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Biomedical subjects

M Ando

Publications and source records attributed to M Ando.

At least 541 records · Page 30Linked to original sources
PubMed1995

Interleukin-13 selectively suppresses the growth of human macrophage progenitors at the late stage.

Interleukin-13 (IL-13) is a pleiotropic cytokine that inhibits the production of inflammatory cytokines of monocytes. We investigated the effects of IL-13 on the clonal growth of human hematopoietic progenitors. IL-13 alone did not support any colony formation. IL-13 markedly suppressed macrophage colonies that were formed in the presence of IL-3 and erythropoietin, granulocyte-macrophage colony-stimulating factor, or macrophage colony-stimulating factor. Macrophage colony cells showed dendritic cell-line morphology and cellular aggregates. IL-13 did not affect granulocyte colony and erythroid burst formation. Delayed addition of IL-13 and replating onto the culture dishes with IL-13 showed that macrophage colony formation was suppressed during days 8 and 14 of culture. These results indicate that IL-13 affects the growth of the late stage of committed macrophage progenitors. Single-cell culture of isolated CD34+CD33+ cells with IL-13 confirmed that macrophage colony formation was significantly suppressed. These results show that IL-13 directly suppresses the proliferation of differentiating macrophages. In addition, these suppressive effects of IL-13 were synergistic with IL-4. Furthermore, in the liquid culture of bone marrow cells in the presence of IL-13, the number of CD14 (monocyte-macrophage antigen)-positive cells decreased and CD18 (LFA-1 beta)-positive cells increased. It is concluded that IL-13 affects the growth of the late stage of macrophage precursors as well as mature monocytes. Induction of differentiation of human monocytes may be correlated with the suppression of their progenitors.

Bone Marrow Cells↗
PubMed1995

Secondary amyloidosis with severe autonomic dysfunctions.

A 46-year-old male underwent hemodialysis because of progressed glomerulo-nephritis. Since he suffered from severe diarrhea during the course of the illness, both gastric and colon biopsies were performed. Significant amyloid deposition was recognized in the submucosal layer of these specimen. This amyloid was positive for anti-AA-protein antibody staining and soluble in KMnO4 solution, indicating secondary induced amyloid. Despite of absence of orthostatic hypotension, examinations revealed extreme reduction in tears and salivary secretion, anhidrosis, a decrease in the coefficiency of variation of the cardiographic R-R interval, and a decrease in the accumulation of [123I]meta-iodobenzylguanidine (MIBG) in the heart, suggesting that severe glandular and visceral autonomic dysfunctions had occurred in the patient.

3-Iodobenzylguanidine↗
PubMed1995

Mitochondrial DNA mutation and muscle pathology in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes.

We sought a relationship between abnormalities of mitochondrial DNA (mtDNA) and muscle pathology in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) at the single fiber level, using histochemistry, in situ hybridization, and single fiber PCR. Most type 1 ragged-red fibers (RRF) showed positive cytochrome c oxidase (COX) activity at the subsarcolemmal region, while type 2 RRF showed little COX activity. However, there was no difference in the amount of total (mutant and wild-type) mtDNAs and the proportion of mutant mtDNA between type 1 RRF and type 2 RRF. These observations suggest that mitochondrial proliferation and nuclear factors affect muscle pathology, including COX activity, in MELAS. Total mtDNAs were greatly increased in RRF. The proportion of mutant mtDNA was significantly higher in RRF than in non-RRF. The amount of both wild-type and mutant mtDNAs was increased in RRF in MELAS, which fact does not support the contention of a replicative advantage of mutant mtDNA. The proportion of mutant mtDNA was significantly higher in the strongly succinate dehydrogenase-reactive blood vessels (SSV) than in non-SSV. The similar morphological behavior in these vessels and fibers suggests that increased mutant mtDNA is responsible for mitochondrial proliferation and dysfunction in both tissues. It seems likely that systemic vascular abnormalities involving cerebral vessels lead to the evolution of strokelike episodes in MELAS.

Arteries↗
PubMed1995

Somatostatin-, vasoactive intestinal peptide-, and granulin-like peptides isolated from intestinal extracts of goldfish, Carassius auratus.

Three new peptides were originally isolated from intestinal extracts of goldfish. They were structurally related with somatostatin, vasoactive intestinal peptide (VIP), and granulin (GRN) and thus termed goldfish somatostatin (gSS-28), gVIP, and gGRN, respectively. The primary structures of these peptides were determined as: SVESSNHLPA 10RERKAGCKNF20YWKGFTSC for the gSS-28; HSDAVFTDNY10SRYRKQMAAK20KYLNSVLA-NH2 for the gVIP, and VIHCDSSTIC10 PDGTTCCLSP20YGVWYCCPFS30MGQCCRDGIH40CCRHGYHCDS50TSTHCLR for the gGRN. The amino acid sequence of the gSS-28 was more similar (79-86% similarity) to somatostatins obtained in anglerfish, flounder, and sculpin, but far (21% similarity) from the catfish somatostatin, whereas goldfish and catfish belong to the same superorder. The structure of the gVIP was closely related to that of the cod VIP; only one residue (Tyr13) being substituted for Phe13 in the cod VIP. Comparing amino acid sequences of VIPs obtained in various vertebrates, the primary structure of this peptide was revealed to be relatively well conserved among vertebrates. In addition, the dose-response curve for the effect of gVIP on the short-circuit current (Isc) across the eel intestine was similar to that of human VIP, suggesting that VIPs in vertebrates have similar effect. The amino acid sequence of gGRN was 96% identical to that of carp GRN-1; only two residues (Ser6-Ser7) being substituted for Ala6-Ala7 in the carp GRN-1. The physiological significance of these peptides is discussed.

Amino Acid Sequence↗
PubMed1995

Induction of rat liver drug-metabolizing enzymes by tetrachloroethylene.

The effect of tetrachloroethylene on Phase I and II drug-metabolizing enzymes in rat liver was examined. Rats were treated orally with tetrachloroethylene daily for five days, at doses of 125, 250, 500, 1,000 and 2,000 mg/kg. The higher doses (> 500 mg/kg) of tetrachloroethylene induced the hepatic microsomal 7-pentoxyresorufin O-depentylase and 7-benzyloxyresorufin O-debenzylase activities associated with the CYP2B subfamily. 7-ethoxyresorufin O-deethylase activity was also induced about 2-fold compared with that of control rats at 500, 1,000, and 2,000 mg/kg dose levels of tetrachloroethylene. However, 7-ethoxycoumarin O-deethylase and 7-methoxyresorufin O-demethylase activities were increased significantly at only the 1,000 mg/kg dose level of tetrachloroethylene (1.4- and 1.5-fold). Although other cytochrome P450-mediated monooxygenase activities such as nitrosodimethylamine N-demethylase, aminopyrine N-demethylase and erythromycin N-demethylase were also induced by tetrachloroethylene, the relative induction to control activity was lower than those of 7-pentoxyresorufin O-depentylase and 7-benzyloxyresorufin O-debenzylase. Western immunoblotting showed that the levels of CYP2B1 and CYP2B2 proteins in liver microsomes were increased at doses of 1,000 and 2,000 mg/kg of tetrachloroethylene. In addition to cytochrome P450-mediated monooxygenases, there was significant induction of the Phase II drug-metabolizing enzymes, DT-diaphorase, glutathione S-transferase activities towards 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene, and UDP-glucuronyltransferase activities towards 4-nitrophenol and 7-hydroxycoumarin. The results indicate that tetrachloroethylene induces both Phase I (CYP2B-mediated monooxygenase) and Phase II drug-metabolizing enzymes (DT-diaphorase, glutathione S-transferase and UDP-glucuronyltransferase) in the rat liver.

Administration, Oral↗
PubMed1995

Polymerase chain reaction fiber analysis and somatic mosaicism in autopsied tissue from a man with Duchenne muscular dystrophy.

Single muscle fibers, obtained at autopsy from a 22-year-old man with Duchenne muscular dystrophy were examined immunocytochemically and also using polymerase chain reaction (PCR). Dystrophin-positive cells were widespread in skeletal, cardiac, smooth muscle, and in brain cells. PCR and Southern blot analyses of DNA from peripheral blood lymphocytes revealed a deletion of exon 45 in the dystrophin gene. With PCR of single fibers, three bands corresponding to exons 44, 45, and 47 were present in the normal control muscle fibers and dystrophin-positive fibers from the patient, while only two bands, exons 44 and 47, were observed in dystrophin-negative fibers. Therefore, in this patient, the genotype of dystrophin-positive fibers differed from that of the dystrophin-negative fibers, possibly because of a somatic mosaicism for deletion in the dystrophin gene. A mutation of the dystrophin gene may have occurred in one cell at an early stage of ontogenesis.

Adult↗
PubMed1995

A histochemical and electron microscopic study of skeletal and cardiac muscle from a Fabry disease patient and carrier.

Histochemical and electron microscopic studies were performed in an attempt to clarify the muscle pathology in an 18-year-old man with Fabry disease, showing proximal limb muscle atrophy, and his 52-year-old mother, who is a Fabry carrier with hypertrophic cardiomyopathy. Despite the relatively mild myopathic changes revealed by histochemistry, electron microscopy demonstrated the widespread accumulation of abundant lamellated bodies in myofibers, associated with increased glycogen granules and autophagic vacuoles. The cardiac muscle of the proband's mother revealed a mosaic pattern of normal-appearing and hypertrophic myofibers containing a number of ring-like, lamellated bodies. Although further studies are necessary to support our findings, skeletal muscle is apparently involved in patients with Fabry disease, and a mosaic pattern of cardiac muscle involvement possibly reflecting Lyonization, may be one of the characteristic findings of a Fabry disease carrier.

Adolescent↗
PubMed1995

Immunohistochemical study of calpain and its endogenous inhibitor in the skeletal muscle of muscular dystrophy.

A calcium-dependent proteinase (calpain) has been suggested to play an important role in muscle degradation in Duchenne muscular dystrophy (DMD). In immunohistochemical studies, calpain and its endogenous inhibitor (calpastatin) were located exclusively in the cytoplasm in normal human muscles. The intensity of the staining was stronger in type 1 than in type 2 fibers. Quantitative immunohistochemical study showed an increase of calpain in biopsied muscles from the patients with DMD and Becker muscular dystrophy. Abnormal increases in calpain and calpastatin were demonstrated mainly in atrophic fibers, whereas necrotic fibers showed moderate or weak immunoreactions for the enzymes. Opaque fibers and hypertrophic fibers were negative. Not all dystrophin-deficient muscle fibers necessarily showed a strong reaction for calpain. We suggest that calpain may play an important role in muscle fiber degradation, especially in the early stage of muscle degradation in muscular dystrophy.

Adolescent↗
PubMed1995

Spontaneous dissecting aneurysm of the main trunk of the superior mesenteric artery: report of a case.

A 47-year-old man with a sudden onset of abdominal pain was diagnosed as having an aneurysm of the main trunk of the superior mesenteric artery (SMA), which induced ischemic colitis of the transverse colon probably because of a transient decrease in the SMA blood flow. The patient was successfully treated by resection of the aneurysm and an end-to-side anastomosis of the SMA to the aorta. A histological examination revealed a spontaneous dissecting aneurysm of the SMA.

Aortic Dissection↗
PubMed1995

The influence of ageing on cisplatin pharmacokinetics in lung cancer patients with normal organ function.

This study was performed to identify any relationship between age and cisplatin (CDDP) pharmacokinetics in lung cancer patients. CDDP was given at a dose of 80 mg/m2 by 1-h intravenous infusion to 23 lung cancer patients. All patients had normal renal, hepatic, and bone marrow functions. We measured ultrafilterable platinum (U-Pt) and total plasma platinum (T-Pt) using atomic absorption spectrometry. There was significant correlation between the age of the patients and U-Pt pharmacokinetic parameters such as the area under the plasma concentration versus time curve (AUC), total clearance (Cl), and peak plasma concentration (Cmax) as well as the AUC of T-Pt (P < 0.05). We performed univariate regression analysis to examine the influence of factors aside from age on the AUC of U-Pt and T-Pt. Creatinine and GPT levels were significantly related to the AUC of U-Pt, and creatinine clearance and creatinine concentrations were significantly related to the AUC of T-Pt. Therefore, stepwise multiple-regression models for the AUC of U-Pt and T-Pt were developed to assess an age effect. Age was consistently an independent and significant predictor of the AUC of U-Pt and T-Pt.

Adult↗
PubMed1995

Alteration of transglutaminase activity in rat and human spinal cord after neuronal degeneration.

We measured the activity of transglutaminase (TG), a Ca(2+)-dependent enzyme and a biochemical marker of cell degeneration, in the adult rat spinal cord after unilateral occlusion of a branch of the dorsal spinal artery, and compared it to the enzyme activity in the tissue on the contralateral side without ischemic damage. The affected half of the spinal cord showed a significant rise in intrinsic (endogenous) TG activity one day after ischemic insult while no apparent morphological changes were observed in the tissue. However, the enzymic activity on the affected side gradually decreased to reach the level in the non-affected tissue, accompanying severe degeneration of neuronal cells at 7 days after the surgery, then it declined to nearly half the level in the intact tissue 30 days after the operation. We also determined the TG activity in transverse sections of the human spinal cord obtained at autopsy from 5 amyotrophic lateral sclerosis (ALS) and 9 non-ALS patients. TG activity in thoracic and lumbar cords was markedly low in ALS patients not only in ventral and lateral regions but also in the dorsal portion. These findings imply that the reduced TG activity in the ALS spinal cord is one of the characteristic features of the disease reflecting exhaustion of the enzyme in the tissue resulting from degeneration of the spinal neurons through cross-linkage of soluble intraneuronal cytoplasmic proteins.

Adult↗
PubMed1995

In vitro investigation of a combination of two drugs, cisplatin and carboplatin, as a function of the area under the c/t curve.

The log/log relationship between the IC50 of cisplatin or carboplatin and the exposure time, determined by human tumor clonogenic assay (HTCA) and MTTAI (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay with additional incubation) using PC-14 cells, exhibited a straight line with a slope of -1, indicating that both drugs have AUC-dependent cytotoxicity (AUC, area under the c/t curve). The combined effect of cisplatin and carboplatin was estimated by the median-effect analysis using HTCA, and it was additive when the AUC ratio (AUC of free platinum from carboplatin/that from cisplatin) was low (3.2, 6.5 or 13.1 in each of PC-7, PC-9, PC-14, H-69, and K562). However, it was significantly worse at a higher AUC ratio (19.5 in PC-7, PC-9, and PC-14). The log/log relationship of each drug, determined by MTTAI using human bone marrow cells, showed that each drug exerts an AUC-dependent cytotoxicity on marrow granulocytes. When cisplatin and carboplatin were combined at an AUC ratio of 14, the therapeutic index was significantly better than that of carboplatin alone and less than that of cisplatin alone using K562, PC-9 and PC-14, indicating the usefulness of this combined therapy for tumor cells with high sensitivity to platinum compounds at this AUC ratio.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

Effects of antecedent anginal episodes and coronary artery stenosis on left ventricular function during coronary occlusion.

We evaluated the effects of antecedent anginal episodes and coronary artery stenosis on left ventricular function during coronary occlusion and the role of collateral filling in 33 patients with angina pectoris who underwent angioplasty. Wall motion abnormalities were investigated by echocardiography and classified into hypokinesia and akinesia. Collateral filling during angioplasty was evaluated by using a second artery catheter. Akinesia was observed as follows: 24% of the patients had > 30 anginal episodes, 38% had 5 to 30, and 87% of the patients had < 5 (p < 0.01); 12% of patients had a lesion of 99%, 47% had a lesion of 90%, and 83% had a lesion of 75% (p < 0.05). Akinesia was observed in none of the patients with grade 3 collaterals, 57% with grade 2, and 67% with grade 1 or 0 (p < 0.01). These observations suggest that the patients with antecedent frequent anginal episodes and severe coronary stenosis have less left ventricular dysfunction during coronary occlusion. This finding may be the result of more extensive collateral development.

Aged↗