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Biomedical subjects

K Maeda

Publications and source records attributed to K Maeda.

At least 865 records · Page 48Linked to original sources
PubMed1993

Reconstitution of rabbit skeletal muscle troponin from the recombinant subunits all expressed in and purified from E. coli.

Three subunits of rabbit skeletal muscle troponin were expressed in and purified from Escherichia coli. The procedures were optimized, and the reconstituted troponin complex is highly homogeneous, stable, and obtainable in large quantities, allowing us to conduct crystallization studies of the troponin complex. The three subunits expressed and purified are beta-TnT(N'-208), TnI(C64A, C133S), and the wild type TnC. beta-TnT(N'-208) is a 25 kDa fragment of beta-troponin T, which consists of 208 amino acids and lacks 58 residues in the N-terminal variable region. TnI(C64A, C133S) is a mutant troponin I, in which Cys-64 and Cys-133 are replaced by Ala and Ser, respectively. Each subunit was separately expressed in E. coli, purified by column chromatography including HPLC, and reassembled to form troponin complex. The reconstituted troponin complex was not distinguishable from authentic troponin prepared from rabbit skeletal muscle; the acto-S1 ATPase rate, as well as the superprecipitation, was calcium-sensitive. Small flat crystals up to 0.2 mm long have been reproducibly obtained in preliminary crystallization trials.

Amino Acid Sequence↗
PubMed1993

Regulation of acute phase gene expression following surgery and endotoxin administration in the anesthetized pig.

BACKGROUND: The hepatic acute phase response (APR) reflects an organism's integrated response to stress. This APR results in augmented synthesis and secretion of specific procoagulants and antiproteases and a complementary decrease in the synthesis and secretion of several constitutive proteins, such as albumin. The cytokines tumor necrosis factor (TNF) or interleukin-6 (IL-6) have been identified as proximal mediators of the APR in response to endotoxin stress. The authors hypothesized that TNF, IL-6, or both would be the proximal mediators of the APR in response to anesthesia and surgical stress. METHODS: The effects of a standardized surgical stress on the APR in pigs under general anesthesia with sodium pentobarbital and ketamine hydrochloride was investigated. Acute phase gene transcription was assayed in nuclei from serial liver biopsies obtained before and after 2.5 h of surgical stress, and after endotoxin administration. Tumor necrosis factor and IL-6 mRNA levels in this liver tissue were examined by Northern blot hybridization, and simultaneous plasma levels of these cytokines were measured using bioassays. RESULTS: The transcription rates of three positive acute phase genes--chymotrypsin inhibitor, inter-alpha-trypsin inhibitor and beta-fibrinogen--increased seven-, six-, and twofold, respectively (P < 0.05), and the transcription rate of albumin, a negative acute phase gene, decreased to 34% of baseline (P < 0.01) during the 2.5 h of anesthesia and surgical stress. During this initial 2.5 h, plasma concentrations of TNF and IL-6 did not change. Hepatic IL-6 mRNA expression was never observed, and TNF mRNA expression was undetectable in six of seven pigs. Subsequent 10-micrograms/kg endotoxin administration caused 20- and 100-fold increases in plasma concentrations of TNF and IL-6, respectively (P < 0.01), and were associated with substantial hepatic expression of the TNF and IL-6 mRNAs. These increments in cytokines were not associated with any further increase in the acute phase gene transcription rates. Thus, the APR was initially regulated at the transcriptional level during surgical stress independent of, and not augmentable by, an endotoxin-provoked increase in either plasma levels or hepatic mRNA expression of TNF or IL-6. CONCLUSIONS: Surgical stress induced hepatic acute phase gene transcription within 2.5 h in the absence of either systemic or local (hepatic) increases in TNF or IL-6. Subsequent endotoxin-induced increases in TNF or IL-6 did not alter this surgical stress-induced acute phase gene transcription.

Acute-Phase Proteins↗
PubMed1993

The pathogenesis of biliary atresia: a morphological study of the hepatobiliary system and the hepatic artery.

Specimens of the extrahepatic biliary trees and wedge liver biopsies were studied in 11 cases of biliary atresia. The hepatic arteries at the porta hepatis were examined with ultrasound in five of the 11 cases. The basic histopathological features were found to be epithelial damage and an inflammatory, sclerosing change of both the intrahepatic and the extrahepatic biliary trees, combined with an arteriopathy manifesting as hyperplasia and hypertrophy of the hepatic arteries in all cases. Based on the results of ultrasonography and histological examination, this arteriopathy was thought to affect the arteries from the trunk of the common hepatic artery to its peripheral branches supplying the entire biliary tree. To determine whether these morphologically abnormal hepatic arteries are related to the pathogenesis of biliary atresia in association with abnormal blood flow and pressure requires further investigation.

Biliary Atresia↗
PubMed1993

Peptide histidine methionine in cerebrospinal fluid of patients with senile dementia of the Alzheimer type.

Immunoreactivities (IRs) of peptide histidine methionine (PHM) as well as somatostatin and vasoactive intestinal peptide (VIP) in the cerebrospinal fluid (CSF) were measured in patients with senile dementia of the Alzheimer type (SDAT) and age-matched control subjects. We found statistically significant reductions in the PHM-IR and somatostatin-IR levels in the CSF from patients with SDAT, as compared with those of the controls. However, the VIP-IR level in the CSF from SDAT was not different from that of the controls. These results suggest that selective degeneration of neurons containing somatostatin and PHM or the alteration in metabolism of PHM in the CSF might occur in SDAT.

Aged↗
PubMed1993

Spontaneous amyloidosis in senile NSY mice.

Senile Nagoya, Shibata, Yasuda (NSY) mice developed amyloidosis and died from renal failure as a result of amyloidosis. NSY mice were first reported as experimental congenital diabetic mice by Shibata et al. in 1980. This study questioned whether NSY mice died from diabetic nephropathy. The authors of the present study investigated the life span and cause of death in these mice. The life span of NSY mice was found to be 618.7 +/- 72.5 days. NSY mice that lived for more than 400 days showed rising blood urea nitrogen and large amounts of amyloid deposits in the glomerulus of the kidneys. NSY mice died of renal amyloidosis. Immunological methods revealed that AApoAII was evident in the amyloid deposits of NSY mice. Apart from the kidneys, amyloid deposition was also found in the tongue, esophagus, stomach, small intestine, large intestine, rectum, lung, heart and adrenal glands. Amyloid deposits were found to a slight degree in the liver and the spleen. The most dominant amyloid deposition in NSY mice was seen in the glomerulus of the kidneys. From the point of view of amyloid depositional distribution, NSY mice were unique compared with other spontaneous amyloid mice.

Amyloidosis↗
PubMed1993

Presynaptic alpha 2 adrenoceptors inhibit glutamate release from rat spinal cord synaptosomes.

The presynaptic regulation of amino acid release from nerve terminals was investigated using synaptosomes prepared from the rat spinal cord. The basal releases of endogenous glutamate (Glu), aspartate (Asp), and gamma-amino-butyric acid (GABA) were 34.6, 21.5, and 10.0 pmol/min/mg of protein, respectively. Exposure to a depolarizing concentration of KCl (30 mM) evoked 2.7-, 1.5-, and 2.9-fold increases in Glu, Asp, and GABA release, respectively. Clonidine reduced the K(+)-evoked overflow of Glu to 56% of the control overflow with a potency (IC50) of 17 nM, but it did not affect K(+)-evoked overflow of Asp, GABA, and their basal releases. Similarly, noradrenaline inhibited the K(+)-evoked overflow of Glu, although phenylephrine and isoproterenol showed no effect. The inhibitory effect of clonidine was counteracted by alpha 2-adrenoceptor antagonists, rauwolscine, yohimbine, and idazoxan, regardless of the imidazoline structures. Because Glu is considered a neurotransmitter of primary afferents that transmit both nociceptive and nonnociceptive stimuli in the spinal cord, these data suggest that part of Glu release may be regulated by the noradrenergic system through alpha 2 adrenoceptors localized on the primary afferent terminals.

Adrenergic alpha-Agonists↗
PubMed1993

Cellular mechanism of U78517F in the protection of porcine coronary artery endothelial cells from oxygen radical-induced damage.

1. The aim of this study was to clarify the role of lipid peroxidation in cellular injury as assessed by lactate dehydrogenase (LDH) release from cultured coronary artery endothelial cells of the pig. Cells exposed to H2O2 at concentrations of 0.1 to 20 mM or to a xanthine and xanthine oxidase (X/XO) reaction mixture released LDH into the medium. Significant release from X/XO-treated cells took place with a delay of 2 h. 2. Superoxide dismutase (SOD), catalase or dimethylthiourea attenuated the release of LDH from X/XO-treated cells. Similarly the putative inhibitor of lipid peroxidation, U78517F attenuated the release of LDH by X/XO with an IC50 of 0.08 microM. 3. H2O2 was continuously produced by the addition of X/XO to the medium alone. However, in the presence of endothelial cells, H2O2 was eliminated at 1 h. U78517F had no effect on either process. 4. The oxygen radical-induced release of LDH was associated with malondialdehyde (MDA) formation. U78517F inhibited the formation of MDA with an IC50 of 0.27 microM. 5. Reduction of the Ca2+ concentration in the incubation medium from 1.6 mM to 0.016 mM markedly attenuated the release of LDH from endothelial cells. Nifedipine (1 microM) did not attenuate the LDH release from the cells. 6. It is likely that porcine coronary artery endothelial cells can be thus injured by oxygen radicals presumably through hydroxyl radicals formed and consequent lipid peroxidation, and that the extracellular Ca2+ concentration plays an important role in the genesis of such endothelial cell damage.

Animals↗
PubMed1993

Continuous hematocrit monitoring method in an extracorporeal circulation system and its application for automatic control of blood volume during artificial kidney treatment.

A two-frequency electrical conductivity method for measuring hematocrit has been developed for use in the continuous monitoring of circulating blood volume during artificial kidney treatment. Using this method, an algorithm for programmed control of blood volume also has been developed. This hematocrit measurement method is based on the beta-dispersion of blood conductivity, and the values measured during hemodialysis are in good agreement with the laboratory hematocrit values obtained by a Coulter counter. Programmed control of blood volume was used 29 times on 11 patients undergoing long-term dialysis. In each case, the blood volume was maintained within 2.5% of the desired level, and stable control was achieved even with disturbances caused by eating, change in body position, and so on. These methods can be used to study the relationship between blood volume and dialysis-induced hypotension during artificial kidney treatment and to achieve adequate ultrafiltration without clinical adverse effects.

Blood Volume↗
PubMed1993

[A clinical study of chronic lower respiratory tract infections with Pseudomonas aeruginosa by transtracheal aspiration].

We investigated the yearly changes of the incidence of Pseudomonas aeruginosa (P. aeruginosa) isolated from chronic lower respiratory tract infections (CLRTI), and also performed a clinical study on CLRTI with P. aeruginosa by transtracheal aspiration (TTA) to clarify the recent trend of P. aeruginosa infection in CLRTI and the predisposing clinical factors to the acute exacerbation. The isolation rate of P. aeruginosa among the total isolated bacteria in CLRTI between December 1978 and March 1983 was 8.4%, but it increased to 23.1% between April 1988 and March 1993. In 69 episodes (40 cases) of P. aeruginosa isolated from CLRTI between April 1983 and March 1993, monomicrobial infections of P. aeruginosa were 42 episodes (60.9%) and polymicrobial infections were 27 episodes (39.1%). When the diseases were classified into acute exacerbated and non-exacerbated phases, polymicrobial infections were seen more in the former phase, and the principal organisms detected with P. aeruginosa were Haemophilus influenzae and Streptococcus pneumoniae. In the acute exacerbated cases, predisposing conditions concerning the exacerbation were divided into four patterns: 1. polymicrobial infections with H. influenzae or S. pneumoniae, 2. after acute upper respiratory tract infections due to viral superinfection, 3. early phase from bacterial replacement by P. aeruginosa, 4. immunocompromised states such as adrenal corticosteroid administration or systemic underlying diseases. These results suggest that the importance of P. aeruginosa in CLRTI is increasing year by year and we must pay attention to the fact that P. aeruginosa alone may also cause acute exacerbation in the latter 2 patterns of the condition.

Adult↗
PubMed1993

[Clinical study of anaerobic respiratory infection].

This clinical study involved 35 cases, anaerobic bacteria were detected by TTA (transtracheal aspiration) or percutaneous lung aspiration, or pleural puncture. These cases were treated over the last 8 years in our department. There were 9 empyema, 9 pneumonitis, 5 lung abscess, 1 necrotizing pneumonia and 11 chronic lower airway infection. In 13 cases (37%), anaerobic bacteria alone were detected, whereas both anaerobic and aerobic bacteria were observed in the other 22 cases (63%). Of all bacteria detected. Bacteroids and Peptostreptococcus were the most common. With respect to host factors involved in the pathogenesis of pleural and parenchymal infection, aspiration was though to be a major trigger in only 11 out of the 24 cases (46%). The other 13 cases (54%) showed no evidence of aspiration, indicating that some other triggers was responsible. In further study, these 13 cases were found either to be heavy smokers with Brinkman index of more than 600, or to show sign of chronic lower airway infection. Both conditions were characterized by an inhibition of the mucociliary transport in the lower airway. Therefore, this study suggested that in the case without apparent aspiration the failure of local defense mechanisms in the airway, as a result of heavy smoking and/or chronic lower airway infection are involved in the pathogenesis of anaerobic respiratory infection.

Adult↗
PubMed1993

[Clinical study of acute bacterial bronchitis].

Eighty-two episodes (77 cases) in which any pathogens were isolated from transtracheal aspiration (TTA) and which satisfied the new clinical criteria of acute bacterial bronchitis were clinically evaluated. Major pathogens isolated from TTA included H. influenzae, S. pneumoniae and B. catarrhalis. Fever developed in 91.5% of the patients. Sputum volume averaged 16.3 +/- 14.9 ml per day. All the patients suffered from coughs, which were so severe as to disturb sleep in 8.5% of the patients. Inflammatory indices included WBC 9738.0 +/- 3158.5/microliter, CRP 10.1 +/- 7.9 mg/dl and ESR 69.0 +/- 38.8 mm/hr on average, PaO2 fell in most cases. Compared to the group of patients with acute bacterial bronchitis from which a single pathogen was isolated, the numbers of elderly patients and smokers were significantly more in the group of multiple pathogens isolated from TTA. Prior episodes related to the development of acute bacterial bronchitis were upper respiratory inflammation in 46.3% and undergoing bronchoscopy in 4.9% of the patients. Antibiotics therapy cured acute bacterial bronchitis in 96.3% of the patients. In spite of treatment, 3 patients developed pneumonia and died.

Acute Disease↗
PubMed1993

[Pneumonia due to respiratory syncytial virus diagnosed by transtracheal aspiration in an adult].

A healthy-looking 44-year-old female was admitted to our hospital complaining of fever and hemosputum. The chest roentgenogram on admission showed patchy infiltrates of the segment 3 and 8 of the right lung. Laboratory studies showed a leukocyte count of 9700/microliters, erythrocytes sedimentation rate of 55 mm/hour and C reactive protein of 8.7 mg/dl. The arterial PO2 was 71.9 torr while the patient was breathing room air. Transtracheal aspiration was performed on admission, and strains and culture for bacteria, acid fast bacilli, fungi and mycoplasma were negative. Respiratory syncytial virus was isolated from transtracheal aspirates. The RSV complement fixing antibody titers rose from 1:40 to 1:16. She became afebrile on the fourth day after admission and her chest roentgenogram improved gradually. RSV infection should be considered in the differential diagnosis of atypical adult pneumonias.

Adult↗
PubMed1993

[Effect of erythromycin on production of cytotoxin and attachment factors of bacteria].

We studied the effect of erythromycin (EM) on the attachment of Pseudomonas aeruginosa and Neisseria gonorrhoeae to HeLa and HT-177 cell and on cytotoxin production of P. aeruginosa. 1. EM inhibited attachment of these bacteria. 2. EM inhibited manifestation of the pili of these bacteria. 3. EM inhibited production of protein II, the second attachment factor of N. gonorrhoeae. 4. EM inhibited production of 66 K cytotoxin of P. aeruginosa. On the basis of these findings, it was suggested that EM might inhibit infection by repressing manifestation of the attachment factor and production of cytotoxin of the bacteria.

Bacterial Adhesion↗
PubMed1993

[Determination of neutrophil function in the respiratory infection by chemiluminescence (CL). I: Change in neutrophil's CL by chemotherapy against the bacterial pneumonia].

We measured neutrophil's CL (CL-index) in 12 patients of the bacterial pneumonia three times per each case: before, during and after chemotherapy. Before the initiation of chemotherapy. CL-index in the six patients remained higher than that in healthy controls, while the remaining six showed lower levels of CL-index compared to the controls. In the 11 cases, their CL-indexes fell to levels lower than those obtained before treatment. Additionally, in the 11 cases their CL-indexes increased after the termination of chemotherapy. Furthermore, in the nine cases the product of the neutrophil number and CL-index was decreased by chemotherapy, and the decrease in the product correlated with improvement in their clinical conditions.

Adolescent↗
PubMed1993

Effect of smoking on pleural thickening in asbestos workers.

It is well known that an interaction exists between smoking and exposure to asbestos in the occurrence of lung cancer, whereas occurrence of malignant mesothelioma has not been related to smoking. In the case of pleural thickening related to asbestos, there is a disagreement in previous studies as to the effect of smoking. This could be because the diagnosis of pleural changes has a subjective element. Taking this into account, in the present work the maximum width of the pleura was used as an index of pleural changes. Study subjects were 134 asbestos workers of a brake manufacturing company who had received medical checks in 1978 and in 1990. The maximum width of the pleura on the chest x ray films of the workers was measured by two examiners who did not know the year of examination or smoking state of the worker. A general linear model was applied to analyse the effects of smoking, the year of examination, age, and duration of exposure to asbestos. The difference between maximum widths measured in 1978 and 1990 suggested chronological progression. The increase in width during the 12 years, however, did not differ significantly between smokers and nonsmokers. This suggests that smoking does not significantly increase pleural thickening in asbestos workers.

Aged↗
PubMed1993

Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin.

Endocardial endothelium is reported to modulate myocardial contraction by releasing diffusible factors, but the nature of the agent(s) responsible is unknown. In the present study we investigated the potential role of endothelin in these effects. Cultured sheep endocardial endothelial cells were found to express endothelin-1 mRNA and to release endothelin-1 into superfusing solution. This superfusate induced positive inotropic effects in isolated rat cardiac myocytes, associated with an increase in the cytosolic Ca2+ transient. Similar positive inotropic effects were induced by vascular endothelial cell superfusate as well as by synthesized endothelin-1, administered at concentrations similar to those present in the superfusate. Incubation of endocardial endothelial cell superfusate with endothelin-1-specific antiserum reduced the free endothelin-1 concentration to undetectable levels and abolished both the positive inotropic effect and the rise in cytosolic Ca2+. These findings indicate that endocardial endothelial cells may modulate myocardial contraction in part through the release of endothelin-1 and suggest that endocardial as well as vascular endothelium could exert potent paracrine effects on myocardium.

Animals↗