Molecular aspects of atrial natriuretic peptides.
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Amino Acid Sequence↗
Biomedical subjects
T Imamura
Publications and source records attributed to T Imamura.
Sinoatrial block induced by oral diltiazem.
A 58-year-old man with variant angina who had no history suggestive of sinus node dysfunction experienced palpitation with pulse deficit after 8 days of diltiazem treatment, 240 mg per day. Electrocardiogram (ECG) revealed frequent occurrence of sinoatrial block. After discontinuation of diltiazem, an ambulatory ECG demonstrated gradual reduction of the occurrence of sinoatrial block, and no recurrence 8 hours after the last dose of the drug. One should note that diltiazem induces not only sinus node suppression and atrioventricular conduction disturbance, but also sinoatrial block.
Administration, Oral↗
Recurrent myocardial infarction and unexpected sudden death in a case of d-loop d-transposition of the great arteries associated with single coronary artery.
A 40-year-old man with d-loop d-transposition of the great arteries associated with single coronary artery type 3 by Hvass died unexpectedly. Postmortem study demonstrated myocardial infarction in the posterior portion of the right ventricle and interventricular septum, and complete obstruction of the proximal right coronary artery. The etiology of the unexpected death is discussed.
Adult↗
Significance of collateral circulation on peri-infarct zone: assessment with stress thallium-201 scintigraphy.
To evaluate the significance of collateral circulation on peri-infarct zone, stress myocardial scintigraphy and contrast left ventriculography (LVG) were performed in 38 patients with recent myocardial infarction (MI). All patients had at least one completely occluded coronary artery corresponding to the infarct area. In patients with good collaterals, stress induced transient enlargement of the perfusion defect, however, in those with poor or no collaterals the enlargement did not occur (p less than 0.05). Wall motion abnormality on LVG was significantly milder in the former patients than in the latter (p less than 0.001). Transient enlargement of the perfusion defect after stress and milder left ventricular asynergy were more frequently observed in patients with anterior MI and good collaterals. These observations indicate that good collaterals may keep some myocardium in the peri-infarct zone viable.
Adult↗
Failure of guinea pig plasma kallikrein to cause neutrophil migration.
Guinea pig plasma kallikrein was apparently chemotactic for guinea pig neutrophils when assayed in Boyden's chamber. However, it was concluded that this phenomenon was artificial due to the following reasons: Kallikrein was only chemotactic in the presence of bovine serum albumin (BSA) in the chamber but not when BSA was substituted by guinea pig serum albumin or egg albumin. Kallikrein injection failed to cause dermal tissue leukocytosis. Kallikrein did not polarize neutrophils. A chemoattractant(s) seemed to be generated from BSA preparation time dependently. Although this generation required the enzymatic activity of kallikrein, the chemotactic activity once generated was resistant to a kallikrein inhibitor (diisopropylfluorophosphate) and antiprekallikrein antibody.
Animals↗
Mechanism of protection against pneumotoxicity caused by O,S,S-trimethyl phosphorodithioate.
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Animals↗
Immunosuppressive effect of an impurity of malathion: inhibition of murine T- and B-lymphocyte responses by O,O,S-trimethyl phosphorothioate.
The effect of O,O,S-trimethyl phosphorothioate (OOS-TMP) on immune responses such as antigen presentation, antibody production, and cytotoxic T-lymphocyte (CTL) function was examined in vitro. The roles of non-enzymatic and enzymatic glutathione (GSH) conjugation of OOS-TMP in these responses were studied. Antibody responses to T-dependent and T-independent antigens were evaluated after (i) direct culture with spleen or B cells; (ii) cocultivation of B cells with T cells with and without preincubation of OOS-TMP with GSH fortified cytosol. Antigen presentation by macrophages was also assessed after such treatment as compared to untreated controls. OOS-TMP preincubated with GSH had an inhibitory effect on the cytotoxic T lymphocyte and the direct hemolytic plaque forming cell responses. This was found to be mediated by a direct inhibitory effect on macrophages, T, and B cells of the immune system and not through the generation of regulatory suppressor T cells. Thus, the mode of suppressive action of OOS-TMP in vitro is due to inhibition of lymphocytic proliferation. This is only possible in the presence of glutathione which was determined to be a prerequisite for the induction of OOS-TMP suppressive effect.
Animals↗
H-2, Ah, and aging: the immune response and the inducibility of P-450 mediated monooxygenase activities, xanthine oxidase, and lipid peroxidation in H-2 congenic mice on C57BL/10, C3H, and A strain backgrounds.
The effects of beta-naphthoflavone (beta-NF, 80 mg/kg i.p. for 2 consecutive days) on P-450-dependent and -independent enzymes, lipid peroxidation and xanthine oxidase were investigated in 9 strains of young (3-month-old) male mice. Three H-2 congenic strains on each of three different genetic backgrounds were studied. The backgrounds were C57BL/10 (abbreviated as B10), C3H, and A strain mice. The reported longevities (weeks) as expressed in 10th decile of survivorship are significantly different among the H-2 congenic strains on each of these backgrounds: it ranges from 155 to 170 weeks in B10, from 138 to 150 in C3H and from 114 to 134 in A background mice. The inducibility of aryl hydrocarbon hydroxylase (AHH) with beta-NF was highest in B10, intermediate in C3H/He and non-inducible in other C3H mice and in all mice on the A strain background. Within the B10 background, inducibility of AHH varied widely among mice of different H-2 haplotypes: 549 +/- 34 (H-2k), 360 +/- 72 (H-2b) and 349 +/- 47 (H-2r) percent of the mean control values (n = 5; mean +/- S.D.), without change in activities of P-450-independent enzymes. In C3H mice the H-2k haplotype showed inducibility (213 +/- 34%), while other haplotypes, specifically H-2b and H-2j, did not. beta-NF increased the activities of xanthine oxidase in B10 and A background strains, without interbackground differences. Lipid peroxidation was significantly increased in A background strains and in an H-2 dependent manner. The relationship between Ah responsiveness and reported longevities of these nine strains is discussed.
Aging↗
Eugenol modulation of the immune response in mice.
The effect of eugenol on selected parameters of the immune response of C57BL/6 mice was studied. In a dose-response study, eugenol at high doses completely inhibited the plaque-forming cell responses of splenocytes to the T-dependent antigen (sheep erythrocytes) both in vitro and in vivo. In vitro, at concentrations higher than 1.0 mM, eugenol was found to be cytotoxic. In vivo, however, at very low doses there appeared to be a suppression of the plaque-forming cell response to sheep erythrocytes, reaching maximal suppression at 0.1 mumol eugenol/kg mouse body weight. This was followed by enhancement of the response, peaking at 0.25 mumol eugenol/kg mouse body weight. These changes correlated fairly well with body weight changes. Thymic weights appeared to remain unchanged for all doses except the 1.0 mumol eugenol/kg body weight, which was significantly (p less than 0.05) higher than the rest of the groups. Natural killer activity at all effector:target ratios (100:1, 50:1, 25:1) was significantly (p less than 0.05) enhanced at both 0.25 and 2.5 mumol eugenol/kg body weight. Overall, eugenol seems to have dose-dependent suppressive and enhancing effects on the immune response. These effects represent an atypical multiphasic response in which an inversed dose-response relationship is observed.
Animals↗
Organophosphorus pesticide immunotoxicity: effects of O,O,S-trimethyl phosphorothioate on cellular and humoral immune response systems.
The time course of immunosuppression induced by acute treatment with O,O,S-trimethyl phosphorothioate (OOS-TMP), an impurity in technical formulations of malathion, was examined in female C57B1/6 mice. Both cell-mediated and humoral immune responses were examined and included allospecific cytotoxic T cells, proliferative response to mitogens, interleukin-2 production and antibody production to sheep red blood cells. OOS-TMP pretreatment led to a reversible suppression of the generation of cytotoxic T lymphocytes and antibody-secreting cells to sheep erythrocytes. However, the mitogenic response of splenocytes from animals treated with nontoxic doses of OOS-TMP (as measured by body weight loss, serum cholinesterase levels and splenic lymphocyte number) to concanavalin A was not significantly suppressed, but the response to the B cell mitogen lipopolysaccharide was slightly decreased on day 1 following treatment. In contrast, interleukin-2 production was elevated by 24 h following treatment, but had returned to control levels by day 7. These data suggest that OOS-TMP was able to block the generation of cytotoxic T lymphocytes and antibody responses at doses of OOS-TMP that did not affect body weight or splenic lymphocyte number and this suppression was reversible.
Animals↗
Modulation of cellular and humoral immune responses by O,S,S-trimethyl phosphorodithioate, an impurity of commercial malathion.
We studied the effect of O,S,S-trimethyl phosphorodithioate (OSS-Me) on macrophage function and the immune responses of both T- and B-cells using an in vitro system. The involvement of glutathione (GSH) in the bioactivation of OSS-Me to suppress such responses was investigated after either direct culture with spleen or B-cells and/or co-culture of B-cells with either B- or T-cells that were or were not preincubated with OSS-Me and glutathione enriched cytosol. Our results show that OSS-Me preincubated with GSH suppresses immune responses through an inhibitory effect on the cell function. Both cytotoxic T-lymphocyte (CTL) generation and antibody production were impaired. Antigen presentation by macrophages was also inhibited. In mixing experiments of pretreated and normal cells, the inhibitory effect was also observed on macrophages and helper T-cells responding to a T-dependent antigen. We concluded that the immunosuppressive effect of OSS-Me is due to impairment of cell function and not mediated through generation of regulatory suppressor T-cells. This inhibitory effect was only detectable in the presence of glutathione in the preincubation mixture, suggesting that an OSS-Me glutathione adduct might be responsible for the toxic effect.
Animals↗
Increased resorption of embryos in O,O,S-trimethyl phosphorothioate-treated rats.
Pregnant rats (N = 7) were dosed p.o. with O,O,S-trimethyl phosphorothioate (OOS-TMP) (LD50 = 85) at 20 mg/kg on days G8 and G10. Seven animals were treated with corn oil and pair-fed. Five control animals were treated with corn oil. The abdomen was palpated on day G15 and in 4 animals out of 7 treated with OOS-TMP, complete resorption was observed. All pair-fed and control animals maintained pregnancy until day G21. Total number of resorption/number of implants was 60/95 (63.2%) in OOS-TMP animals, 21/82 (25.6%) in pair-fed animals and 4/65 (6.5%) in control animals. Incidence of complete resorption and % resorption were significantly higher (P less than 0.03 and P less than 0.01) in comparison with those in pair-fed animals. Fetuses from OOS-TMP mothers showed slight growth retardation. By skeletal examination, a missing vertebra and delayed ossifications were found in animals treated with OOS-TMP (20 mg/kg).
Abnormalities, Drug-Induced↗
Similarity of isozyme pattern of serum lactate dehydrogenase following treatments with O,O,S-trimethyl phosphorothioate and paraquat.
Oral administration of O,O,S-trimethyl phosphorothioate (OOS-TMP) causes delayed mortality and lung injury in rats. The present study was carried out to determine whether serum lactate dehydrogenase (LDH) activity and its isozyme pattern were capable of detecting lung injury and possible other organ damages caused by OOS-TMP. Carbon tetrachloride (CCl4, 1 ml/kg, i.p., 24 h) and paraquat (25 mg/kg, i.p., 48 h) were selected as standard chemicals for liver injury, and lung and kidney injuries, respectively. The activity of serum LDH increased to 4 times above control following treatment of rats with OOS-TMP (20 mg/kg, p.o., 72 h). Treatment with CCl4 increased the activity to 8 times while paraquat only slightly increased the activity. Isoelectrophoresis of serum samples showed that OOS-TMP increased the activities of isozymes LDH 1 and LDH 2. This isozyme pattern was similar to the pattern of paraquat but quite different from the pattern in animals treated with CCl4, where LDH 5 was most predominant, or in control animals. Thus, the isozyme pattern strongly suggests that OOS-TMP causes the similar organ damage evoked by paraquat, lung and kidney.
Administration, Oral↗
Increasing pre-excitation ("concertina effect") during vasospastic angina.
A patient with Wolff-Parkinson-White syndrome and variant angina developed progressive ST-segment elevation in the inferior leads after hyperventilation-induced right coronary artery spasm. At the same time, increasing pre-excitation ("concertina effect") developed with gradual prolongation of the AH interval on His bundle ECG. The ECG changes promptly disappeared after sublingual nitroglycerin, with termination of the chest pain. Transient ischemia induced by coronary artery spasm can be an etiology of increasing pre-excitation.
Angina Pectoris, Variant↗
Suppressive effect of O,O-dimethyl, S-ethyl phosphorothioate on immune response.
The effect of O,O-dimethyl, S-ethyl phosphorothioate (OO-Me S-Et) on macrophage function and the responses of T- and B-cells of the immune system were investigated using an in vitro model. The role of glutathione (GSH) enhancement of OO-Me S-Et suppression of immune responses was studied after either direct culturing with spleen or B-cells alone or coculture of B-cells with either B- or T-cells with or without preincubation with OO-Me S-Et and glutathione enriched cytosol. The results indicated that OO-Me S-Et, when preincubated with GSH, suppresses immune responses through an inhibition of B- and T-cell functions. Both cytotoxic T-lymphocyte (CTL) generation and antibody production were impaired. In mixing experiments of pretreated and normal cells, the inhibitory effect was also observed on macrophages and helper T-cells responding to a T-dependent antigen. It appears that the immunosuppressive effect of OO-Me S-Et is due to impairment of collaboration of T- and B-cells, i.e., mainly due to impairment of T-cell functions. The immunotoxic effect was only detectable when glutathione was present in the preincubation mixture.
Animals↗
Pseudomembranous colitis in a patient of paraquat intoxication.
A 49 year-old man drank paraquat 7-8 fold of human fatal dose, and died of severe respiratory failure in 24 days in spite of intensive therapy. The autopsy revealed diffuse pulmonary fibrosis caused by prolonged intoxication of paraquat. An interesting finding was many raised plaques from 1 mm to 10 mm in diameter, observed in whole colon. Histologically, these plaques were composed of necrotic mucosa ("pseudomembrane"), disrupted crypts and edematous submucosa with fibrin education, intervening in normal colon tissue with sharp margins, and diagnosed as non-antibiotic-induced pseudomembranous colitis. Since the edematous submucosa of the raised plaque had a stratified fibrin education around a dilated capillary, it was speculated that the vessel injury by paraquat might play a role in the pathogenesis of pseudomembranous colitis.
Administration, Oral↗
Expression of hepatitis B virus core antigen gene in Saccharomyces cerevisiae: synthesis of two polypeptides translated from different initiation codons.
Two recombinant plasmids were constructed that allow expression of the hepatitis B core (HBc) antigen gene in the yeast Saccharomyces cerevisiae under the control of the repressible acid phosphatase promoter. One plasmid was designed to produce polypeptide I, which consists of 183 amino acids, and the other plasmid was designed to produce polypeptide II, which has an additional 29-amino-acid sequence at the amino terminus of polypeptide I. The viral genome may code for either one or both of these two polypeptides, depending upon the selection of initiation codons. Both polypeptides produced in yeast cells reacted with anti-HBc antibody and were assembled into spherical particles approximately 27 nm in diameter. Particles made of polypeptide I were stable, whereas those made of polypeptide II readily dissociated when exposed to high salt levels. The antigenicity of the HBc (as defined by its reactivity to anti-HBc antibody in the reversed passive hemagglutination assay) disappeared as the particle dissociated, leaving materials that sedimented slowly and that reacted to anti-hepatitis B e antibody. These observations strongly suggest that native viral cores are mostly (if not all) made of polypeptide I, because it is reasonably stable, and that the N-terminal portion of this polypeptide has some, but not a profound, influence on the assembly of polypeptides into particles.
Capsid↗
Initial pulmonary artery involvement in Takayasu arteritis.
Although the pulmonary artery is involved in many cases of Takayasu arteritis, few cases have been reported in which the pulmonary artery was initially involved. Two such cases are reported here. Both of these cases had been initially diagnosed as chronic pulmonary embolism. The importance of considering Takayasu arteritis in cases of chronic pulmonary arterial obstruction of unknown cause is emphasized. Bronchial-pulmonary artery communication and coronary-bronchial artery communication in Takayasu arteritis are also discussed.
Adult↗