[Intravenous sedation in dentistry. Use of intravenous sedation with flunitrazepam in dental treatment for handicapped patients].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Kishimoto.
Explore the source record for details and available documents.
Intensive proteinuria accompanied by marked renal enlargement occurs in rats bearing functioning pituitary tumor MtT SA5. Urinalysis showed that protein excretion was up to 700 mg/day, and that the excreted protein consisted mostly of albumin. However, serum total protein and albumin levels remained almost unchanged. Histological examination revealed glomerular lesions, hyaline casts in the tubules, and proliferation of the tubular epithelium. The glomerular lesions consisted of accumulation of proteinaceous material in the subcapsular space; its organization and formation of fibrous crescents was with or without epithelial crescents. Electron microscopy revealed loss of foot processes and accumulation of absorption droplets in glomerular epithelial cells. Removal of the tumor resulted in a rapid reduction in urinary protein excretion. However, proteinuria persisted for at least 4 weeks after tumor removal with levels of approximately one-fourth of those before tumor removal. Histological changes of the kidneys resolved to some extent but damage still remained in the glomerular epithelial cells 4 weeks after tumor removal. Although proteinuria in animals bearing functioning pituitary tumors has long been implicated in hyperprolactinemia, the present study suggests that proteinuria in tumor-bearing rats is a control mechanism for overproduction of albumin in the liver stimulated by elevated serum growth hormone since hyperalbuminemia and possibly the hyperfibrinogenemia would cause the elevation of blood viscosity, resulting in thrombosis, unless control mechanisms were present. This proteinuria may serve for studies of glomerular permeability disorders as a model for homologous protein-overload proteinuria.
To study the effects of ethanol and its metabolite on albumin metabolism, we examined the hepatic albumin synthesis and secretion in male Wistar rats in vitro, following acute and chronic ethanol administration. After acute ethanol administration, proalbumin synthesis in rat liver in vitro, declined to 47% of the control level at 4 hrs, the lowest level, and increased thereafter to slightly higher than the control level at 16 hrs. On the other hand, chronic ethanol administration for 4 weeks, increased proalbumin synthesis to 1.5 times that of the control level. In the acute ethanol group, a significant negative correlation was observed between proalbumin radioactivity and the concentration of hepatic ethanol and acetaldehyde. The variation between proalbumin radioactivity and hepatic ethanol concentration was wider than the variation between proalbumin and hepatic acetaldehyde. In the chronic ethanol group, ethanol was not detected in the liver. No significant differences from the proalbumin/albumin ratio were seen at any time point after acute or chronic ethanol administration. These findings suggest that the effects of ethanol on hepatic albumin synthesis differ with the method of ethanol administration, and acetaldehyde and/or ethanol is involved in the reduction in albumin synthesis, however, proalbumin-albumin conversion is not disturbed.
A case of unresectable advanced gastric cancer (portion A, Min, S3 infiltrating into pancreas, N3, por., Borrmann III-type, hen's egg size) was treated with cis-dichlorodiammine platinum (CDDP) at a dosage of 30 mg/day for five days every month following surgery. After three courses of administration, examinations revealed that the tumor had disappeared and an evaluation of complete response was made. Four months later, a second-look operation was performed. It was found that the cancer was less than thumbsize and was able to be resected radically. No significant side effects were observed during CDDP therapy.
Fatty acyl-CoA synthetase purified from rat liver microsomes was immobilized on either CNBr-activated Sepharose 4B or activated CH-Sepharose 4B, and the enzymatic activities of the syntheses of CoA esters from lignoceric acid (C24:0) and palmitic acid (C16:0) were studied and compared. The ratio of activities of the synthesis of lignoceroyl-CoA to palmitoyl-CoA increased 4.5 fold with CH-Sepharose, but only slightly with CNBr-Sepharose. The effects of a detergent and chaotropic agent on both substrates were significantly altered by the immobilization. The results of this study thus indicate that the stability and fatty acid specificity of fatty acyl-CoA synthetase are significantly affected by the physical state of the enzyme.
Myelin of several Caudata (Urodela) species appears to be unique in the fact that it lacks hydroxycerebrosides and hydroxysulfatides although it contains their non-hydroxy counterparts. Comparison of the nerve conduction velocities in the Urodeles Necturus (salamander) and Notophthalmus (newt) with that in a reptile, Anolis (chameleon) which contains hydroxycerebrosides and -sulfatides indicated that the values were significantly reduced in the urodeles. Furthermore, urodele myelin thickness remained uniformly the same regardless of the size of the nerve fiber. Despite these differences the myelins appeared structurally similar. Electron microscopic and X-ray diffraction studies did not disclose any structural difference between the two orders. A teased fiber technique established that the ratio of internodal distance and fiber diameter in urodele nerves was essentially similar to that in Anolis. These findings suggest that the absence of hydroxycerebroside and -sulfatide may be related to the reduction in nerve conduction velocity and unusual myelin thickness in the urodele nervous system.
As part of a long-term study of sphingolipid metabolism in brain, we have purified and partially characterized a long-chain acyl-CoA synthetase from microsomes of developing rat brain and compared it with the hepatic microsomal enzyme from the same animals. Both enzymes were solubilized from microsomes by treatment with Triton X-100 and then chromatographed successively on Blue-Sepharose and DEAE-Sepharose. Blue-Sepharose chromatography yielded a single peak with acyl-CoA synthetase activity, whereas DEAE-Sepharose chromatography of both brain and liver preparations yielded two peaks. Elution patterns of lignoceroyl-CoA synthetase and palmitoyl-CoA synthetase activities were identical throughout these steps and were similar in brain and liver. Gel filtration of each DEAE-Sepharose fraction on Sephadex G-200 also yielded two peaks of activity. The more rapidly eluted material contained much more lignoceroyl-CoA synthetase activity, while the activity for palmitoyl-CoA synthetase was higher in slower eluting peaks. In all preparations the ratio of lignoceroyl-CoA synthetase activity to palmitoyl-CoA synthetase activity was much higher in brain than in liver. These results suggest that although the brain acyl-CoA synthetase is chromatographically similar to the liver enzyme, there are differences in substrate specificity.
Phospholipid methylation is thought to modulate such vital cellular processes as calcium transport, receptor function, and membrane microviscosity. As these processes are fundamental to the function of muscle cells and are thought to be altered in disease states, we have characterized several features of phospholipid methylation reactions in skeletal muscle and have defined appropriate assay conditions. In rat leg muscle, methyltransferase activity was assayed radiometrically by measuring the incorporation of methyl groups from S-adenosyl-L-[methyl-3H]methionine into membrane phospholipids, the methylated derivatives of which were separated by thin-layer chromatography. Contrary to previous investigations of whole muscle, phospholipid methyltransferase activity was clearly present in skeletal muscle membranes, being highly localized in sarcoplasmic reticulum and present to a lesser extent in sarcolemma. Both the reaction products and the reaction kinetics were consistent with sequential methylation of phospholipids by two methyltransferase enzymes. S-adenosylhomocysteine and its analogues were potent inhibitors of phospholipid methylation in sarcoplasmic reticulum. The predominant localization of phospholipid methyltransferase activity in sarcoplasmic reticulum suggests that its functional role in skeletal muscle may be in calcium transport.
Galactocerebrosides and sulfatides are major characteristic components of vertebrate myelin. In contrast, glucocerebroside is the major glycosphingolipid of shrimp nerve. In this study, the concentrations of these glycosphingolipids in the nervous systems of animals from several evolutionary branches were determined by use of high-performance liquid chromatography. In nerves of protostome animals only glucose-containing glycosphingolipids were detected, whereas glycosphingolipids from deuterostomes contained predominantly galactose. Neither the glycolipids containing alpha-hydroxy fatty acids nor sulfate esters of the glycolipids, both of which always accompany galactocerebrosides in deuterostome myelin, were present in protostome nerves. This correlation suggests an evolutionary trend from gluco- to galactocerebrosides, which corresponds with changes in the nervous system from loosely structured membrane-enwrapped axons to multilamellar highly structured myelin.
As part of a systematic study of the evolution of the nervous system, the lipid composition of the ventral nerves of earthworms was examined. The nerve axons are wrapped in copious layers of loosely bound membrane, superficially resembling the myelin sheath of vertebrates. However, neither galactocerebroside nor sulfatide, both of which are considered to be markers for myelin, was present, and only traces of glucocerebroside, which is abundant in shrimp nerve, were detected. The lipids were rich in cholesterol (15.3 mumol/g of fresh tissue) and phospholipids (21.7 mumol/g of fresh tissue). The phospholipids were composed of phosphatidylethanolamine, -choline, -serine, and -inositol in the ratio of 41:44:8:7. Most of the ethanolamine-containing phospholipids were in the form of plasmalogens. The fatty acid moieties of these phospholipids were predominantly 18:1, 18:0, and 20:1, whereas the aldehyde moieties of plasmalogen were mostly 18:0. Sphingomyelin, which is considered a ubiquitous component of animal membranes, was not detected. How the unique structure of the membranes of earthworm nerves may be related to the function of the nervous system in this organism is discussed.
Non-obese diabetic (NOD) mice spontaneously develop diabetic signs akin to those of Type I diabetes in man. Insulitis, i.e., lymphocytic infiltration around and into the pancreatic islets is one of the characteristics of such mice. It is also the etiologic pathological lesion in the development of diabetes mellitus in NOD mice. Thus, we chose insulitis as a marker for genetic analysis of the development of diabetes mellitus in NOD mice and clarified the mode of its inheritance. In breeding studies between NOD and C57BL/6J mice, insulitis was not observed in the F1 and (F1 X C57BL/6J) backcross generations, but was found with incidences of 3.9% in females and 1.4% in males in the F2 generation and 23.7% in females and 12.1% in males in the (F1 X NOD) backcross generation. These incidences in the F2 and (F1 X NOD) backcross females corresponded approximately to 1/16 and 1/4 of the incidences of 89.7% in the NOD females, respectively. A similar relationship was observed between the F2 and (F1 X NOD) backcross males and the NOD males. When the gene expressivity of both sexes for a double recessive homozygote was assumed to be the incidences of insulitis in 9-week-old NOD females and males, respectively, the expected numbers of both sexes with and without insulitis in the F2 and backcross generations agreed well with the observed ones. These observations suggest that two recessive genes on independent autosomal chromosomes are necessary for the development of insulitis in NOD mice.
Catecholamines were measured in the amniotic fluid and in the first voided newborn urine obtained from appropriate-for-date infants of term deliveries. Catecholamine values in the amniotic fluid and urine were nearly equal when expressed in terms of creatinine. Significant positive correlations were observed between the amniotic fluid and urine of norepinephrine and epinephrine. In normal cases (n = 32) that underwent uneventful vaginal delivery, the 95% confidence limits for norepinephrine and epinephrine in the amniotic fluid were 1.53 to 2.33 ng/ml and 0.16 to 0.30 ng/ml, respectively. In cases of moderate stress (n = 12), only norepinephrine showed significantly higher values than the normal cases, while in cases of severe stress (n = 12), norepinephrine became more significantly high, and epinephrine was found to be elevated significantly. A significant difference was noted in the incidence of fetal stress between the infants with more than and those with less than 2.30 ng/ml of norepinephrine, the upper limits of the normal 95% confidence limits. However, for epinephrine such a significant difference was not noted. It was concluded that amniotic fluid catecholamines are of fetal origin and reflect fetal sympathoadrenal activity directly, even during labor, and that their level may be a good indicator of fetal condition and stress.
Syrian golden hamsters were administered 8-nitroquinoline, at a concentration of 0.05%, in a 10% ethanol solution as drinking water for 104 weeks. The animals were kept under observation until 112 weeks of age when the experiment was terminated. Both control and treated groups developed tumors in a pattern indistinguishable from that usually observed in Syrian golden hamsters. Thus the result of this experiment indicates that 8-nitroquinoline given orally at a concentration of 0.05% is not carcinogenic in Syrian golden hamsters.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Fasting serum bile acid (FSBA) was serially measured by a fluorescent enzyme method in a follow-up study of 61 patients with chronic liver disease. In chronic inactive hepatitis, fluctuation of FSBA was within the normal range in both the exacerbated state and in remission. In chronic active hepatitis, FSBA was abnormally elevated in both states, but the difference was not significant. In chronic active hepatitis where FSBA was elevated in the remission state above its value in the exacerbated state, exacerbation of the disease occurred repeatedly during the follow-up period. In compensated liver cirrhosis progressing into the decompensated form, FSBA levels increased before a decrease in the serum values of albumin, cholesterol, and cholinesterase, and an elevation of bilirubin. In liver cirrhosis, FSBA levels increased above 100 microM, 1-4 months before the appearance of ascites.
To elucidate the significance of adrenal medulla and brain catecholamines (CA) in perinatal adaptation, their developmental changes, responses to hypoxia and the relation between brain energy metabolism and secreted CA were investigated using fetal rats. The following results were obtained. Adrenal norepinephrine (NE) showed a gradual linear increase during the last week of gestation. Epinephrine (E) increased rapidly during the last 3 days to become predominant over NE. A gradual increase in brain NE was observed with advancing gestational age. In the term fetal rats, adrenal NE and E decreased significantly by 18.7% and 17.0% respectively after 30 minutes of hypoxia in utero. Brain NE decreased significantly during both hypoxia and recovery up to 60 minutes. The blood glucose levels were elevated markedly, reaching a peak at 30 minutes of recovery which corresponded to the peak of diminution of adrenal CA. The brain energy charge potential [(ATP) + 0.5(ADP)]/[(ATP) + (ADP) + (AMP)] fell significantly during hypoxia, followed by rapid recovery after hypoxia. It is concluded that matured fetal adrenal medulla responds to acute hypoxia, discharging both NE and E with sufficient reserve, and secreted CA plays an important role in maintaining the brain energy level during recovery after hypoxia. And the changes in brain NE content caused by hypoxia may be a causative factor in the neurological sequela of hypoxia.
The alpha-oxidation of [1-14C]phytanic acid of high specific activity was studied in postnuclear and various subcellular fractions from rat liver. alpha-Oxidation in the postnuclear fraction required ATP, Mg2+, nicotinamide, and molecular oxygen for activity. alpha-Oxidation was inhibited by iron-specific chelating agents and respiratory chain inhibitors. Partial inhibition by carbon monoxide indicated a possible involvement of cytochrome P-450. However, phenobarbital-treated rat liver postnuclear fraction did not stimulate phytanic acid alpha-oxidation above that of control. Subcellular fractionation indicated that in addition to the mitochondrial fraction, cytosol was required for activity. The cytosolic factor appeared to be dialyzable; it was inactivated by heat treatment, but not affected by trypsin digestion. NAD, CoA, ascorbic acid, and catalase did not replace cytosolic activity nor did the recently characterized heat-stable factors in brain hydroxylation, namely, adenosine nucleotides and glutamate.