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Biomedical subjects

H Kikuchi

Publications and source records attributed to H Kikuchi.

At least 883 records · Page 49Linked to original sources
PubMed1980

Partial purification of a stimulatory factor of RNA polymerase B in nonhistone proteins; correlation with nuclear protein kinase.

A stimulatory factor of DNA-dependent RNA polymerase B (nucleosidetriphosphate: RNA nucleotidyltransferase, EC 2.7.7.6) in nonhistone proteins was partially purified from rat liver nuclei on a column of daunomycin-CH Sepharose 4B and of phosphocellulose. In the process of purification, the stimulatory factor was separated from the main fraction of nuclear protein kinase (ATP: protein phosphotransferase, EC 2.7.1.37). This factor enhanced specifically the activity of RNA polymerase B on rat liver DNA as template and did not affect RNA polymerase A and Escherichia coli RNA polymerase at all. The polynucleotide elongation rate was increased by the addition of this factor.

Animals↗
PubMed1980

Halothane-induced changes in neuronal activity of cells of the nucleus reticularis gigantocellularis of the cat.

The ability of 0.5% and 1.0% halothane to suppress neuronal activity of cells in the nucleus reticularis gigantocellularis (NRGC) was studied in decerebrate cats. These drug effects were examined in order to substantiate further the potential involvement of the NRGC in the modulation of transmission of pain information. Only cells of the NRGC, which were excited exclusively by electrical stimulation of A-delta fibers in the superficial radial nerve, were studied. Both concentrations of halothane caused a significant, dose-dependent reduction of spontaneous and evoked activity of all cells studied. These findings correlate well with previous reports of other anesthetics suppressing NRGC activity. In light of the selective depression by anesthetics and narcotic analgesics of spinal cord dorsal horn cells associated with noxious stimuli, these findings, when combined with anatomic, physiologic, and behavioral studies of NRGC, provide further evidence of the involvement of NRGC in the signaling of noxious stimuli and the analgesic effects of halothane exerted at this site.

Animals↗
PubMed1980

Intracranial transplantation of the omentum for cerebrovascular moyamoya disease: a two-year follow-up study.

Intracranial transplantation of the omentum was performed on a patient with moyamoya disease who presented with diffuse cerebral ischemic symptoms and blindness. Anastomoses were made between the superficial temporal artery and the gastroepiploic artery of the transplanting omentum, and between the superficial temporal and gastroepiploic veins. Postoperative angiography demonstrated branches of the middle cerebral artery through the anastomosed gastroepiploic artery. Postoperatively the patient was able to walk with a cane without further ischemic attacks for the next two years. The blindness did not improve.

Arterial Occlusive Diseases↗
PubMed1980

Subependymal hematoma in "Moyamoya" disease.

A 27-year-old woman in the ninth month of her pregnancy suddently developed nausea and motor weakness of her right lower extremity while shopping. Subsequently a disturbance of consciousness and right-sided hemiparesis developed. Spinal puncture yielded clear CSF but CT scan demonstrated a left subependymal hematoma. Angiographical examination led to a diagnosis of "Moyamoya" disease. The source of the intracranial hemorrhage could not be identified. The hematoma could not have been diagnosed accurately without the CT scan.

Adult↗
PubMed1980

[A histopathological study of the brain of patients who died of cerebral vasospasm after rupture of cerebral aneurysm (author's transl)].

It is said that cerebral angiospasm affects very seriously the prognosis of the patient with ruptured aneurysm. Of 44 patients with ruptured aneurysm who died from cerebral ischemia due to cerebral angiospasm, we performed histopathological studies of brains of 18 patients without iatrogenic factors (radical surgical operation, prolonged artificial breathing and so on). In all of the cases, cerebral infarctions were observed in the area fed by the artery with angiospasm. The size and extent of the cerebral infarction were various. In 12 cases who died in the acute stage (within 3 weeks after subarachnoid hemorrhage), those who survived longer showed more severe and wide cerebral infarction, while those who died earlier showed more localized infarction in the basal ganglia and thalamus. In 6 cases who died in the chronic stage (more than 3 weeks after subarachnoid hemorrhage), the cerebral infarction was slight. No ischemic changes were observed in the brain stem, except for secondary petechial hemorrhage due to incisural herniation in cases with extensive cerebral infarction.

Adult↗
PubMed1979

Effects of ketamine on nociceptive cells in the medial medullary reticular formation of the cat.

Anatomic, physiologic and behavioral evidence suggests that the neurons in the nucleus reticularis gigantocellularis of the medial medullary reticular formation may act as a relay station for the transmission of nociceptive information from the spinal cord to higher brain centers. The nucleus reticularis gigantocellularis may also be the site of action of analgesic agents, such as ketamine hydrochloride. Utilizing extracellular microelectrodes in 23 decerebrate cats, the authors measured the effect of ketamine on neurons in the nucleus reticularis gigantocellularis that were excited by electrical stimulation of peripheral nerves. The frequency of spontaneous single-unit firing activity in the nucleus reticularis gigantocellularis was suppressed by 31 +/- 11 (mean +/- 1 SE) and by 62 +/- 7 per cent with ketamine, 1.0 and 2.5 mg/kg, iv, respectively. The frequency of evoked single-unit activity was suppressed by 57 +/- 9 and 79 +/- 5 per cent with ketamine, 1.0 and 2.5 mg/kg, respectively. Ketamine produces significant depression of single-unit activity of the cells in the nucleus reticularis gigantocellularis, suggesting that this may be an important site of its analgesic action.

Animals↗
PubMed1979

Stabilization and purification of glucosamine 6-phosphate isomerase from rat kidney.

1. Glucosamine 6-phosphate (GlcN-6-P) isomerase of rat kidney was resistant to heating at 50--55 degrees in crude extract but not after several purification steps. GlcN-6-P and N-acetylglucosamine 6-phosphate were found to stabilize the isomerase under these conditions. They also protected the enzyme from tryptic digestion, but only GlcN-6-P was effective against inactivation by p-chloromercuribenzoate. 2. When GlcN-6P isomerase was purified from fresh kidney and kidney stored at -20 degrees, separately and under GlcN-6-P, the two preparations were different in elution profile from a hydroxyapatite column. It was subsequently found that storage of crude extract at -20 degrees resulted in molecular alterations of the enzyme. Prolonged purification appeared to affect the enzyme similarly. The molecular alterations, however, were suppressed if the extract was stored at -70 degrees. 3. These findings have been utilized to develop a procedure, which enables us to purify rat kidney GlcN-6-P isomerase without any molecular alteration and in good yield.

Aldose-Ketose Isomerases↗