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Biomedical subjects

Y Oka

Publications and source records attributed to Y Oka.

At least 433 records · Page 24Linked to original sources
PubMed1989

[Direct percutaneous transluminal coronary angioplasty (PTCA) for treatment of acute myocardial infarction: comparison with PTCA immediately after thrombolysis].

We studied 73 patients with acute myocardial infarction (AMI) treated by percutaneous transluminal coronary angioplasty (PTCA) without thrombolysis (direct PTCA) and 52 patients with AMI treated by PTCA immediately after thrombolysis (PTCR + PTCA). The initial results, angiographic findings and preservation of ventricular functions of the direct PTCA group were compared with those of the PTCR + PTCA group. 1. The success rate of coronary recanalization was higher in the direct PTCA group than in the PTCR + PTCA group, but there was no statistical significance (89% vs 77%; p = NS). 2. Major complications occurred in 4.1% of the direct PTCA group and in 5.8% of the PTCR + PTCA group (p = NS). 3. The incidence of acute coronary reocclusion was higher in the PTCR + PTCA group than in the direct PTCA group (7.4% vs 22%; p less than 0.05). 4. Angiographic haziness at the dilated site following PTCA was seen more frequently in patients in the PTCR + PTCA group than in those of the direct PTCA group (43% vs 23%; p less than 0.05). 5. Patients with haziness at the dilated site had a significantly higher incidence of acute coronary reocclusion than did the patients without such haziness (28% vs 6.3%; p less than 0.05). 6. Left ventricular ejection fraction and regional wall motion were better preserved in the direct PTCA group than in the PTCR + PTCA group, but there was not statistical significance. It was suggested that direct PTCA is safe and can be performed with good success rates. It is superior to PTCR + PTCA in avoiding acute coronary reocclusion, and thus we supposed that the response of lesions to angioplasty may be altered by the administration of thrombolytic agents.

Adult↗
PubMed1989

[Effects of early myocardial reperfusion on left ventricular function in patients with acute myocardial infarction].

The effect of early myocardial reperfusion (within six hours after the onset of symptoms) on left ventricular (LV) function in 106 patients with acute myocardial infarction was studied. The subjects consisting of 26 with conventional therapy, 19 with percutaneous transluminal coronary recanalization (PTCR), 16 with percutaneous transluminal coronary angioplasty (PTCA) after PTCR, 32 with direct-PTCA and 13 with coronary artery bypass graft (CABG) were randomly observed after 1981. In these patients, left ventricular ejection fraction (LVEF), regional wall motion, end-diastolic pressure and the contractility index were measured as the indices of LV function. 1. Compared to the conventional therapy group, LVEF and regional wall motion improved significantly in all groups with reperfusion therapy except in the PTCR group. This LV function in patients with subtotal obstruction or good initial collaterals significantly improved compared to patients with total obstruction and no collateral circulation. Patients with a 75 percent or more residual stenosis after reperfusion therapy had significantly decreased LV function compared to those with residual stenosis of less than 75 percent. These findings support the potential role for reperfusion therapy in patients with acute myocardial infarction.

Aged↗
PubMed1988

Studies with antipeptide antibody suggest the presence of at least two types of glucose transporter in rat brain and adipocyte.

Three antipeptide antibodies were prepared by immunizing rabbits with synthesized short peptides corresponding to residues 215-226, 466-479, and 478-492 predicted from the cDNA of both the human hepatoma HepG2 and rat brain glucose transporters. All three antibodies were found to precipitate quantitatively the [3H]cytochalasin B photoaffinity-labeled human erythrocyte glucose transporter. Each antibody also recognized the rat brain protein of Mr 45,000 on immunoblots, and a similar molecular weight protein was labeled with [3H]cytochalasin B in a D-glucose-inhibitable manner, suggesting that this protein is glucose transporter. However, only up to 30% of the labeled rat brain glucose transporters were precipitated, even by repeated rounds of immunoprecipitation. In addition, these antibodies were observed to be unable to immunoprecipitate significantly the [3H]cytochalasin B-labeled rat adipocyte glucose transporter. Further, one-dimensional peptide maps of [3H]cytochalasin B-labeled human erythrocyte and adipocyte glucose transporters generated distinct tryptic fragments. Although Mr 45,000 protein in rat adipocyte low density microsomes was detected on immunoblots and its amount was decreased in insulin-treated cells, the rat adipocyte low density microsomes were much less reactive on immunoblots than the rat brain membranes in spite of the fact that the rat adipocyte low density microsomes contained more [3H]cytochalasin B-labeled glucose transporters. In addition, the ratio of cytochalasin B-labeled glucose transporter per unit HepG2-type glucose transporter mRNA was more than 10-fold higher in rat adipocyte than in rat brain. These results indicate that virtually all the human erythrocyte glucose transporters are of the HepG2 type, whereas this type of glucose transporter constitutes only approximately 30 and 3% of all the glucose transporters present in rat brain and rat adipocyte, respectively; and the rest, of similar molecular weight, is expressed by a different gene.

Adipose Tissue↗
PubMed1988

Enhanced synthesis and secretion of apolipoprotein E from sciatic nerves of streptozotocin-induced diabetic rats after injury.

To elucidate the pathogenesis of diabetic neuropathy, synthesis and secretion of apolipoprotein E (apo E) from sciatic nerves after injury was studied in normal and streptozotocin-induced diabetic rats. Seven, 14, 28, 45 and 59 days after making crush injury on sciatic nerves with concomitant administration of streptozotocin (50 mg/kg body weight), the nerves were taken out and incubated with [35S]methionine. The [35S]labeled apo E was precipitated with specific antiserum. The amounts of apo E secreted into medium by nerves of diabetic rats were 7 times greater than those of non-diabetic rats 7 days after injury. This enhanced secretion of apo E was relatively selective for this protein, since the ratio of the immunoprecipitable apo E to the TCA preciptitable protein in the medium increased in diabetic rats. Intriguing possibility deduced from these results is that the secretion of apo E is involved in the development of diabetic neuropathy.

Animals↗
PubMed1988

Cloning of a rabbit brain glucose transporter cDNA and alteration of glucose transporter mRNA during tissue development.

A full-length cDNA clone that codes for glucose transporter protein was isolated from a rabbit brain cDNA library by using synthetic oligonucleotide probe derived from the sequence of human glucose transporter cDNA. The coding region shared 93.2% nucleotide and 97.0% amino-acid similarities with those of human glucose transporter and 89.4% nucleotide and 97.4% amino-acid similarities with those of rat transporter. Northern blot analysis revealed that glucose transporter mRNA is most abundant in the placenta and that it is also abundant in the brain. The fat tissue, heart, liver, and skeletal muscle of adult rats contained a very small amount of mRNA, while heart, liver, skeletal muscle and kidney of fetal rats contained a very high amount of glucose transporter mRNA. These results suggest that this type of glucose transporter might be closely related with cell proliferation and tissue development.

Aging↗
PubMed1988

Vestibular ototoxicity following intratympanic applications of chlorhexidine gluconate in the cat.

Our previous studies have shown that the disinfectant chlorhexidine gluconate (CH) has an ototoxic effect on the cochlea following its topical application in the middle ear space. The purpose of the present investigation was to demonstrate morphologically if CH also has the potential to injure the vestibular organs in the inner ear and, if so, what structures are most strongly damaged. Nine cats were used for the study. The drug dose of CH and the number of its applications to the middle ear were the same as used in our previous study to produce middle ear injuries. In the 2% CH group of cats pronounced degeneration was found in afferent nerve endings and both types of sensory cells. These nerve terminals showed edematous dilatations and contained degenerated mitochondria. Highly dark-stained degenerated mitochondria were distributed in the sensory cells and the afferent nerve terminals in the 0.05% CH group, but these degenerative changes were much less than in the 2% CH group. No otolithic crystals or synaptic vesicles could be seen in the 2% CH group. The results from this study showed that CH as a disinfectant has an ototoxic effect on the labyrinthine vestibule in which the sensory cell-nerve ending complex is affected as the main target. Even when used in dilute clinical concentrations, vestibular disturbances are a likely complication if the drug solution flows into the middle ear through a perforated eardrum.

Administration, Topical↗
PubMed1988

Mucosal injuries following intratympanic applications of chlorhexidine gluconate in the cat.

We investigated the morphological changes of the middle ear mucosa of the cat exposed to two different concentrations of the disinfectant, chlorhexidine gluconate. In the high concentration (2%) group, notable destructive changes were found on the mucosal surfaces in the tympanic cavity and were especially most severe in that area lined with few ciliated cells under normal conditions. Cilia were twisted and decreased in length in this site. At the tympanic orifice of the eustachian tube, cilia were distributed densely and showed little destructive changes on the surface. In the clinical concentration (0.05%) group, mucosal injuries generally seemed more slight when compared with those in the high concentration group. However, a decrease in the number of cilia or actual loss of cilia was one of the features in this group. Infrequent defects of the superstructures of the epithelial cells were noted on the mucosal surface, but these injuries appeared to spare the basal lamina. In both groups, there were no calcified pathologies seen and no complete obliterations by thickened mucosa or granulations. Deterioration of the ciliary system by chlorhexidine gluconate seems to produce subsequent cell destruction of the middle ear mucosa.

Animals↗
PubMed1988

Epidermal growth factor in the mouse kidney: developmental changes and intranephron localizations.

The developmental changes in epidermal growth factor (EGF) have been studied in tissue homogenates, kidney slices, and microdissected nephron segments of the mouse. Immunoreactive EGF concentration per milligram of protein increased in the kidney by about 20-fold from 1 week to 3 weeks of life, reaching the highest levels between 5 and 7 weeks, and decreasing by 10 weeks of life. The time course of the changes was different from those of submaxillary and urinary EGF. Above 7 weeks of age, kidney EGF was higher in female than in male mice. Among various zones of the kidney (outer cortex, inner cortex, outer medulla I, II and papilla), the outer medulla I and II contained the highest quantities of EGF per gram of wet tissue. The highest EGF content per millimeter length was observed in the medullary and cortical thick ascending limbs of Henle's loop. The amounts exceeded by about 4.5-fold those found in glomeruli and in proximal convoluted and proximal straight tubules, and by about 3-fold those present in distal and collecting tubules. Unilateral nephrectomy resulted in no significant changes in EGF levels in the contralateral kidney. The results suggest that the ontogeny of kidney EGF is different from that of the EGF found in the submaxillary gland, and that there is nephron heterogeneity in EGF content.

Animals↗
PubMed1988

Class switching from gamma 3 to gamma 2b in a murine pre-B cell line.

Class switching from gamma 3 to gamma 2b production at pre-B cell stage was observed in an Abelson virus-transformed murine immature cell line that is able to perform VH to DJH recombinations followed by class switch recombinations. A series of Southern blotting experiments indicates that the class switching from gamma 3 to gamma 2b was mediated by the deletion mechanism of the intervening CH genes on the expressed chromosome and that the break points in the switch recombinations might be different from each other among six independent switching events from gamma 3 to gamma 2b. This in vitro switching system should provide us with much information on the mechanisms of class switch recombination.

Abelson murine leukemia virus↗
PubMed1988

An analysis of the macronuclear actin genes of Oxytricha.

We have cloned and sequenced a 1.6-kb macronuclear molecule encoding actin from the hypotrichous ciliate Oxytricha nova. High-stringency Southern hybridization to native and digested macronuclear DNA shows that there is only one 1.6-kb actin-encoding molecule in O. nova. The 227-nucleotide 5' leader sequence contains AT-rich stretches punctuated by short GC regions. The AT-rich regions contain TATA-like sequences. However, other known eukaryote transcription regulatory sequences were not found. The 249-nucleotide 3' trailer sequence is also AT-rich and does not contain any obvious known eukaryotic mRNA processing signals. Sequence comparison with a closely related species, O. fallax, shows an 87% sequence similarity in the coding regions and an almost total lack of similarity in the noncoding regions of the molecules. However, a few small sequence similarities and motifs appear in the noncoding regions of the actin-encoding molecules of these two species. The actin-encoding molecule of O. nova could encode a polypeptide 374 amino acids long, the same size as some vertebrate cytoplasmic actins. Contrary to a previous report, we show that the actin-encoding molecule of O. fallax also codes for a polypeptide 374 amino acids long.

Actins↗
PubMed1988

Exchange blood transfusion for acute hepatic failure: its limited availability depending on the type of injury in rats.

The efficacy of exchange blood transfusion for acute hepatic failure was evaluated using rats. Rats receiving a dose of carbon tetrachloride died later than 24 h after dosing. When their blood was replaced with blood from normal rats at 24 h, survival time was prolonged, and hepatic protein synthesis was enhanced at 36 h with improved prothrombin time (PT). Those rats surviving 120 h showed better histological grade of recovery from injury after treatment. In contrast, dimethylnitrosamine (DMN)-intoxicated rats showed no such improvement in survival time or PT. In rats given a nonfatal dose of carbon tetrachloride, serum glutamic-pyruvic transaminase values were five times higher than those in rats given DMN despite similar maximal PT. The benefit of exchange transfusion for acute hepatic failure may differ depending on the mechanism of development in rats. Enhanced hepatic protein synthesis may contribute to its effect.

Acute Disease↗
PubMed1988

Reflow of obstructed capillaries in the maculae of humans with diabetic retinopathy, observed by fluorescein angiography.

As diabetic retinopathy progresses, the non-perfused area in the retina gradually enlarges as the capillaries are obstructed. To elucidate the process of capillary obstruction we examined macular capillaries in 104 diabetics, using fluorescein angiography. The follow-up period was three to eight years. We found that some capillaries in the macular were obstructed, then became unobstructed. Reflow of blood into the macula after the obstruction was observed in nine patients (8.7%). The time between obstruction and reflow varied from two months to four years. There were four cases of simple, three of preproliferative, and two of proliferative retinopathy. Reflow in the capillaries was confirmed as occurring at the same position and in vessels with the same diameter as seen before the obstruction. There was no leakage of the fluorescein dye from the capillary where reflow took place. We tentatively conclude that one of the causes of this phenomenon is a functional obstruction.

Adolescent↗
PubMed1988

Intravascular coagulation in acute liver failure in rats and its treatment with antithrombin III.

Liver damage was induced in rats by injection of dimethylnitrosamine (DMN) or carbon tetrachloride (CCl4). Fibrin clots were observed in the hepatic sinusoids at 12 hours and soluble fibrin monomer complexes were markedly detected at 24 hours only in the rats given DMN. When antithrombin III concentrate was infused at 12 hours there was a dose dependent improvement of the values of serum total bilirubin, SGPT, prothrombin time, peripheral platelet count, and plasma fibrinogen and coagulation factor VIIIC and of the histological degree of liver injury at 24 hours in the DMN group. The CCl4-group showed no such improvement. Intravascular coagulation may complicate the course of certain types of acute liver injury and contribute to its aggravation in rats. Under such circumstances, treatment with antithrombin III concentrate would be beneficial.

Animals↗
PubMed1988

Glucagon and insulin for the treatment of hepatic failure in dimethylnitrosamine-intoxicated rats.

When rats received dimethylnitrosamine every 24 h until death, plus hormone treatment after the first 24 h, the survival was enhanced between 100 and 140 h compared with the control rats, with attenuated derangements of prothrombin time and serum albumin levels at 120 h. In rats given a single dose of dimethylnitrosamine, hepatic DNA synthesis peaked at 48 h. The synthesis was increased after hormone treatment when started immediately, but not when delayed for 24 h. Hormone treatment for 3 days starting 24 h after a single dose of dimethylnitrosamine produced a rapid normalization of decreased hepatic protein content on day 9, although hepatic DNA content was not affected. These results suggest that this treatment is effective for hepatic failure, and the promotion of restoration of liver function is a contributing factor to its effect, in addition to the stimulation of hepatocyte proliferation.

Animals↗