In addition to results obtained from microelectrode experiments, the actions of quinidine and apamin on membrane currents were assessed using the single cell voltage clamp method. Quinine (above 0.2 mmol/l) and quinidine (above 0.08 mmol/l) depolarized the membrane, increased the membrane resistance and blocked generation of the after-hyperpolarization of the spike. Higher concentrations of both agents reduced the amplitude of the action potential and further depolarized the membrane. Quinidine and quinine possessed much the same action, with the former being more potent than the latter. Apamin, an inhibitor of the Ca-dependent K current, did not inhibit the after-hyperpolarization of the spike and had no effect on the membrane potential. In voltage clamp experiments, a depolarizing pulse (above -30 mV from -60 mV; 200 ms duration) elicited an inward current, followed by an outward current. With application of 2.5 mmol/l Mn instead of Ca, the outward current was subclassified into the Mn sensitive (Ca-dependent) and Mn resistant (voltage-dependent) K currents. Apamin (0.1 mumol/l) did not modify membrane currents evoked in the circular muscle cell, while, 0.1 mmol/l quinidine inhibited both the Ca- and voltage-dependent K outward currents, and Ca inward current. Our observation suggest that apamin-insensitive Ca-dependent K channels are present in the smooth muscle membrane and that they probably participate in the falling phase and after-hyperpolarization of the action potential.

Action Potentials↗
PubMed1986

A newly identified Ca2+ dependent K+ channel in the smooth muscle membrane of single cells dispersed from the rabbit portal vein.

We found a new type of Ca2+-dependent K+ channel in smooth muscle cell membranes of single cells of the rabbit portal vein. A slope conductance of the current was 180 pS when 142 mM K+ solution was exposed to both sides of the membrane (this channel was named the KM channel, in comparison to the known KL and KS channels from the same membrane patch; Inoue et al. 1985). This KM channel was less sensitive to the cytoplasmic Ca2+ concentration, [Ca2+]i, but was sensitive to the extracellular Ca2+, [Ca2+]o, e. g. in the outside-out membrane patch, lowering the [Ca2+]o in the bath markedly reduced the open probability of this channel, and also in cell-attached configuration, lowering of the [Ca2+]o using the internally perfused patch clamp electrode device reduced the opening of KM channel. TEA+ (1-10 mM) reduced the amplitude of the elementary current through the KM channel applied from each side of the membrane, but this agent inhibited the KM channel to a greater extent when applied to the inner than to the outer surface of the membrane. Furthermore, this KM channel had a weak voltage dependency, and the open probability of the channel remained much the same within a wide range of potential (from -60 mV to +60 mV). Whereas most Ca2+-dependent K+ channels are regulated mainly by [Ca2+]i and possess a voltage dependency, these properties of the KM channel differed from other Ca2+-dependent K+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The stabilization of vascular smooth muscle by procaine.

Procaine acts on the cell membrane as a depolarizing agent. It inhibits K-conductance; as a consequence, the membrane is depolarized and the spike potential is readily generated by outward current pulses. This inhibition of the K-conductance of membrane induced by procaine is discussed in relation to the K channel classified by the patch clamp procedure. The authors' observations indicate that procaine acts as a stimulant rather than as a stabilizer of the membrane. Furthermore, procaine inhibits the release of Ca from the store site, with no effect on the contractile protein. This local anaesthetic agent acts not only on the surface membrane but also on the internal membrane, the sarcoplasmic reticulum. Procaine reduces mechanical activity and stabilization of vascular smooth muscles occurs.

Animals↗
PubMed1986

Leu 11+ T gamma cell chronic lymphocytic leukemia with partially activated natural killer function and its further activation by recombinant IL2 in vitro.

A patient with T gamma cell chronic lymphocytic leukemia with the Leu 11+ phenotype and novel function of activated natural killer cells is reported. The peripheral blood mononuclear cells of this patient showed large granular lymphocytes by May-Giemsa staining and lamellipodia by scanning electron micrography. Tests on reactivity with monoclonal antibodies showed that most cells were Leu 11+, OKT3-/Leu 1-, OKT4-, OKT8-, Leu 7-, OKM1-, and Tac-. Freshly collected cells lysed not only K562, which is highly sensitive to natural killer cells, but also Raji cells and Daudi cells, which are not. Leu 11+ cells were triggered by recombinant interleukin 2 (rIL2) to proliferate, produce gamma-interferon (gamma IFN), and show enhanced HLA-DR antigen expression, and 30% of the Leu 11+ cells became positive for IL2 receptor antigen (Tac). The spectrum of cytotoxic activity of these cells against target cells was extended by rIL2; after treatment with rIL2, the cells also lysed HeLa cells and even fresh cancer cells. This stimulation also increased the activities of acid phosphatase and tartrate-resistant acid phosphatase of the cells and resulted in the appearance of nonspecific esterase activity. The expanded cell population may represent a neoplasm, but these findings provide information on a novel differentiation stage of activated NK cells.

Aged↗
PubMed1986

Transcatheter partial splenic arterial embolization in patients with hypersplenism: a clinical evaluation as supporting therapy for hepatocellular carcinoma and liver cirrhosis.

Eleven cases with hypersplenism, one with liver cirrhosis and ten with hepatocellular carcinoma (HCC) associated with liver cirrhosis, underwent transcatheter partial splenic arterial embolization. In four of ten HCC cases, the spleen was accidentally infarcted during the procedure of transcatheter hepatic arterial embolization (TAE). The mean infarcted area of the spleen was 55.7%. An increase in the peripheral platelet count was particularly remarkable and continued over one year after the embolization. High fever and abdominal pain were observed in all cases. The fever was seen for 18.0 days and pain was noted for an average of 12.8 days after the embolization. Other adverse effects such as pleural effusion and ascites were transitorily observed. Splenic embolization is an effective supporting therapy for hypersplenism in patients with cirrhosis or HCC.

Adult↗
PubMed1985

Accelerated protein turnover in the skeletal muscle of dystrophic mice.

The excretion of 3-methylhistidine increased in the urine of dystrophic mice C57BL/6J. The content of 3-methylhistidine residue decreased in the muscle proteins of dystrophic mice, but not in other organs. Methylated proteins in the skeletal muscle, actin and myosin, were partially purified from the dystrophic and control muscles. The amount of 3-methylhistidine residue in unit weight of the actin and myosin preparations was normal in dystrophic muscle. These three facts indicate that the turnover rates of actin and myosin are increased in the muscle of the dystrophic mice.

Actins↗