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Biomedical subjects

S Abe

Publications and source records attributed to S Abe.

At least 415 records · Page 23Linked to original sources

Electrocardiographic abnormalities in patients receiving hemodialysis.

We assessed standard 12-lead and Holter electrocardiographic (ECG) abnormalities in maintenance hemodialysis (HD) patients. Of 221 outpatients receiving HD, 143 (65%) had ECG abnormalities. Rates were higher in male, elderly, hypertensive, and diabetic patients than in female, younger, normotensive, and nondiabetic patients. The prevalence of ECG changes correlated inversely with HD duration. Serial ECGs were compared in 87 patients whose average HD duration was 7.5 +/- 2.5 years. Thirty-four patients (39%) showed normal ECGs throughout, 27 (31%) relatively stable abnormalities, 22 (25%) worsening, and 4 (5%) reversion to normal. Age, hypertension, and diabetes are factors related to abnormal ECG findings. Among the 142 Holter recordings from 72 patients, 70 (97%) were basically in sinus rhythm, and 2 (3%) were in atrial fibrillation. The average frequency of supraventricular premature contractions (SVPCs) was 1597 +/- 9725 per 24 hours, and that of ventricular premature contractions (VPCs), 556 +/- 1415. VPCs were multifocal in 9%, in runs in 25%, and early in 1%. In 29 (40%) of recordings, VPCs appeared mainly during and for several hours after HD. ST-T changes were seen in 43 (60%). In 11, ST depression occurred during and a few hours after HD. Patients receiving HD showed diverse ECG abnormalities. Holter ECGs revealed a high incidence of arrhythmias and ST-T changes, which frequently appeared in relation to HD timing.

Adolescent↗

Impaired hyperemic response of brachial artery with the presence of diabetes mellitus in patients with coronary artery disease: a preliminary study.

Microvascular reactivity was assessed in reactive hyperemic response of brachial artery in 10 patients with non-insulin-dependent diabetes mellitus and 34 non-diabetic patients. Each subject was diagnosed clinically as having angina pectoris and was examined by coronary angiography. Brachial arterial flow was determined by a pulsed Doppler velocity measurement, guided by a high-resolution B-mode imaging of the forearm. Peak systolic velocity at the basal state in diabetic and non-diabetic patients was comparable (0.53 +/- 0.03 versus 0.61 +/- 0.04 m/s, respectively; P = NS). The velocity ratio of the peak systolic flow at the basal state to the maximum velocity during hyperemia of 2 min arterial occlusion tended to be less in diabetic than in non-diabetic patients (1.76 +/- 0.14 versus 2.15 +/- 0.13, respectively; P = NS). The duration of hyperemic flow was less in diabetic than in non-diabetic patients (6.7 +/- 0.7 versus 9.9 +/- 0.6 s, respectively; P < 0.02). Such alterations in reactive hyperemia may be relevant to the microvascular disorder of the peripheral vessel in the presence of diabetes mellitus.

Aged↗

Circulating soluble intercellular adhesion molecule-1 (sICAM-1) in patients with sarcoidosis.

sICAM-1 has been elevated in sera of specific inflammatory diseases, and circulating sICAM-1 concentrations reflect disease activity in these diseases. We measured circulating sICAM-1 concentrations and serum angiotensin-converting enzyme (SACE) activity in patients with sarcoidosis. Patients with sarcoidosis had significantly increased circulating sICAM-1 concentrations (62.8 +/- 33.5 U/ml) and SACE activity (23.7 +/- 7.4 U/l) compared with controls (circulating sICAM-1 50.9 +/- 12.1 U/ml, and SACE 13.5 +/- 3.8 U/l). Successive measurements showed that circulating sICAM-1 values changed in parallel with disease activity in sarcoidosis. In the progressive disease group (progressed or without change for 2 years or more), circulating sICAM-1 values (102.2 +/- 35.3 U/ml) at the time of diagnosis were significantly increased compared with those in the regressive disease group (disappeared or regressed within 2 years) 46.4 +/- 12.6 U/ml). However, there was no significant difference in SACE activity of the regressive and progressive disease groups. Fifteen patients with a high value of circulating sICAM-1 (> 75 U/ml, mean of controls + 2 s.d.) all had progressive disease, while only 15 of 44 patients with a high value of SACE had progressive disease. Circulating sICAM-1 will be a useful blood marker to predict outcome and to monitor disease activity in sarcoidosis.

Adolescent↗

Prognostic significance of proliferating cell nuclear antigen (PCNA) in squamous cell carcinoma of the esophagus.

Proliferating cell nuclear antigen (PCNA) has been shown to be of prognostic significance in some gastrointestinal tumors. Immunohistochemical analysis was performed to determine whether PCNA is useful for predicting the outcome of patients with squamous cell carcinoma of the esophagus. Using a mouse monoclonal antibody, PC 10, the expression of PCNA was studied in resected squamous cell carcinomas of the esophagus from 59 patients who had undergone curative esophagectomy. None had received any preceding therapy. The proliferation rate was assessed in terms of the percentage of the PCNA-positive nuclear area relative to the total area of cancer nuclei using a cell analysis system (CAS). Clinicopathological variables including PCNA staining were assessed in relation to prognosis. Survival rate was obtained by the Kaplan-Meier method. The PCNA indices (percentage of the positive nuclear area) of the tumors varied from 4.4% to 96.2%. Among the clinicopathological variables, only tumor size (5 cm) and depth of invasion were correlated significantly with PCNA index (P<0.05). Microscopically, PCNA was stained in non-keratinized cells but not in keratinized cells. However the histological grade was not correlated with PCNA index. The survival rate was significantly worse in patients with high PCNA indices (> or = 40%) than in those with low indices (<40%) (P<0.05). However, multivariate analysis revealed that PCNA index was not an independent prognostic factor.

Aged↗

Cooperative anti-Candida effects of lactoferrin or its peptides in combination with azole antifungal agents.

The effects of lactoferrin (LF), an antimicrobial protein secreted in body fluids, and its peptides in combination with azole antifungal agents were investigated by the micro-broth-dilution method in a study of Candida albicans. In the case of LF, its pepsin hydrolysate (LFhyd) or the LF-derived antimicrobial peptide Lactoferricin B (LF-B), the concentrations required to inhibit the growth of Candida decreased in the presence of relatively low concentrations of clotrimazole (CTZ). The minimum inhibitory concentration (MIC) of all azole antifungal agents tested was reduced by 1/4-1/16 in the presence of a sub-MIC level of each of these LF-related substances. Polyene and fluoropyrimidine antifungal agents did not show such a combined effect with these LF-related substances. The anti-Candida activity of LF or LF-B in combination with CTZ was shown to be synergistic by checkerboard analysis. These results indicate that LF-related substances function cooperatively with azole antifungal agents against C. albicans.

Antifungal Agents↗

Prophylactic effect of Enterococcus faecalis FK-23 preparation on experimental candidiasis in mice.

The prophylactic effects of heat-killed cells of Enterococcus faecalis FK-23 (FK-23 preparation) on experimental candidiasis were investigated in normal and leukopenic mice. In cyclophosphamide-induced leukopenic mice, oral or intraperitoneal administration of the FK-23 preparation at a daily dose of 1.25 or 5 mg/mouse for 3 consecutive days prior to Candida albicans infection significantly prolonged survival periods of the infected mice, and decreased viable counts of C. albicans recovered from their kidneys. In normal mice, the FK-23 preparation administered at dosages ranging from 0.63 to 10 mg/mouse/day for 3 consecutive days was ineffective, while in leukopenic mice, the FK-23 administered orally caused a facilitated recovery in the number of white blood cells including neutrophils. Furthermore, intraperitoneal administration of the FK-23 preparation into mice augmented the anti-Candida activity of immunocompromised peritoneal exudate cells obtained from the animals. These results suggested the potential usefulness of the FK-23 preparation as a prophylactic agent for the management of patients with opportunistic fungal infections.

Animals↗

Some effects of nipradilol, a beta-antagonist possessing a nitroxy group, on smooth muscle of the pig coronary artery.

1. The effects of nipradilol, a beta-adrenoceptor antagonist which possesses a nitroxy group, on cytosolic Ca2+ concentration ([Ca2+]i), and on tension development were simultaneously measured by front-surface fluorometry and fura-2-loaded strips in the proximal portion of pig coronary arteries. 2. Nipradilol reduced in a concentration-dependent manner both the [Ca2+]i and tension, irrespective of whether the strips were unstimulated or exposed to either high K+ or histamine containing solutions. However, both in the case of contractions induced by high K+-depolarization and histamine stimulation, for a given [Ca2+]i elevation the tension which developed in the presence of nipradilol was smaller than that generated in its absence, so that the [Ca2+]i-tension curves during the contraction were shifted to the right. 3. In the absence of extracellular Ca2+, the [Ca2+]i elevation due to the release of Ca2+ from histamine-sensitive store was inhibited by nipradilol. Nipradilol had no effect on the [Ca2+]i elevation due to the release of Ca2+ from caffeine-sensitive stores; however, it did inhibit the caffeine-induced increase in tension. A derivative of nipradilol, which lacked a nitroxy molecule (Nip(-N)), had no effect on the [Ca2+]i and tension elevated by histamine or caffeine in the absence of extracellular Ca2+. 4. The beta-adrenoceptor agonist, isoprenaline, reduced [Ca2+]i tension when applied to steady state contractions induced by high K+, or at the peak level of tension to histamine. The reduction of [Ca2+]i and tension induced by isoprenaline was inhibited by Nip(-N) in a concentration-dependent manner and nipradilol inhibited the isoprenaline-induced relaxation with bell-shaped concentration-response curves. At lower concentrations, nipradilol acted as a beta-blocker, the IC50- value being smaller than that of Nip(-N), and at higher concentrations, it acted as a nitrovasodilator. 5. Thus, it is suggested that, at lower concentrations, nipradilol, an antianginal drug, acts as a beta-adrenoceptor antagonist. At higher concentrations, it relaxes the proximal portion of the coronary artery by directly reducing [Ca2+]i and the Ca2+-sensitivity of the myofilaments, apparently due to the presence of the nitroxy molecule.

Adrenergic beta-Agonists↗

A glucocorticoid antagonist, mifepristone affects anti-Candida activity of murine neutrophils in the presence of prednisolone in vitro and experimental candidiasis of prednisolone-treated mice in vivo.

The effects of a glucocorticoid-antagonist, mifepristone on the suppressive action of prednisolone for anti-Candida activity of murine neutrophils were examined. Prednisolone suppressed inhibitory activity of neutrophils to mycelial growth of Candida albicans. This suppression was cancelled in the presence of 10(-7)-10(-6) M of mifepristone in vitro. Corresponding to this in vitro action, mifepristone protected prednisolone-treated mice from lethal C. albicans infection in vivo. These results suggest that glucocorticoid-induced vulnerability to Candida infection may be recovered or normalized by application of mifepristone.

Animals↗

[Suppression of anti-Candida activity of human neutrophils by glucose and diminishment of the glucose effect by an amino acid mixture].

Effects of a glucose and amino acid mixture prescribed for parenteral alimentation on anti-Candida activity of neutrophils were examined. Neutrophils obtained from peripheral blood of healthy humans inhibited the growth of Candida albicans in vitro. More than 1.0% of glucose inhibited the anti-Candida activity of the neutrophils in a dose-dependent manner. This glucose effect was reduced by the addition of an amino acid mixture clinically prescribed with a carbohydrate solution (PN-twin) in Japan. The amino acid mixture neutralized the suppression of anti-Candida activity of neutrophils by dexamethasone. These results suggest that an amino acid mixture prescribed in an alimentation solution may play a role as a neutralizer of the suppressive action of glucose for anti-Candida activity of neutrophils in a limited area near the top of a catheter in a blood vessel.

Amino Acids↗

Significance of serum lipase in patients undergoing hemodialysis.

Serum levels of lipase (Lp) during the end of the dialysis showed a significant increase after the administration of heparin in hemodialysis patients. However, serum Lp levels were not increased after the administration of the anti-coagulant nafamostat mesylate in hemodialysis patients. Serum levels of Lp were significantly correlated with serum levels of lipoprotein lipase (LPL), hepatic triglyceride lipase (H-TGL) and nonesterified fatty acid (NEFA) 20 min after the administration of heparin during maintenance hemodialysis. Lp activity did not appear with the NEFA ligand for determining the NEFA activity. Inhibitors of LPL and H-TGL reduced the measured Lp activity in vitro. The main mechanism of elevated measured serum Lp activity in hemodialysis patients was determined to be cross-reactivity with LPL or H-TGL. Furthermore, measurement of Lp may be a method for determining optimal coagulation time in patients with hemodialysis.

Adult↗

Elevated progastrin-releasing peptide(31-98) concentrations in pleural effusions due to small-cell lung carcinoma.

Progastrin-releasing peptide (ProGRP) is a specific and actively secreted product from small-cell lung carcinoma (SCLC) cells. Recently, an enzyme-linked immunosorbent assay, which uses monoclonal and polyclonal antibodies to recombinant proGRP(31-98), a common region of ProGRP, was established. We measured concentrations of ProGRP (31-98), neuron-specific enolase (NSE) and carcinoembryonic antigen (CEA) in carcinomatous and infectious pleural effusions. Significantly increased ProGRP(31-98) and NSE values were found in carcinomatous pleurisy due to SCLC compared to the other carcinomatous pleurisy and infectious pleurisy. CEA values were significantly increased in carcinomatous pleural effusions compared with those in infectious effusions. The ProGRP(31-98) values were not correlated to NSE values in carcinomatous pleurisy due to SCLC. The determination of ProGRP(31-98) in pleural effusions will be helpful for diagnosing carcinomatous pleurisy due to SCLC.

Biomarkers, Tumor↗

Lipid analysis and surfactant-associated protein expression in lung adenocarcinoma cells from pleural effusion.

Primary lung adenocarcinomas originate from the progenitor cells of peripheral airway cells. Alveolar type II cells and Clara cells are the major progenitor cells of peripheral airway cells. Alveolar type II cells produce a lipid-protein complex called surfactant, which contains surfactant proteins SP-A, SP-B, SP-C and SP-D. Phosphatidylcholine (PC) and phosphatidylglycerol (PG) are believed to be essential for the surfactant function. Clara cells also express SP-A, SP-B and SP-D but not SP-C. In this study we examined the properties of the cancer cells isolated from the pleural effusion of a patient with primary lung adenocarcinoma by analyzing lipids, proteins and mRNAs. The cancer cells, designated as LC117 cells, were isolated from the pleural effusion of a patient with primary lung adenocarcinoma. The percent distributions of [14C]-acetate incorporated into PC and PG in the cancer cells were 55.7 and 1.1%, respectively. The disaturated species in total PC was 46.2%. Immunoblotting analysis using anti-SP-D monoclonal antibody revealed that the pleural effusion from a patient with lung adenocarcinoma contained SP-D. We determined the concentrations of SP-A and SP-D by enzyme-linked immunosorbent assay. The pleural effusions from this patient and the media incubated with cancer cells exhibited significant levels of SP-D as well as SP-A. Reverse transcriptase-polymerase chain reaction demonstrated that the tumor cells expressed mRNAs for SP-C as well as the other surfactant proteins. The results demonstrate that tumor cells from lung adenocarcinoma express all of surfactant-associated proteins, indicating that LC117 cells originate from alveolar type II cells. This study indicates that the combination of analyses of lipids, proteins and mRNAs in the cancer cells isolated from pleural effusion is useful to understand the property of lung adenocarcinoma.

Adenocarcinoma↗

Transvenous hemodynamic assessment of arteriovenous malformations and fistulas. Preliminary clinical experience in Doppler guidewire monitoring of embolotherapy.

BACKGROUND AND PURPOSE: Transvenous monitoring of blood flow through intracranial vascular malformations was performed with an intravascular Doppler guidewire to assess hemodynamic changes during endovascular embolotherapy. METHODS: Flow velocity was assessed in the intracranial venous sinuses of two patients with arteriovenous malformations and seven patients with dural arteriovenous fistulas. In all cases, the Doppler guidewire was positioned in the dural sinuses coaxially through a 2.1F microcatheter. The Doppler guidewire was then advanced to the site of arteriovenous shunting for sampling of venous average peak velocity (APV) and pulsatility index. In two cases, simultaneous feeding artery flow velocity was monitored by transcranial color-coded duplex sonography. RESULTS: Before embolotherapy, the flow pattern in the venous sinuses was pulsatile, with a mean (+/-SD) APV of 39.0 +/- 22.5 cm/s. Total or near-total embolization was achieved in six of the nine cases. After embolization, the flow pattern became less pulsatile and the APV was reduced to a mean of 21.2 +/- 14.6 cm/s (P = .0123, one-tailed paired t test). The pulsatility index was used to calculate the maximum minus the minimum peak velocity (MxPV-MnPV). This was reduced from an average of 27.0 +/- 8.7 cm/s to 13.5 +/- 8.3 cm/s after treatment (P = .0456). A parallel reduction in APV of the feeding arteries was observed with embolization. CONCLUSIONS: Preliminary clinical experience indicates that transvenous assessment of two parameters, APV and MxPV-MnPV, is useful in the hemodynamic evaluation of intracranial arteriovenous shunts. This valuable hemodynamic information may be used for objective and quantitative monitoring during embolotherapy of intracranial vascular malformations.

Adolescent↗

Progastrin-releasing peptide(31-98) in idiopathic pulmonary fibrosis and sarcoidosis.

Gastrin-releasing peptide (GRP) is present in the lung and functions as a growth factor for bronchial epithelial cells and fibroblasts. GRP may stimulate release of cytokines from alveolar macrophages. However, in interstitial lung diseases, the role of GRP has not been clarified, in part because of the instability of GRP. Progastrin-releasing peptide (ProGRP) molecules are the actual GRP gene products. ProGRP molecules contain common extension peptides(31-98) [ProGRP(31-98)], which are not homologous with other proteins unlike GRP. With the ELISA, we measured ProGRP(31-98) concentrations in sera and bronchoalveolar lavage (BAL) fluids from patients with sarcoidosis and idiopathic pulmonary fibrosis (IPF). Significant increased ProGRP(31-98) concentrations were found in sera and BAL fluids from patients with IPF or sarcoidosis when compared with healthy subjects. Serum ProGRP(31-98) values significantly correlated with BAL fluid ProGRP(31-98) values. In IPF and sarcoidosis, the release of the actual GRP gene products is increased in the lung and the bloodstream, and GRP may play a role during the processes of inflammation and remodeling in interstitial lung diseases.

Adolescent↗

Effects of interleukin-2 and cyclosporin A on pathologic features in Mycoplasma pneumonia.

To elucidate the immunopathologic mechanisms of Mycoplasma pneumonia, the effects of interleukin-2 (IL-2) and cyclosporin A (CYA) on Mycoplasma pneumonia in mice were investigated. Mice were intranasally inoculated with Mycoplasma pulmonis (M. pul) and treated with IL-2, CYA, or minocycline (MINO) every day between Days 3 and 9. They were killed at Days 7, 14, or 21 after the inoculation. Cell-mediated immunity (CMI) of the host was assessed by delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC). Peribronchial and perivascular lymphocyte cuffing and the accumulation of macrophages at the ends of bronchioles were exacerbated (p < 0.05) in IL-2-treated mice at Day 14 and reduced (p < 0.05) in CYA-treated mice at Day 7. Although the DTH responses to SRBC of saline-inoculated, IL-2-treated mice were increased at Days 7 (p < 0.01) and 14 (p < 0.05), those of M. pul-inoculated, IL-2-treated mice at Day 7 could not recover to the control level. The CMI levels of M. pul-inoculated, CYA-treated mice were decreased at Days 7, 14 (p < 0.05), and 21 (p < 0.01). Mycoplasma organisms in the lung showed the greatest decrease (p < 0.05) in MINO- and IL-2-treated mice, but increased at Day 21 (p < 0.05) in mice treated with IL-2 alone. These results suggest that the pathologic features of Mycoplasma pneumonia could be modified by the degree of host CMI.

Animals↗

Relationships between radiological pattern and cell-mediated immune response in Mycoplasma pneumoniae pneumonia.

The aim of this study was to determine the relationship between the radiological pattern of Mycoplasma pneumoniae and the level of cell-mediated immunity of the host. Computed tomographic (CT) scans of the chest and the results of the purified protein derivative (PPD) test were studied during the acute stage of infection in 54 patients with M. pneumoniae pneumonia. The CT findings were used to divide the patients into two groups: one group had a predominance of nodular opacities with a centrilobular distribution (Group N; n = 29); and the other showed a predominance of an airspace consolidation (Group C; n = 25). Forty out of 54 subjects had negative tuberculin skin tests ( < 10 mm induration). The positive rate of PPD reaction was higher in Group N (13 out of 29) compared to Group C (1 out of 25) (p = 0.0005); whilst pleural effusion appeared more frequently in Group C (10 out of 25) than in Group N (3 out of 29) (p = 0.023). There was no significant difference between Groups N and C in white blood cell and lymphocyte counts, level of antibodies to M. pneumoniae in sera, and severity of the disease. These findings suggest that the characteristics of the host cell-mediated immunity might influence the pattern of pulmonary lesions in M. pneumoniae infection.

Adult↗

Circulating factors and insulin resistance. II. The action of the novel myo-inositol cyclic 1,2-inositol phosphate phosphoglycan insulin antagonist from human plasma in regulating pyruvate dehydrogenase phosphatase.

A novel low mol wt inositol phosphoglycan antagonist of insulin action of oxidative glucose metabolism in isolated rat adipocytes was partially purified from normal human plasma and shown to be increased in type II diabetic plasma. It was characterized chemically as a myo-inositol phosphoglycan containing a cyclic 1,2-phosphate. This antagonist, termed fraction V3, is now shown to inhibit the action of an inositol glycan insulin pH 2.0 mediator that stimulates pyruvate dehydrogenase phosphatase in a similar manner to insulin. In addition, fraction V3 inhibits stimulation of the pyruvate dehydrogenase (PDH) phosphatase by Mg2+, the enzyme's required metal, and by spermine, a polyamine. Fraction V3 does not inhibit active PDH itself. The inhibitory effect is dose dependent and apparently noncompetitive or nonsurmountable for the insulin inositol glycan pH 2.0 mediator, thus comparing kinetically with its insulin antagonistic action on intact adipocytes. Its inhibitory action on PDH phosphatase is dose dependent and competitive for Mg2+ stimulation of the phosphatase. Additionally, fraction V3 is shown to inhibit stimulation by Mg2+ of cloned recombinant PDH phosphatase catalytic subunit. Inhibition by fraction V3 of Mg(2+)-stimulated PDH phosphatase and its cloned catalytic subunit helps explain its mechanism of action to inhibit insulin-stimulated oxidative glucose metabolism in adipocytes and its potential clinical significance in insulin resistance.

Animals↗