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Biomedical subjects

A Nagashima

Publications and source records attributed to A Nagashima.

At least 55 records · Page 3Linked to original sources
PubMed1995

Influence of a high salt diet on glomerular injury and the preventive effects of amiloride in adriamycin nephropathy.

The effects of a high salt diet on glomerular hypertrophy and sclerosis were examined in a focal glomerular sclerosis rat model. Sprague-Dawley rats were injected twice with Adriamycin (ADR, 2.5 mg/kg body weight) and then divided into 3 groups: (1) ADR rats fed a 1% sodium chloride (NaCI) diet (control ADR rats); (2) ADR rats fed an 8% NaC1 diet (ADR-NaC1 group), and (3) ADR rats fed a 10% sodium bicarbonate (NaHCO3) diet (the ADR-NaHCO3 group), and were then observed for 8 weeks. There were no differences in the blood pressure levels between the control ADR and ADR-NaC1 groups. The urinary protein excretion was significantly less in the ADR-NaC1 and ADR-NaHCO3 groups than in the control ADR group. However, a progressive increase in the blood urea nitrogen and serum creatinine associated with extensive glomerular sclerosis and hypertrophy was only observed in the ADR-NaC1 group. An increase in the glomerular diameter preceded the development of glomerulosclerosis in this group. Furthermore, a daily administration of amiloride, a Na+/H+ exchanger inhibitor, to the ADR-NaC1 rats prevented the development of glomerular hypertrophy and sclerosis. These results therefore suggest that the aggravated effect of a high salt diet on glomerular sclerosis may be related to glomerular hypertrophy which is associated with the stimulation of the Na+/H+ exchanger.

Amiloride↗
PubMed1994

Increased expression of Na+/H+ exchanger in the injured renal tissues of focal glomerulosclerosis in rats.

The renal mRNA expression of Na+/H+ exchanger (NHE) and the effects of NHE inhibitor, amiloride, on renal injury were investigated in adriamycin (ADR)-induced glomerulosclerosis model in rats, which progressively developed extensive glomerulosclerosis and interstitial fibrosis. NHE-1 mRNA from the cortex of the ADR rats progressively increased at weeks 4 and 8 and then peaked at week 16, which paralleled with the degree of glomerular sclerosis and interstitial fibrosis. The interstitial fibrosis in the ADR-rats was prevented by a daily administration of amiloride. A simultaneous analysis of the effects of a high salt diet on NHE-1 mRNA expression or renal injury was performed in the ADR rats at weeks 2 and 8. Renal or glomerular hypertrophy was observed in the control or ADR rats fed an 8% NaCl diet at week 2 and 8 compared to a 1% NaCl diet, while the NHE-1 mRNA expression was not up-regulated by an 8% NaCl diet at week 2. At week 8, the NHE-1 mRNA expression or glomerulosclerosis and interstitial fibrosis were enhanced in the ADR rats fed an 8% NaCl diet compared to a 1% NaCl diet. This histological aggravation by an 8% NaCl diet was prevented by a daily administration of amiloride but not by furosemide. In conclusion, the increased NHE-1 mRNA expression and the preventive effects of amiloride on the renal lesions suggest a potential importance of NHE in the progressive process of ADR-nephropathy. The high salt diet had a hypertrophic and destructive effect on kidney or glomeruli in the ADR rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1994

Clinical significance of growth hormone-binding protein measurements in children.

To investigate the role of growth hormone (GH) and its downstream axis in normal growth and growth disorders, we measured serum GH-binding protein (GHBP) levels in children by ligand-mediated immunofunctional assay (LIFA). Samples were taken from 512 healthy children of normal stature, 146 healthy neonates, 153 short but otherwise normal children, and 27 patients with GH deficiency. Serum GHBP showed no significant diurnal variation. Serum GHBP levels were low in neonates, acutely rose within 6 months, and gradually increased toward midpuberty in normal children (r = 0.2, P < 0.01, assessed among subjects over 1 year old). Neither significant sexual dimorphism nor rapid pubertal changes were observed. In normal short children and patients with GH deficiency, GHBP was lower than normal, but not significant. These data suggest that one of the etiologies for growth disorder in children could be resistance to, or low efficacy for, utilization of GH.

Adolescent↗
PubMed1994

Specific reactivity of human monoclonal antibody AE6F4 against cancer cells in tissues and sputa from lung cancer patients.

In vitro immunization of normal human peripheral lymphocytes by the co-cultivation with A549 cells (a human lung adenocarcinoma cell line), followed by the hybridization with the partner cell line A4H12, resulted in the efficient generation of hybridomas which produce human monoclonal antibodies of IgG or IgM isotype. Immunohistochemical and immunocytological studies showed that one of those monoclonal antibodies, termed AE6F4, was specifically reactive to lung cancer tissues as well as cancer cells in sputa.

Antibodies, Monoclonal↗
PubMed1994

[Nephrotic syndrome due to membranous glomerulopathy in hypocomplementemic urticarial vasculitis syndrome;--a case report].

We report a case of hypocomplementemic urticarial vasculitis syndrome (HUVS) with membranous glomerulopathy in a 62-year-old man who had a 2-month history of secondary iritis. He was transferred to our hospital because of uncontrollable edema and respiratory dysfunction. Physical examination revealed anasarca, pulmonary edema, hypertension and urticaria-like eruption on his arms. Urinalysis, blood chemistry and serological studies showed massive proteinuria (10.5g/day) with numerous granular casts, hypoalbuminemia (1.5g/dl), renal dysfunction (creatinine; 1.6mg/dl, BUN; 86mg/dl), hypercholesterolemia (total cholesterol; 455mg/dl), positive results for antinuclear factor, microsome test, thyroid test, lupus anticoaglant, antithyroglobulin test and rheumatoid factor, but LE cell or double-strand anti DNA antibody was negative. Serum complement levels were persistently low as CH50 of 13 U/ml and Clq of 6.0 micrograms/dl. The patient serum precipitated with normal human Clq by immunodiffusion analysis, indicating the presence of anti-Clq antibody. Renal biopsy revealed membranous glomerulopathy with prominent fine granular deposition of Clq along the glomerular basement membrane by immunofluorescent study and subepithelial dense deposit by electron microscopy. Corticosteroid treatment was ineffective for hypocomplementemia and nephrotic syndrome. Acute subendocardial infarction occurred on the 25th hospital day and he died of acute respiratory distress syndrome on the 45th hospital day. Autopsy revealed leucocytoclastic vasculitis in the alveolar wall. HUVS was confirmed by clinical symptoms, such as iritis and urticaria-like eruption, serum anti-Clq antibody, the absence of any specific autoantibody for systemic lupus erythematosus (SLE) and leucocytoclastic vasculitis in the alveolar wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1993

Pharmacokinetics of cisplatin instilled into the pleural cavity following panpleuropneumonectomy in patients with malignant pleurisy due to lung cancer.

The pharmacokinetics of cisplatin instilled into the pleural cavity in patients with malignant pleurisy due to lung cancer were studied. Higher concentrations of total and free platinum in pleural effusion have been maintained for longer than 72 hours in patients who were subjected to panpleuropneumonectomy than in those who received simple drainage. Early rapid drop of total platinum within 6 hours was significant in the drainage group. Total platinum level in the serum of the panpleuropneumonectomy group gradually increased during 1-72 hours, however, that of the drainage group was highest at 1 hour after instillation and declined gradually with time. Free platinum in the serum was also present at lower concentrations in the panpleuropneumonectomy group than in the drainage group. These facts may be ascribed to the absorptive activity of parietal pleura which is present in the drainage group but absent in the panpleuropneumonectomy group. In summary, removal of the parietal pleura by panpleuropneumonectomy could cause cisplatin to be not only more active but also less toxic in patients with malignant pleurisy due to lung cancer.

Adenocarcinoma↗
PubMed1993

Effect of postoperative intrapleural instillations of interleukin-2 in patients with malignant pleurisy due to lung cancer.

Thirteen patients with resectable lung cancer and concomitant malignant pleurisy which could not be detected by preoperative chest roentgenograms were treated with surgical resection of the primary lesions and postoperative intrapleural instillations of interleukin-2 (IL-2). All of the patients demonstrated disappearance of cancer cells from pleural effusion after the IL-2 therapy. Four of the 13 patients survived over 5 years and 2 of them are in disease free state at this moment (January 31, 1993). The first recurrent sites were distant organs in 8 of 11 patients with recurrence and lymph nodes in 3 of them. No pleural recurrence was observed. These results indicate that the postoperative intrapleural IL-2 therapy may be one of hopeful adjuvant therapies in patients with resectable lung cancer and concomitant malignant pleurisy, although distant metastasis and lymph node recurrence could not be suppressed completely.

Adenocarcinoma↗
PubMed1993

The pharmacological characterization of FK 739, a new angiotensin II-receptor antagonist.

The pharmacological properties of FK 739, a new angiotensin II-receptor antagonist, were examined. FK 739 inhibited the specific binding of [125I]-angiotensin II to rat aortic smooth muscle cell membrane with an IC50 value of 8.6 nM, but did not displace the specific binding of [125I]-angiotensin II to bovine cerebellum membrane. In isolated helical strips of rabbit aorta, FK 739 shifted the concentration-response curve of angiotensin II-induced contraction in parallel to the right, and the values of the slope and pA2 were 1.06 and 8.45, respectively. In in vivo studies, oral administration of FK 739 at 10 mg/kg significantly inhibited the angiotensin I-induced pressor response in normotensive rats and dogs, and it caused a fall of mean blood pressure in renal hypertensive rats and dogs. In spontaneously hypertensive rats, FK 739 at 32 and 100 mg/kg significantly decreased the mean blood pressure in a dose-dependent manner. Additionally, we studied whether FK 739 would cause side effects such as dry cough, like other ACE inhibitors did. Oral administration of FK 739 (10 and 32 mg/kg) did not affect the capsaicin-induced bronchial edema. On the other hand, captopril (10 mg/kg) significantly enhanced capsaicin-induced bronchial edema. These results indicate that FK 739 is a potent and competitive antagonist for AT1-type receptors, and suggest that FK 739 might be a safe and useful agent for the treatment of hypertension in clinical trials.

Angiotensin I↗
PubMed1993

[Hemodynamic changes in acute pancreatitis].

Hemodynamics studies were carried out from days 1-5 following the onset of illness in 7 patients with severe pancreatitis (group A) and in 7 patients with moderate pancreatitis (group B). Patients in both groups had a higher cardiac index (CI) and a lower systemic vascular resistance (SVR) than normal patients during 5 days of illness, and patients in group A had a higher CI of 5.38 +/- 0.841 x min/m2 and lower SVR of 889 +/- 234dyn.sec/cm5 than those in group B on day 4. Patients in group A had a lower pulmonary vascular resistance than normal patients on days 1, 3, and 4, but those in group B did not show this hemodynamic change. Group A patients had a higher pulmonary wedge pressure of 11.9 +/- 8.4mmHg and depressed left ventricular stroke work index of 59.8 +/- 17.8g.m/m2 as compared with group B (5.6 +/- 3.4mmHg, 77.7 +/- 23.6g./m2, respectively). These findings indicate that a hyperdynamic hemodynamic state may exist in the early stages of moderate and severe pancreatitis and myocardial depression may be evident in severe pancreatitis.

Acute Disease↗
PubMed1991

The central pressor actions of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide.

Intracerebroventricular (i.c.v.) injections of a novel tachykinin peptide, gamma-preprotachykinin-(72-92)-peptide amide (neuropeptide gamma, NP gamma), caused dose-dependent increases in blood pressure. The NP gamma-induced pressor responses (1 microgram i.c.v.) were blocked by peripheral administration of pentolinium (10 mg/kg i.v.) and phentolamine (10 mg/kg i.v.), but were not inhibited by a vasopressin antagonist. These results suggest that central NP gamma increases the blood pressure via sympathetic nerve activity.

Animals↗
PubMed1991

[A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid lactic acidosis].

A case of metoclopramide-induced neuroleptic malignant syndrome with cerebrospinal fluid (CSF) lactic acidosis was reported. A 44-year-old Japanese woman noted tarry stool on July 2, 1988 and was treated with metoclopramide and cimetidine for nausea and vomiting. Hydroxyzine pamoate was also administered for insomnia at 3:10 am and she became comatose with muscle rigidity at 3:40-4:30 am on July 3. Tachycardia and high fever (39.5 degrees C) were evident at 8:00 am on July 4. She was transferred to the Kyushu University Hospital. On admission, serum creatine kinase was elevated to 1640 IU/1; MM fraction was 100%. She was diagnosed as malignant syndrome. Cerebrospinal fluid was normocellular with protein 38 mg/dl and glucose 122 mg/dl. Cerebrospinal fluid lactate increased markedly to 3.43 mmol/l, CSF pH was 7.264, HCO3- 14.4 mEq/l, indicating CSF metabolic acidosis. She became afebrile after the 10th hospital day, and gradually but completely recovered within a month. She was discharged on August 16, 1988. The anti-dopaminergic activity of metoclopramide was considered to be primarily responsible for the development of malignant syndrome in this case. Cerebrospinal fluid lactic acidosis seemed to reflect hyperpyrexia or malignant syndrome induced derangement of the brain metabolism.

Acidosis, Lactic↗
PubMed1991

[A clinical study on intrathoracic malignant lymphoma with chronic tuberculous pyothorax].

The authors reported 3 male patients of malignant lymphoma developing from long-standing pyothorax. They had been suffering from tuberculous pyothorax for more than 30 years, after artificial pneumothorax therapy for pulmonary tuberculosis. The most common symptom was chest pain. It was difficult to detect the tumor mass by chest X-ray because of old inflammatory changes. Computed tomography and 67Ga scintigraphy were useful. The lesions tended to grow destroying the surrounding lung, chest wall and ribs. Histologically, 2 cases were diffuse large cell type and one was diffuse intermediate sized cell type. Immunologically, 2 cases were B-cell type lymphoma but one was not clearly classified. They received radiotherapy, but 2 cases died of respiratory failure. These findings suggest that B cell lymphoma might arise following chronic tuberculous pyothorax. Therefore such cases should be followed up carefully.

Empyema, Pleural↗
PubMed1990

Role of central tachykinin peptides in cardiovascular regulation in rats.

The mechanisms of action of tachykinin peptides thought to be involved in central cardiovascular regulation were examined. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dose-dependent increases in blood pressure and heart rate. The pressor responses to substance P (SP) (10 micrograms, i.c.v.) and neurokinin A (NKA) (10 micrograms, i.c.v.) were blocked by peripheral administration of pentolinium or phentolamine, and partially attenuated by adrenalectomy. In contrast, the only initial pressor response to the neurokinin B (NKB) analogue senktide (10 micrograms, i.c.v.) was blocked by pentolinium or phentolamine. The pressor response to senktide was inhibited by pretreatment with a vasopressin V1 receptor antagonist (d(CH2)5OMe(Tyr)AVP) (10 micrograms/kg, i.v.), and senktide (10 micrograms, i.c.v.) caused an increase in plasma vasopressin level. However, the vasopressin antagonist did not influence the SP- and NKA-induced pressor responses. These results suggest that central SP and NKA increase the blood pressure and heart rate via sympathetic nerve activity, whereas central NKB increases the blood pressure mainly via release of vasopressin from the hypothalamus.

Adrenal Glands↗
PubMed1989

Central pressor actions of neurokinin B: increases in neurokinin B contents in discrete nuclei in spontaneously hypertensive rats.

The regional distributions of neurokinin B-like immunoreactivity and substance P-like immunoreactivity in the central nervous system in spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto rats (WKYs) were examined. The distribution of neurokinin B-like immunoreactivity in WKYs was not exactly the same as that of substance P-like immunoreactivity. The neurokinin B-like immunoreactivity contents of the supraoptic nucleus of the hypothalamus and the caudal part of the nucleus tractus solitarii were higher in SHRs than in WKYs. Injections of selective neurokinin B receptor peptides, senktide (suc-[Asp6,Me-Phe8]-substance P6-11) and [Pro7]-neurokinin B, into the lateral brain ventricle of the normotensive rats caused dose-dependent increases in the blood pressure, and blockade of peripheral vascular vasopressin receptors reduced these pressor responses, but did not affect the substance P-induced pressor response. These findings suggest that the novel tachykinin peptide, neurokinin B has an important role in central pressor action in rats.

Animals↗