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Biomedical subjects

M Shoji

Publications and source records attributed to M Shoji.

At least 199 records · Page 11Linked to original sources
PubMed1994

The 14-3-3 protein as the antigen for lung cancer-associated human monoclonal antibody AE6F4.

Human monoclonal antibody (MAb) AE6F4, which had been shown potentially useful for the immunocytological detection of lung cancer cells in sputum, was characterized for its antigen(s). Of the three MAb-reacting materials found in A549 cells by the immunoblotting analysis, the cytoplasmic 31-kDa protein extractable with phosphate-buffered saline was evidenced as the most plausible antigen by its highest content and outstanding affinity to the MAb AE6F4-derivatized Sepharose 4B column. This 31-kDa protein was identified by the amino acid sequence analysis of the CNBr-cleaved fragment as the 14-3-3 family of proteins, the members of which are known to play important physiological roles such as in the regulation of neurotransmitter levels and intracellular signal transduction. The purified 14-3-3 protein from bovine brain showed a comparable MAb-reacting activity to that of the 31-kDa protein from A549 cells in the enzyme-linked immunosorbent assay (ELISA). The significant reactivity of bovine 14-3-3 protein by MAb AE6F4, shown by the cross inhibition of antibody binding to the coated 31-kDa antigen in ELISA as well as by the inhibition of immunostaining with lung cancer tissues, consistently demonstrated that the antigen(s) recognized by the MAb was involved in the 14-3-3 protein family. It was found that the expression of the 14-3-3 protein was significantly enhanced in lung cancer tissues compared with the neighboring normal part of the lung as examined by the immunoblotting method. These results implicated that some member(s) of the 14-3-3 protein family can be the tumor marker(s), providing a rational basis for the immunocytological diagnosis of lung cancer with this human MAb.

14-3-3 Proteins↗
PubMed1994

[A study of relationships among solvent inhalation, personality and expectancy; especially on affinity to hallucination, sensation seeking and neurotic tendency].

94 delinquents in two homes for resocialization were surveyed to elucidate the relationship among the status of volatile solvent inhalation, expectancy and personality. The subjects were classified into solvent-inhalation group and non-solvent-inhalation group, and the former was divided into solvent dependence group and abuse group according to DSM-III-R. Each group was given personality tests; general health questionnaire (GHQ), sensation seeking scale (SSS), the vividness of visual imagery (VVIQ), test of visual imagery control (TVIC) and Yatabe-Guilford test (YG). In addition we investigated expectancy and mental symptoms caused by inhalation in it. The results are summarized as follows; 1. Inhalation group scored higher on SSS than non-inhalation group. 2. Compared with abuse group, dependence group presented with 1) higher GHQ score meaning neurotic tendency; 2) higher TVIC score meaning imagery-control-ability; 3) a higher incidence of day-dream and hallucination, especially egosyntonic type; 4) higher expectancy of "enhancement of positive affection", "reduction of negative affection" and "hallucination seeking"; 5) lower expectancy of "association with friends". 3. Higher scored inhalers on TVIC showed visual hallucinations, especially egosyntonic type more frequently than lower ones. 4. Significant correlations were recognized between GHQ score and expectancy of "reduction of negative affection", and between lack of objectiveness score of YG subscale and "hallucination seeking" expectancy. These results suggested that 1) beginning of inhalation is associated with sensation seeking trait, 2) progression to solvent dependence is correlated with three expectancies, i.e., seeking egosyntonic hallucinations paralleling high imagery-control-ability and subjectivity, reducing negative affection paralleling neurotic tendency, and enhancing positive affection. According to the findings, indulgence to drug induced positive imagery led delinquents into splitting of personality. In their treatment we need to help them to integrate high imagery ability and sensation seeking for recovery.

Adolescent↗
PubMed1994

Different mechanisms of inhibition by alkyl-lysophospholipid and phorbol ester of granulocyte-macrophage colony-stimulating factor binding to human leukemic cell lines.

We investigated the effects of rac-1-O-octadecyl-2-O-methyl-glycero-3-phosphocholine (ET-18-OCH3) and 12-O-tetradecanoylphorbol-13-acetate (TPA) on granulocyte-macrophage colony-stimulating factor (GM-CSF) binding to human leukemic cell lines HL60, U937, KG-1, KG-1a, and K562. HL60, U937, and KG-1 exhibited the high-affinity receptors, but KG-1a and K562 revealed no demonstrable receptors. ET-18-OCH3 inhibited GM-CSF binding to HL60, U937, and KG-1 cells with a half-maximal inhibitory concentration of 16, 10, and 78 microM, respectively. ET-18-OCH3 at 10 microM reduced GM-CSF binding sites on HL60, U937, and KG-1, but had little effect on the dissociation constant (Kd). ET-18-OCH3 at 10 and 30 microM significantly (p < 0.01) decreased, in a dose-dependent manner, the total uptake, surface binding, and internalization of GM-CSF. The internalization of GM-CSF was more profoundly inhibited than its surface binding. TPA at 1 and 10 nM inhibited GM-CSF binding. Inhibition of GM-CSF binding by a combination of ET-18-OCH3 (10 microM) and TPA (1 or 10 nM) was less than additive, and ET-18-OCH3 partially inhibited TPA-induced protein kinase C (PKC) depletion in the cytosol and translocation to the particulate fractions. It is suggested that the inhibition of GM-CSF binding by ET-18-OCH3 is due in part to disruption of the plasma membrane and that the inhibition of GM-CSF binding by TPA is due to activation of PKC.

Antineoplastic Agents↗
PubMed1993

Human and baboon integrin beta 5 subunit-encoding mRNAs have alternative polyadenylation sites.

A cDNA probe, encoding part of the human integrin polypeptide, GPIIIa (beta 3), was used to screen a cDNA library derived from baboon smooth muscle polyadenylated mRNA. One cross-hybridizing clone, lacking the baboon equivalent of 478 bp of the human sequence, was found to be 98% similar to a human cDNA encoding the beta 5-chain of the receptor for vitronectin, a cell adhesion molecule. The baboon mRNA terminates at 3' position 212 nucleotides upstream from the polyadenylation site of the aligned human mRNA.

Amino Acid Sequence↗
PubMed1993

Production of amyloid beta protein from normal amyloid beta-protein precursor (beta APP) and the mutated beta APPS linked to familial Alzheimer's disease.

The approximately 4 kD (39-43 amino acid) polypeptide (amyloid beta protein, A beta) deposited as amyloid in Alzheimer's disease (AD) is derived from a set of 695-770 residue precursor proteins collectively referred to as the amyloid beta-protein precursor (beta APP). Using immunoblotting techniques, metabolic labeling, and sequencing we have analyzed beta APP derivatives in medium conditioned by: (1) human mononuclear leukemic (K562) cells expressing a model beta AP-bearing carboxyl-terminal beta APP derivative (2) human neuroblastoma (M17) cells transfected with constructs expressing full length beta APP and (3) M17 cells expressing only endogenous beta APP. In each case, we observed the release of a approximately 4 kD beta APP derivative essentially identical to the A beta found in AD amyloid. A similar, if not identical, beta APP fragment was readily detected in CSF from both Alzheimer's disease patients and controls. These observations indicate that the A beta is produced and released by normal processing of the beta APP. To determine if the production of A beta or A beta-tearing COOH-terminal beta APP derivatives is altered in cells expressing the mutant beta APPs linked to familial AD, we have compared M17 cells expressing wild type beta APP with those expressing mutant beta APPs (beta APP delta I or beta APP delta NL). After continuous metabolic labeling for 8 hours, cells expressing the beta APP delta NL mutant showed a 5-fold increase in the relative amount of an approximately 11.4 kD A beta-bearing carboxyl-terminal beta APP derivative, and they released 6-fold more 4 kD A beta into the medium. These observations provide strong evidence that: (1) the pathway producing A beta in cultured cells is highly relevant to AD and (2) the beta APP delta NL mutant causes AD because its processing is altered in a way that releases increased amounts of A beta.

Alzheimer Disease↗
PubMed1993

Central effects of interleukin-1 on blood pressure, thermogenesis, and the release of vasopressin, ACTH, and atrial natriuretic peptide.

To assess the central role of interleukin 1-beta (IL-1 beta) in the release of ACTH, vasopressin (AVP) and atrial natriuretic peptide (ANP) and in the regulation of blood pressure and thermogenesis, 3 ng (0.173 pM) x 100-1 x BW-1 (LIL), 30 ng (1.73 pM) x 100g-1 x BW-1 (MIL), and 150 ng (8.63 pM) x 100g-1 x BW-1 (HIL) of human IL-1 beta dissolved in sterile saline were injected intracerebroventricularly to conscious rats. In the control rats, saline alone (5 microliters) was administered. In three other groups, rats were pretreated with indomethacin, a cyclooxygenase inhibitor, given i.v. (1 mg x 100g-1 x BW-1); medium and high doses of IL-1 beta or its vehicle were given. In the LIL group, IL-1 beta increased blood pressure, body temperature and plasma AVP and ANP without any changes in heart rate (HR) and plasma ACTH. In the MIL group, plasma ACTH was increased, and changes in the other parameters were similar to those in the LIL group. In the HIL group, however, the pressor and thermogenetic responses were attenuated; plasma AVP, ACTH, and ANP were increased; and HR was unchanged. In the control (CON) group, none of these parameters was changed throughout the studies. Indomethacin abolished the AVP and ACTH responses to IL-1 beta, but potentiated the pressor and hypothermic responses and increased plasma ANP. These data suggest that the actions of IL-1 beta on AVP and ACTH release and thermogenesis, but not on blood pressure and the release of ANP, are modulated by the stimulated central production of prostaglandins.

Adrenocorticotropic Hormone↗
PubMed1993

Characterization of a cDNA encoding the beta-chain of baboon receptor glycoprotein GPIb.

A cDNA probe, encoding part of the baboon integrin polypeptide, GPIIb, was used to screen a cDNA library derived from baboon platelet polyadenylated mRNA. One cross-hybridizing clone was found to be 94% similar to a human cDNA encoding the beta-chain of the receptor for von Willebrand factor, a major component of the platelet-subendothelium attachment mechanism.

Amino Acid Sequence↗
PubMed1993

Amyloid beta protein precursor accumulates in swollen neurites throughout rat brain with aging.

We immunocytochemically studied the expression of amyloid beta protein precursor (APP) in the brains of normal aged rats, and found APP accumulation in swollen neurites, most of which were axons. These swollen neurites appeared throughout the central nervous system of aged rats; most of them were negative for neurofilament, ubiquitin, and tau. Such widely distributed APP accumulation in swollen neurites may reflect impaired fast axonal transport due to aging. APP immunostaining may be a good method to detect widely distributed age-related changes.

Aging↗
PubMed1993

Diagnostic significance of skin immunolabelling with antibody against native cerebral amyloid in Alzheimer's disease.

Skin taken from patients with Alzheimer's disease (AD) and control patient groups were immunolabelled using antisera against either purified native cerebral beta protein or synthetic beta peptide. Native amyloid antiserum frequently labelled vascular walls in AD skin but rarely in control skin. Semi-quantitative analysis of the positive vessels showed a significant difference between the two groups. Sweat glands and dermal nerves were labelled in both groups. However, synthetic beta peptide antiserum showed no significant difference. Vascular wall labelling in skin with native amyloid antiserum is useful in the differential diagnosis of AD.

Aged↗
PubMed1993

Structure-function relationships of alkyl-lysophospholipid analogs in selective antitumor activity.

This investigation was initiated in order to delineate the structure-function relationship of the anticancer alkyl-lysophospholipids and assess their degree of selective cytotoxicity toward neoplastic cells. A series of glycerol phosphocholine analogs with varying substitutions in the sn-1 and sn-2 position were tested for their inhibitory activity as measured by thymidine incorporation, clonogenic assays and effects on protein kinase C activity against a series of human leukemic cell lines and healthy bone marrow progenitor cells. The IC50 was determined for each of the compounds in each cell line and healthy bone marrow cells following a 4-h incubation. The data indicated that a 16-18 carbon chain at the sn-1 coupled with a short substitution at sn-2 had the broadest antitumor activity and was the least toxic to normal bone marrow cells. The results provide a number of useful leads toward the design and development of potentially more active phospholipid compounds.

Antineoplastic Agents↗
PubMed1993

Differential expression of alpha 1-antichymotrypsin in the aged human brain.

The localization of alpha 1-antichymotrypsin (ACT) mRNA and ACT immunoreactivity (ACT-IR) were examined in 12 brains obtained at post-mortem from elderly patients, four of whom had Alzheimer's disease. A biotinylated oligonucleotide probe was used for in situ hybridization histochemistry and the relationship between the expression of both ACT mRNA and ACT-IR and the extent of beta protein or tau deposition were investigated. The extent of beta-plaques, tau-tangles, and ACT-IR were rated from (-) to (++). In brains without plaques and tangles, there were no detectable ACT mRNA signals in the gray matter, and those in the white matter were weak; in these brains, ACT-IR was generally weak. The brains with beta-plaques but no tangles showed weak ACT mRNA expression in astrocytes of both the gray and white matter; they also showed weak ACT-IR in the astrocytes. In the brains from patients with Alzheimer's disease with both plaques and tangles, ACT mRNA was expressed intensely in a majority of the astrocytes in the white and gray matter. Some senile plaques-associated astrocytes expressed ACT mRNA and ACT-IR was strong in the white matter astrocytes. ACT-IR and ACT mRNA expression in astrocytes was correlated with the extent of beta and tau depositions.

Aged↗
PubMed1993

The roles of GABA in the central regulation of AVP and ANP release and blood pressure in hypertonic saline infusion and hemorrhage.

In order to assess the central effects of gamma-aminobutyric acid (GABA) on arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) release and cardiovascular function, the following two experiments (Exp) were carried out in conscious rats (n = 24). Experiment I: GABA (10 micrograms/kg.min) was intracerebroventricularly (i.c.v.) administered into conscious rats receiving an intravenous (i.v.) infusion of 2.5 M NaCl, and the vehicle alone was i.c.v. administered under i.v. 2.5 M NaCl in the control group. Experiment II: GABA (12 micrograms/kg.min) was infused i.c.v. in conscious rats during hemorrhage (1.6% of BW) and the vehicle alone was i.c.v. administered during hemorrhage in the control study. In Experiment I, plasma AVP and ANP and mean arterial blood pressure (MABP) increased in response to 2.5 M NaCl, but heart rate (HR) slightly decreased. I.C.V. GABA attenuated the AVP and ANP responses, but did not affect MABP and HR. In Experiment II, plasma AVP increased due to decreases in MABP induced by hemorrhage, but plasma ANP and HR never changed. I.C.V. GABA did not affect plasma AVP and ANP, MABP and HR. These results show that i.c.v. GABA has an inhibitory effect on AVP and ANP release in response to hypertonic NaCl, but not to hemorrhage, but never affected hypertonic NaCl-induced increases in blood pressure.

Animals↗
PubMed1993

Effects of intraduodenal administration of "kyushin," a senso (toad venom)-containing drug, on systemic hemodynamics, cardiacfunction and myocardial oxygen consumption in anesthetized dogs.

The effects of "Kyushin" (KY), a Senso (toad venom)-containing drug, on the cardiovascular system were examined by intraduodenal administration of KY in anesthetized open-chest dogs. KY (3 or 10 mg/kg) dose-dependently increased the peak positive first derivative of left ventricular pressure ((+)LVdP/dt) and mean aortic pressure, and decreased the left ventricular end-diastolic pressure (LVEDP). Myocardial oxygen consumption (MVO2) and heart rate (HR) were not significantly influenced by KY. KY produced a cardiotonic effect without any increase in MVO2, because the increase in MVO2 due to the cardiotonic effect of KY may have been cancelled by a decrease in MVO2 due to reduction of preload and the lack of increase in HR. In order to clarify the relationship between the cardiovascular effects of KY and the drug concentration in plasma, the concentration of anti-bufalin IgG reactive substance (BRS) in plasma was measured by enzyme immunoassay. The maximum BRS concentrations 20 min after administration of 3 and 10 mg/kg KY were dose-dependent. From the relationship between changes in (+)LVdP/dt and changes in BRS concentration after administration of KY, it is inferred that the effective concentration of BRS in plasma at which KY produces a cardiotonic effect in dogs is approximately 2-3 ng/ml.

Anesthesia↗
PubMed1993

Pharmacological actions of "kyushin," a drug containing toad venom(2): effects on urinary volume and electrolyte excretion.

A study was conducted on the pharmacological actions of the toad venom-containing drug "Kyushin" (KY-2 and KY-R) on urinary volume and electrolytes excretion, regional blood flow, renal artery blood flow and carrageenin-induced hind-paw edema. In rabbits, KY-2 and KY-R significantly increased urinary volume after intravenous administration of 8 mg/kg. In guinea pigs, KY-2 and KY-R produced a significant increase in urinary volume after intraduodenal administration (i.d.) of 80 mg/kg. In guinea pigs treated with propranolol, KY-2 at 20 and 40 mg/kg p.o. and KY-R at 40 mg/kg p.o. increased urinary volume. At 40 mg/kg i.d. both KY-2 and KY-R produced an increase in regional blood flow, as determined by the hydrogen gas clearance method, of the brain areas including the amygdaloid nucleus, but did not affect regional blood flow in liver, kidney and skeletal muscle, or renal artery blood flow. In rats, carrageenin-induced hind-paw edema was inhibited by KY-2 or KY-R at 600 mg/kg p.o.

Animals↗
PubMed1993

Pharmacological actions of "kyushin," a drug containing toad venom (3): Effects on experimentally induced arrhythmia.

The pharmacological effects of the toad venom-containing drug "kyushin" on aconitine- and thyroxine-induced arrhythmia in guinea pigs, on the conduction system in Langendorff preparations of rabbit hearts and on the autonomic nervous system in cats were studied. "kyushin" significantly inhibited the aconitine-induced arrhythmia after intraduodenal administration (i.d.) with 80 mg/kg, and the thyroxine-induced arrhythmia with 40 mg/kg i.d. Although "kyushin" itself did not affect the conduction system with 30 mg/ml of the maximal concentration being able to be prepared, bufalin and cinobufagin as constituents of toad venom produced inhibition with 0.3 mg/ml and 1 mg/ml, respectively. The decrease in heart rate induced by electrical stimulation to the parasympathetic nerve (vagus nerve) was potentiated by "kyushin" at 30 mg/kg i.d. The anti-arrhythmic effects of "kyushin" may be attributable to both possible inhibitory effect on the conduction system and potentiating effect on the parasympathetic nervous system.

Aconitine↗
PubMed1993

Effects of acute hypotensive hemorrhage on arginine vasopressin gene transcription in the rat brain.

To determine whether hypotensive hemorrhage has an effect on arginine vasopressin (AVP) gene expression, 16 ml/kg of arterial blood was drawn over 10 min in conscious unrestrained rats. Mean arterial blood pressure (MABP) and heart rate (HR) were measured, and the rats were decapitated before and 10 min, 1, 3, 6, 9, 12, and 24 h after the initiation of hemorrhage. The hypothalamic or cerebro-hypothalamic tissue was used to measure AVP mRNA by Northern blot analysis, and the trunk blood to measure plasma AVP, osmolality and hematocrit. Hemorrhage brought about rapid and transient decreases in MABP and HR accompanied by transient increases in plasma osmolality and AVP. Hematocrit decreased after the bleeding and reached a stable level 6 h after hemorrhage and thereafter. AVP mRNA was detected in the hypothalamus and not in the extrahypothalamic cerebral brain tissue under basal and posthemorrhage conditions. AVP mRNA in the cerebro-hypothalamic tissue increased by 1.8-fold at 6 h and 2.1-fold at 9 h after hemorrhage. These results indicate that AVP mRNA in the brain increases 6 h after increased AVP release in response to hypotensive hemorrhage.

Acute Disease↗
PubMed1993

Role of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion.

To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCl alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined. Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D-HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.

Animals↗