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Biomedical subjects

T Takano

Publications and source records attributed to T Takano.

At least 631 records · Page 35Linked to original sources
PubMed1982

Long terminal repeat (LTR)-derived recombination of retroviral DNA: sequence analyses of an aberrant clone of baboon endogenous virus DNA which carries an inversion from the LTR to the gag region.

Nucleotide sequences of a cloned proviral DNA of baboon endogenous virus M7 were analyzed, which carried an internal inversion. The inversion of 2.2 kilobase pairs was occurred between the junction of two tandem LTRs and a site locating in the p30 region of the gag gene. The ATAA sequence was a target for recombination generating the inversion, which was duplicated at both ends of the inverted segment. AAA and CA were lost at the 5'- and 3'-ends of the LTRs by the inversion, respectively. On both sides of the target sequence, long AG-rich stretches were detected, which may specify the site of recombination together with the target sequence. The characteristic base changes in the inversion are concluded to result from an illegitimate recombination associated with LTRs, as well as in case of provirus integration into the host cell DNA. We propose and discuss models to explain the processes of recombination to generate both inversion and integration.

Amino Acid Sequence↗
PubMed1982

Retrovirus-related sequences in human DNA: detection and cloning of sequences which hybridize with the long terminal repeat of baboon endogenous virus.

Human DNA sequences which hybridized with the long terminal repeats (LTR) of baboon type C virus M7 were detected by non-stringent blot hybridization. About 7 to 10 discrete bands of the LTR-related sequences were commonly observed in the DNAs from four independent human cell lines after digestion with either Eco RI, Hind III or Bam HI. The amounts of these sequences were more abundant in tumor cell lines than in a non-malignant cell line. The human sequences related to the M7 LTR seemed to be located at relatively specific sites on the cell DNA. The human DNA clones which hybridized with M7 LTR were detected in the human DNA library described by Lawn et al. (Cell 15, 1157-1174, 1978), at a frequency of about 300 per haploid genome. Five clones were isolated which shared different extent of homology with M7 LTR and whose restriction maps were totally different one another. The DNA structures of two of them resembled the genome of retroviruses. These results suggest the presence of various types of the LTR-related sequences in human DNA: some of them might represent endogenous virus genomes of human cells.

Animals↗
PubMed1982

Restoration by cyclic AMP of the differentiated phenotype of chondrocytes from de-differentiated cells pretreated with retinoids.

Parathyroid hormone (PTH) increases the cyclic AMP level in rabbit costal chondrocytes in culture. PTH, dibutyryl cyclic AMP (DBcAMP), and 8-bromo cyclic AMP (8-Br cAMP)induce ornithine decarboxylase (ODC) and expression of the differentiated phenotype of chondrocytes in this cell system. On the other hand, retinoids inhibit expression of the differentiated phenotype of chondrocytes. In the present study, the effects of PTH, DBcAMP, and 8-Br cAMP on rabbit costal chondrocytes pretreated with retinoids were examined. PTH did not increase the cellular cyclic AMP level in de-differentiated cells that had been pretreated with retinyl acetate or retinoic acid for three days, but it did increase the cyclic AMP level four days after removal of retinoids. PTH did not stimulate ODC activity or expression of the differentiated phenotype of chondrocytes in the de-differentiated state. On the other hand, DBcAMP or 8-Br cAMP stimulated expression of the differentiated phenotype of chondrocytes even in de-differentiated cells, as judged by morphological and histological changes of the cells and increase in glycosaminoglycan synthesis. Cyclic AMP analogues also induced ODC in these cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

The molecular structure of d(ICpCpGpG), a fragment of right-handed double helical A-DNA.

The DNA tetramer d(ICpCpGpG) or ICCGG crystallizes as a double-stranded 4-base pair (bp) segment of an A helix. Two such tetramer helices are packed together in the crystal with local helix axes nearly coincident, simulating an 8-bp helix, and four such octamers make up the tetragonal unit cell. Restrained energy and reciprocal space refinement has led to an R factor of 20.5% at 2.1 A resolution. The ICCGG helix has a twist corresponding to 10.7 bp per turn, a 19 degree base tilt and a 2.3 A rise per base pair along the helix axis. The mean propeller twist of 18 degree is comparable with, and has the same rotational sense as that observed in the B-DNA dodecamer CGCGAATTCGCG at similarly high alcohol concentration. Backbone phosphate groups in A-DNA are extensively hydrated, including a network across the opening of the major groove, whereas base edge N and O groups in major and minor grooves are less hydrated than in B-DNA. The minor groove spine of hydration observed in B-DNA is totally absent. These observations of relative hydration confirm and extend the model for the B- to A- helix transition proposed earlier on the basis of the B helix structure.

Base Composition↗
PubMed1982

Overlapping genes in the heat-labile enterotoxin operon originating from Escherichia coli human strain.

We have determined the nucleotide sequence at the distal end of the heat-labile enterotoxin subunit A (LT-A) gene (toxA) originating from human enterotoxigenic Escherichia coli. The sequenced region covers the entire LT-A2 region and a part of the LT-A1 region. In confirming our previous prediction based on product analysis of clones toxA regions, the data suggest the overlapping of the distal end (5'-TTA TGA) of toxA with the proximal end (5'-ATG AAT) of the LT subunit B gene (toxB), in the sequences 5'-TTATGAAT. Some additional characteristics of the LT operon as well as of the products are discussed.

Amino Acid Sequence↗
PubMed1982

Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats.

Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less then 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5h and then the aortic blood pressure (BP) was reduced to 60-80 mm Hg by blood depletion and ganglion-blockage for 1h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilatation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.

Animals↗
PubMed1982

Tocofibrate (tocopheryl 2-(p-chlorophenoxy) isobutyrate); a new peroxisomotropic compound, and its hypocholesterolemic activity in cholesterol-fed rats.

The effect of tocofibrate (tocopheryl 2-(p-chlorophenoxy) isobutyrate) on cholesterol levels in rats fed a high-fat cholesterol diet was investigated. The efficacy of tocofibrate in reducing blood cholesterol levels was comparable to that of clofibrate, a compound with known hypocholesterolemic activity. To investigate further the mechanism underlying the action of tocofibrate, the intracellular distribution of the compound in liver was examined. The results indicate that the distribution of tocofibrate clearly differs from that of both clofibrate and alpha-tocofibrate is primarily associated with its effect upon liver peroxisomes.

Animals↗
PubMed1982

Identification and characterization of a proton pump on lysosomes by fluorescein-isothiocyanate-dextran fluorescence.

Fluorescein isothiocyanate-conjugated dextran was introduced preferentially into hepatic lysosomes by intraperitoneal injection into rats. The pH in isolated lysosomes, measured by fluorescein fluorescence, was approximately 5 and gradually increased in KCl (to 7.0) at 25 degrees C. In the presence of Mg2+, ATP caused acidification of lysosomes that was reversed by the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone. Mn2+, Co2+, and Fe2+ could replace Mg2+ but Ca2+ could not. Cu2+, Zn2+, and Cd2+ were inhibitory. A membrane-permeant anion, in practice chloride, was required for this acidification. ATP analogues, including 5'-adenylyl imidodiphosphate, could not be substituted for ATP. ATP-driven acidification was sensitive to N-ethylmaleimide and quercetin but insensitive to oligomycin, ouabain, and vanadate. There were some differences between "normal" lysosomes and tritosomes; the acidification was resistant to azide and N,N'-dicyclohexylcarbodiimide in normal lysosomes but sensitive to these reagents in tritosomes. These results provide evidence for the presence of an electrogenic proton pump driven by MgATP (H+-ATPase) on lysosomes.

Adenosine Triphosphate↗
PubMed1982

Acridine orange as a fluorescent probe for lysosomal proton pump.

Acridine orange was found to accumulate in pure lysosomal particles (tritosomes) in vitro, and the quenching of its fluorescence correlated well with the delta pH (inside acid) across the lysosomal membrane. Use of this dye showed that Mg-ATP caused lysosomal acidification. This acidification was sensitive to N,N'-dicyclohexylcarbodiimide, N-ethylmaleimide, and azide, but not to oligomycin, ouabain or vanadate. These results supported the idea of the existence of a lysosomal H+-pump, suggested in a previous paper (Ohkuma et al. (1982) Proc. Natl. Acad. Sci. U.S. 79, 2758-2762).

Acridine Orange↗
PubMed1982

Electron microscopic observations of experimental carbon monoxide encephalopathy in the acute phase.

The cerebral and cerebellar lesions of the cats that were exposed to 0.3% carbon monoxide gas under artificial respiration were examined by an electron microscope at different intervals. During the first few days, the most outstanding features were segmental empty axonal swelling, dilatation of the extracellular space, swelling and necrosis of astrocytes and oligodendroglias, and lamellar separation of the myelin sheath predominantly in the deep cerebral white matter. These changes subsided within one week. Instead, collapsed myelin increased in number and phagocytosis of disintegrated myelin was occasionally observed. Astrocytes and oligodendroglias became prominent in size and number. Changes suggestive of selective damage of myelin or oligodendroglia was not encountered. We proposed that CO-followed by Wallerian degeneration. The pathogenesis of CO-encephalopathy was also discussed.

Animals↗
PubMed1982

Sequence analysis of the heat-labile enterotoxin subunit B gene originating in human enterotoxigenic Escherichia coli.

In this study, we determined the amino-terminal coding sequence, covering the signal peptide and the amino-terminus of the mature peptide, of the heat-labile enterotoxin subunit B (LT-B) gene originating in human enterotoxigenic Escherichia coli. Neither the signal sequence nor the amino-terminal sequence of the mature LT-B was identical to those sequences from porcine enterotoxigenic E. coli, but there was an extensive homology.

Amino Acid Sequence↗
PubMed1982

Unloading effects of vasodilators on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction.

Effects of three representative vasodilators on peripheral and cardiac hemodynamics were studied in 20 patients with heart failure due to acute myocardial infarction (PCWP greater than 18 mmHg, C1 greater than 2.20 L/min/m2) using venous occlusion plethysmography and a Swan-Ganz catheter. Sublingual isosorbide dinitrate (ISDN) significantly increased calf venous capacitance (CVC) from 5 to 60 min (p less than 0.01) and calf blood flow (CBF) in the initial 15 min (p less than 0.05), while simultaneously lowering PCWP (p less than 0.05) and central venous pressure (p less than 0.05). Calf vascular resistance (CVR), cardiac index, blood pressure, and total systemic peripheral resistance (TSPR) were not affected significantly. Nitroglycerin ointment (NGO) significantly decreased CVR (p less than 0.05) and increased CVC (p less than 0.05) from 60 to 240 min, simultaneously with lowering of PCWP (p less than 0.01), central venous pressure (p less than 0.05), and TSPR (p less than 0.05). Oral prazosin (Pz) increased CBF (p less than 0.01) and CVC (p less than 0.05) from 60 to 240 min, simultaneously with significant lowering of PCWP (p less than 0.01) and TSPR (p less than 0.05), resulting in increased stroke work index (p less than 0.05). These data confirm that ISDN predominantly causes capacitance vessel dilatation and reduce excessive venous return, while Pz and NGO dilate not only capacitance vessels but also resistance vessels, consequently reducing systemic vascular resistance and resulting in increased peripheral blood flow and cardiac performance. It was observed that the higher the base-line calf vascular resistance rose, the better the response to the vasodilator treatment appeared in terms of a decrease in calf vascular resistance.

Adult↗
PubMed1982

Effect of chlorinated ethanes and ethylenes on electron transport in rat liver mitochondria.

For all members of the chlorinated ethane and ethylene series except monochloroethylene, the effects on the oxygen consumption of isolated rat mitochondria were studied. All the tested compounds inhibited glutamate and malate oxidation, and their inhibitory potency increased in the order of the number of contained chlorines. The eight compounds of greatest potency were also investigated for their inhibition of succinate oxidation in mitochondria and inhibition of NADH oxidation in sonicated submitochondrial particles. The data obtained suggested that the inhibition of substrate oxidation was due to blockade of electron transport and the most susceptible portion was located from NADH to CoQ.

Animals↗