[Adrenomedullary scintigraphy with I-131 metaiodobenzylguanidine].
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Biomedical subjects
Publications and source records attributed to Y Ohta.
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With the use of a stereoscopic microscope, observations were made on the course of the proper digital nerve of the thumb on ten upper limbs in adult cadavers. By observation from the dorsal side after removal of the bone, it was possible to clearly see the ramification of the digital nerve from the subcutaneous tissue to the dermis. Ramification from the palm to the level of the interphalangeal joint was segmental. The digital nerve of the thumb trifurcates from the proximal site of the distal palmar thumb crease into the main, medial, and lateral branches. The main branch is thick and extends from the center of the pulp toward the fingertip. Ramification at the pulp of the thumb is of a radiating rather than segmental type, and its control can be considered as spotty or intermittent. Distribution of pacinian corpuscles is dense in the subcutaneous tissue of the distal palmar thumb crease. These observations are of clinical importance not only for avoidance of injury to the digital nerve in surgical procedures such as the incision and drainage for felon and the trigger thumb release but also for precise repair of the digital nerve in the reconstructive surgery of the thumb.
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Ectopic pituitary transplantation induced a high incidence of adenomyosis in SHN mice. Early signs of the development of adenomyosis were the penetration of stromal connective tissue into myometrium followed by uterine gland invasion. Associated with these changes, the inner layer of myometrium showed the involution of smooth muscle cells and distended intercellular spaces.
In order to elucidate the anthranilic acid metabolism in animal tissue, the metabolism was studied in the isolated perfused liver of rats. A sensitive and rapid method was devised for determination of anthranilic acid and its related substances using high-performance liquid chromatography with electrochemical detection. 5-Hydroxyanthranilic acid and anthranilamide, which have not been detected in animal tissue, were found in the perfusate and in the bile secreted from the perfused liver, respectively. In addition, a non-enzymatic production of anthranilamide from anthraniloyl glucuronide in the presence of ammonium and bicarbonate ions was also observed. These present results suggest that, apart from undergoing glycine or glucuronide conjugation, anthranilic acid is metabolized to 5-hydroxyanthranilic acid and anthranilamide in the rat liver.
The mechanism of an inhibitory effect of histamine on the sensitivity of frog skeletal muscle endplate was analyzed by studying the dose-response relation between the quantity of ACh applied iontophoretically and the ACh-induced postsynaptic current (ACh current), and also the interaction between histamine and erabutoxin-b (ETX-b). The results obtained show that histamine, like curare, decreased the sensitivity of ACh-receptor in a competitive manner.
Enhancement of decidual cell reaction (DCR) following adrenalectomy was reversed by corticosterone as well as indomethacin. The results suggest the adrenal involvement in DCR through uterine prostaglandin production.
An abnormal globin gene from a patient heterozygous for Hemoglobin Miyada was cloned and sequenced. The results indicated that the 5' flanking region and the 5' side of the gene were identical to those of a beta-globin gene and that the 3' side was identical to that of a delta-globin gene. The part of the gene identical to a beta-globin gene shifted to the part identical to the delta-globin gene somewhere in a homologous sequence region between the third nucleotide of the 17th codon and the second nucleotide of the 22nd codon of these two genes. Thus, results of analysis of the nucleotide sequence support the idea that the abnormal globin gene of Hemoglobin Miyada was generated as a fusion gene by unequal crossing over between a beta- and a delta-globin gene.
Restriction mapping of the globin genes from a homozygous delta beta thalassemia patient from Israel indicates that at least a 10-kilobase deletion is present extending 3' from within the large intervening sequence (IVS 2) of the delta globin gene and including the entire beta globin gene. Unique bands are seen when cellular DNA from this patient is digested with a variety of restriction endonucleases and hybridized with a probe specific for the delta IVS 2. Extensive analysis of the Israeli delta beta thalassemia DNA as well as material from an Italian delta beta thalassemia homozygote with enzymes which cleave more frequently in delta IVS 2 has localized the 5' end of the deletion to a 107-base pair region within delta IVS 2. This region contains a unique repetitive sequence (TG)4 which has been reported to be a specific recognition signal for recombination and may be involved in the formation of these mutant genes. Two homozygous delta(0) thalassemia DNA samples from Japan were also analyzed for gene rearrangements or other changes by restriction enzyme mapping. No changes from normal were seen using 14 different enzymes indicating the absence of large deletions in the region around the delta globin gene. More specifically, both the 5' and 3' splice junctions of the IVS 2 appear to be normal from hybridization of restriction fragments generated by HphI and AluI, respectively, with a delta IVS 2 specific probe. We have also shown that point mutations which could lead to termination codons are not present at codons 35, 37, 43, 61, and 121, since restriction enzymes which recognize these sites produce normal patterns. The delta(0) thalassemia phenotype in these two subjects is most likely due to a point mutation either at one of the other 24 potential termination codons not accessible to restriction analysis or to other single nucleotide changes which could either decrease delta globin gene transcription or lead to abnormal processing or transport of delta globin mRNA.
Substance P and luteinizing hormone-releasing hormone (LHRH), neurotransmitter candidates for peptidergic neurotransmission in peripheral autonomic ganglia, facilitated the desensitization of nicotinic acetylcholine (ACh)-receptor at the skeletal muscle endplate. In the presence of these peptides, the desensitization proceeded with a biphasic time course, i.e. fast and then slow components of desensitization. We suggest that neuropeptides such as substance P and LHRH may regulate the sensitivity of nicotinic ACh-receptors by modulating the process of desensitization.
Hemoglobin Miyada, an anti-Lepore hemoglobin, represents the protein product of a nonhomologous crossover between beta and delta genes. The mutant globin is beta-like from the N terminus to amino acid 12, and delta-like from amino acid 22 through the C terminus, thus predicting a crossover site in the first coding region of the gene. DNA analysis, using multiple restriction endonucleases and hybridization to delta and beta globin gene-specific probes, confirms that the beta delta hybrid gene 1) is located on a single chromosomal fragment between normal delta and beta genes, and 2) has 5' beta promoter sequences, delta IVS 1 and 2, and 3' coding and flanking sequences.
Three new actin-binding proteins having molecular weights of 26,000, 21,000, and 19,000 were isolated from porcine brain by DNase I affinity column chromatography. These proteins were released from the DNase I column by elution with a solution of high ionic strength. They were further purified by column chromatographies using hydroxyapatite, phosphocellulose, and Sephadex G-75. All of these actin-binding proteins behaved as monomeric particles in the gel filtration chromatography. After elution of the three actin-binding proteins, actin and profilin were recovered from the DNase I column with 2 M urea solution. The eluted was further purified by a cycle of polymerization and depolymerization and finally by gel filtration. Little difference in polymerizability was detected between the purified brain actin and muscle actin. After sedimentation of the polymerized brain actin, profilin was purified by DEAE-cellulose and gel filtration column chromatographies. In the assay of the action of these actin-binding proteins, the 26K protein was found to cause a large decrease in the rate of actin polymerization, while showing little effect on the extent of polymerization. The 21K protein decreased the steady-state viscosity of actin solution in a concentration-dependent manner irrespective of whether it was added before or after actin polymerization. It reacted with actin at a 1:1 molar ratio.
We have isolated a protein factor from rat liver which stimulates anthranilamide hydroxylation by the microsomes in the presence of NADPH and oxygen and showed this factor to contain Cu and Zn and to have superoxide dismutase activity [Biochim. Biophys. Acta 365, 148-157 (1974)]. In the present study, this protein factor was confirmed to be a superoxide dismutase (SOD) by comparison of the recovery of SOD activity with that of anthranilamide hydroxylation-stimulating activity at each step of its purification, by inhibition of SOD activity with NaCN and hydrogen peroxide (H2O2), and by recovery of the SOD activity of the protein factor after reconstitution with Cu2+ and/or Zn2+. At a given SOD activity level, there was no difference among the rat liver SOD, Cu,Zn-SOD from bovine erythrocytes, and Mn-SOD from Serratia marcescens in their ability to stimulate anthranilamide hydroxylation not only by rat liver microsomes, but also by the reconstituted cytochrome P-450-containing monooxygenase system. Rat liver SOD stimulated anthranilamide hydroxylation by the reconstituted system in proportion to its amount below a protein concentration of 1 microgram/ml. In anthranilamide hydroxylation by the reconstituted system without SOD, only a slight hydroxylase activity was found at the initial stage of the reaction and a marked increase in the amounts of NADPH oxidized and H2O2 formed was observed after a lag time. In the presence of rat liver SOD, however, the hydroxylase activity was markedly and continuously increased almost proportionally to reaction time with a concomitant decrease in the amounts of NADPH oxidized and H2O2 formed. In addition, a trace of 3-OH anthranilamide, one of the products, not only stimulated NADPH-dependent H2O2 formation in the reconstituted system, but also inhibited the apparent reduction of cytochrome P-450 by NADPH in the reconstituted system. These effects of 3-OH anthranilamide were diminished by rat liver SOD. When a trace of 3-OH anthranilamide were added to a system composed of NADPH-cytochrome c (P-450) reductase and NADPH, H2O2 formation and NADPH oxidation were markedly stimulated. However, on addition of 3-OH anthranilamide to the system containing rat liver SOD, no stimulation on either H2O2 formation or NADPH oxidation was found.(ABSTRACT TRUNCATED AT 400 WORDS)