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Biomedical subjects

K Koike

Publications and source records attributed to K Koike.

At least 631 records · Page 35Linked to original sources
PubMed1989

[The effect of bilateral vagal blockade on respiration].

Although respiratory regulation has been extensively studied so far, the relation between the vagal nerves and respiratory reflex in man is still open to controversy. This paper describes the effect of bilateral vagal blockade on respiration. 1) Dyspnea due to unilateral bronchial occlusion. This type of dyspnea is caused by extreme depression of the intrabronchial pressure on the occluded side and is accompanied by a rapid increase in respiratory rate and a rapid decrease in tidal volume. This type of dyspnea is relieved by blockade of the ipsilateral cervical vagal nerve. 2) Animal experiments on bilateral lung transplantation, heart-lung transplantation and bilateral cervical vagal blockade. The respiratory changes induced by CO2 inhalation, low O2 inhalation, respiratory stimulant. Loss of blood or fever stimulation in the manipulated dogs were compared with those in normal controls. CO2 inhalation alone produced differences in the respiratory rates and tidal volumes between the two groups. The tidal volume increase under CO2 inhalation was suppressed by the inflation reflex but other afferent vagal nerves seemed to be closely associated with the increased respiratory rate. 3) Vagal nerve reflex in humans. Blockade of the bilateral cervical vagal nerves in an awake state resulted in irregular PETCO2 in cases that had been stable and sometimes produced a pattern of Cheyne-Stokes respiration. Inhalation of 5% CO2 restored the regular rhythm of respiration and enhanced the response to CO2. When subjected to bilateral vagal blockade in an awake state, the patient expressed an unbearbly uneasy dyspneic sensation as if he were pulled into a bottomless abyss. This was demonstrated by the unstable FRC level.

Animals↗
PubMed1989

[Pulmonary fibrosis after endotoxin-induced permeability edema].

To know the pathogenesis of the lung fibrosis after ARDS, we investigated the role of PMN-elastase after endotoxin-induced pulmonary edema in awake sheep with chronic lung lymph fistulas. The permeability of the pulmonary circulation increased 2 hours after endotoxin injection. Four hours after endotoxin injection, WBC migrated to the lung interstitium and the number of WBC in BALF increased. Endotoxin increased PMN-elastase in plasma and lymph whereas the level of alpha-1-protease inhibitor (alpha-1-PI) did not change. The activity of alpha-1-PI measured by trypsin inhibitory capacity was zero in the exudative phase. The level of PMN-elastase in lymph was significantly higher 1 week after endotoxin injection than baseline levels. Histologically, pulmonary fibrosis developed 1 week after endotoxin injection. These results suggest that inflammatory mediators released from PMN play an important part in progress to the fibrotic phase after ARDS.

Animals↗
PubMed1989

[A case of reexpansion pulmonary edema during thoracotomy].

A case of reexpansion pulmonary edema during thoracotomy is presented. A high edema fluid-plasma protein concentration ratio suggested an increase in pulmonary vascular permeability. A marked increase in the percentages of polymorphonuclear leukocytes (PMN) and high concentration of PMN-elastase in edema fluid suggested activated PMN-mediated vascular endothelial injury, which caused an increase in permeability. Edema fluid and plasma contained high concentrations of Thromboxane B2 and 6-keto-PGF1 alpha at the stage of increased permeability. This suggested these chemical mediators participated in the mechanisms of increased permeability in reexpansion pulmonary edema.

Adult↗
PubMed1988

Synergism of BSF-2/interleukin 6 and interleukin 3 on development of multipotential hemopoietic progenitors in serum-free culture.

We investigated the effects of B cell stimulatory factor 2/interleukin 6 (BSF-2/IL-6) on the development of murine hemopoietic progenitors using serum-containing culture and serum-free culture. In serum-containing culture, BSF-2 mainly supported multipotential blast cell colonies from spleen cells of normal and 5-fluorouracil (5-FU)-treated mice. In serum-free culture, no colony growth was seen in the presence of BSF-2. Addition of BSF-2 to the serum-free culture containing IL-3 resulted in a significant increase in the number of colonies formed from multipotential progenitors in spleen cells and bone marrow cells of 5-FU-treated mice, whereas no effects were seen on the number of single or oligolineage colonies formed by the spleen cells of normal mice. These results suggested that BSF-2 and IL-3 act synergistically on the multipotential progenitors but not on the maturer progenitors. When BSF-2 was added to a culture containing low concentrations of IL-3 (1 U/ml, 4 U/ml), which had little effect on colony formation, the number of total colonies formed by the spleen cells and bone marrow cells of 5-FU-treated mice increased significantly. The combination of BSF-2 and 40 U/ml of IL-3 resulted in a significant enlargement of GMM colonies. Thus, BSF-2 appears to enhance the sensitivity of multipotential hemopoietic progenitors to IL-3.

Animals↗
PubMed1988

Chondrodysplasia punctata with X;Y translocation.

We have studied a family in which the mother and her son were carriers of an X;Y translocation, der(X)t(X;Y) (p22.3;q11). The mother was of slightly short stature and had mildly short upper extremities. The son had epiphyseal punctate calcifications, mildly short extremities, a flattened nasal bridge, and mental retardation (chondrodysplasia punctata). The extra bands on the short arm of the X chromosome were identified as deriving from the long arm of the Y chromosome, using in situ hybridization with a Y-chromosome-specific DNA probe (pHY10). The chondrodysplasia punctata seen in our case may be associated with the abnormality of the distal short arm of the X chromosome caused by X;Y translocation.

Chondrodysplasia Punctata↗
PubMed1988

Possible involvement of lipoxygenase pathway of arachidonic acid in rat pituitary hormone release in vitro.

The roles of arachidonic acid (AA) and its lipoxygenase products in control of secretion of anterior pituitary hormones were studied in vitro using cultured cells. AA (10(-4)M) and 5-hydroxy-eicosatetraenoic acid (5HETE) (5 x 10(-6)M) significantly (p less than 0.05) stimulated the releases of LH, TSH, GH, PRL, ACTH and beta-endorphin (beta-E). Added leukotriene B4 (LTB4) (5 x 10(-6)M) also caused significant increases in the secretions of LH, GH, ACTH and beta-E. The other lipoxygenase metabolites tested, 12HETE, 15HETE, LTA4, LTC4 and LTD4, had no effect on the releases of anterior pituitary hormones. These results suggest that AA and 5-lipoxygenase metabolites may be involved in the control of the releases of anterior pituitary hormones.

Adrenocorticotropic Hormone↗
PubMed1988

Characterization of hepatitis B virus X gene: in vitro translation of mRNA from COS-1 cells transfected with the X gene.

To elucidate the biological role of the X region of HBV DNA, we constructed an expression plasmid pSV2HBx by inserting the StuI/BglII fragment of HBV DNA into the pSV2 vector. Although X region products were not identified in vivo in transfected COS-1 cells, transcripts were translated in vitro and a 17-k Da protein was immunoprecipitated with an antibody raised against a synthetic peptide corresponding to the carboxy terminus of the X region open reading frame. Among 68 HBV carrier sera tested, two were found to contain antibodies reactive to the in vitro translation product. These results suggest that the X region is a gene which can be actually expressed at some stage of HBV infection.

Animals↗
PubMed1988

Cytogenetic characterization of a T-cell line, ATN-1, derived from adult T-cell leukemia cells.

A T-cell line, ATN-1, was established by culturing peripheral blood mononuclear cells derived from a patient with adult T-cell leukemia/lymphoma (ATL/L). Identities of the patterns of chromosomal abnormalities, cell surface phenotypes, morphologic findings, rearrangement patterns of T-cell receptor beta chain gene, and an integration site of human T-cell leukemia virus I proviral genome indicated that ATN-1 was derived from original leukemic cells. Both ATN-1 and the original leukemic cells showed a variety of patterns of chromosomal abnormalities that include 3q-, 6q-, rearrangements involving 2q31, 7q11.2, 8q11, 8q24, 19p13.3, and also 14q11 and 14q32, where genes for the T-cell receptor alpha chain and the immunoglobulin heavy chain are located. Availability of a genuine ATL/L cell line with these chromosomal abnormalities may greatly facilitate the biologic analysis of ATL/L.

Antibodies, Monoclonal↗
PubMed1988

The selectivity of newly synthesized ergot derivatives to alpha 1- and alpha 2-adrenoceptors, D1- and D2-dopaminergic receptors, muscarinic acetylcholinoceptors and beta-adrenoceptors.

1. We tested affinities of newly synthesized ergot derivatives to alpha 1- and alpha 2-adrenoceptors, D1- and D2-dopamine receptors, muscarinic acetylcholinoceptors and beta-adrenoceptors using radioligand binding techniques. 2. BAM-1110 was alpha 2-selective, though its affinity to alpha 2-adrenoceptors was one tenth less than that of yohimbine. 3. BAM-1303, which was non-selective, had high affinity to alpha-adrenoceptors. The pKi-values for BAM-1303 was 10.11 against both [3H]prazosin (alpha 1-ligand) and [3H]rauwolscine (alpha 2-ligand). 4. New ergot derivatives were selective to D2-dopamine receptors. BAM-1125 and BAM-1303 had high selectivity to D2-receptors. 5. They had less affinity to muscarinic receptors and beta-adrenoceptors.

Animals↗
PubMed1988

Ca-entry blockers, verapamil and diltiazem, on alpha 1-adrenoceptors in thoracic aorta, renal artery and portal vein from rabbit.

1. Verapamil caused a parallel shift of the concentration-response curve for norepinephrine in rabbit thoracic aorta and the reduction in norepinephrine-induced maximum response with shifts of the concentration-response curve for norepinephrine in renal artery and portal vein. 2. Diltiazem was without any effects on the response of thoracic aorta to norepinephrine, while the responses of renal artery and portal vein to norepinephrine were inhibited noncompetitively by diltiazem. 3. Verapamil but not diltiazem diminished markedly dibenamine-induced inhibition of maximum response to norepinephrine in all the preparations used. 4. Specific bindings of [3H]prazosin to both the membrane fractions derived from thoracic aorta and renal artery were displaced concentration-dependently by verapamil and diltiazem, but the effective concentrations of diltiazem were more than those for Ca-entry blocking activity. 5. These results suggest that verapamil might antagonize norepinephrine at alpha 1-adrenoceptors and the effective concentration for Ca-entry blocking activity of diltiazem were less than those for the interaction of diltiazem with alpha 1-adrenoceptors.

Animals↗
PubMed1988

The effects of co-administration of selenium and cis-platin (CDDP) on CDDP-induced toxicity and antitumour activity.

The therapeutic antitumour activity and host toxicity of cis-platin (CDDP), which was administered with selenium (sodium selenite) was studied on the growth of a human yolk sac tumour grown in nude mice. Treatment consisted of CDDP single agent chemotherapy (3 weeks) or preliminary PVB combination chemotherapy (CDDP + vinblastine + bleomycin, 2 weeks). Selenium was co-administered from day 1 to 5 with each therapeutic regimen. The administration of CDDP alone caused significant reduction in tumour burden but at higher doses there was significant host toxicity. The co-administration of selenium together with CDDP (CDDP: selenium, molar ratio = 3.5:1) did not affect the anti-tumour activity of CDDP but it did cause a decrease of parameters of host toxicity including lethality, increasing the 50% lethal dose (LD50) from 9.3 mg kg-1 to 17.5 mg kg-1. The parameters of host toxicity which were altered by selenium co-administration were nephrotoxicity, myeloid suppression and weight loss. Our study suggested that selenium co-administration allows higher doses of CDDP with reduction of apparent toxicity, resulting in a higher therapeutic index and possibly indicating a potential increase in the utilization of CDDP in clinical cancer chemotherapy.

Animals↗
PubMed1988

Cloning and sequencing of cDNAs encoding alpha and beta subunits of human pyruvate dehydrogenase.

The cDNAs encoding fragments of the alpha and beta subunits (PDH alpha and PDH beta) of human pyruvate dehydrogenase (PDH, EC 1.2.4.1) were isolated from a HeLa cell cDNA library in the lambda gt11 expression vector by immunoscreening. Phage cDNA fragments were subsequently used to screen a human foreskin fibroblast cDNA library by colony hybridization. Nucleotide sequence analyses of the positive plasmid clones (pHPDA and pHPDB) revealed an insert of 1.36 kilobases (kb) for PDH alpha and one of 1.69 kb for PDH beta, respectively, allowing us to predict the complete amino acid sequences of the precursor and mature proteins of these two subunits. A putative leader sequence of 29 amino acid residues was identified in pHPDA, resulting in a precursor protein of 392 amino acid residues (Mr 43,414) and a mature protein of 363 residues (Mr 40,334). A similar leader sequence of 30 amino acid residues in pHPDB was also identified, resulting in a precursor protein of 359 amino acid residues (Mr 39,046) and a mature protein of 329 residues (Mr 35,911). The amino acid sequences of NH2-terminal regions of the two subunits of human PDH were highly homologous with those of mature porcine PDH. The amino acid sequences of phosphorylation sites determined in PDH alpha of bovine and porcine enzymes were also conserved in the human PDH alpha. Blot analysis of HeLa cell poly(A)+ RNA showed a single mRNA of 1.8 kb for PDH alpha and 1.7 kb for PDH beta, respectively. The precursor proteins of PDH alpha and PDH beta were detected by immunoprecipitation from an 35S-labeled cell-free translation system.

Amino Acid Sequence↗