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Biomedical subjects

F Murakami

Publications and source records attributed to F Murakami.

At least 91 records · Page 5Linked to original sources

Axonal-growth-associated intracellular molecule in the rat central nervous system recognized by the monoclonal antibody 5H.

In order to discover molecules involved in axonal outgrowth during development of the central nervous system (CNS), monoclonal antibodies (MAbs) were raised against homogenates of the early postnatal rat cerebral cortex. A novel MAb, 5H, was obtained which recognizes a developmentally regulated antigen in the CNS. In the cerebral cortex of postnatal (PN) day 0-6 rats, 5H-immunoreactive punctate or fiber-like processes were observed. In the PN day 12 cortex, 5H immunostaining was mostly present as puncta. The expression of the 5H antigens decreased in the second PN week and completely disappeared from the cortex of rats older than PN day 18. In the hippocampal region, 5H immunoreactivity exhibited similar developmental changes, but with a more prolonged period of expression of the antigen (up to 5 weeks postnatally). They were also absent from the hippocampus of the adult rat. Similar developmental changes were also observed in the other CNS regions, but the only region in the adult CNS that showed 5H immunoreactivity was the olfactory bulb, in which synaptic turnover normally occurs even in the adult. Immunoelectron microscopy revealed that 5H immunoreactivity was localized to the cytoplasm of neuronal processes, including synaptic boutons. The expression of the 5H antigen in neurons cultured from rat cerebral cortex obtained from embryonic day 16 to PN day 6 was mostly restricted to neurite tips, including growth cones. These results suggest that the MAb 5H antigen is associated with axonal outgrowth during early development in the CNS.

Aging↗

[A case of octogenarian left atrial myxoma].

We reported a case of left atrial myxoma in advanced age. The case was eighty years old man. He admitted with congestive heart failure. He was diagnosed as left atrial myxoma by echocardiography. The open heart surgery was done. The myxoma was 79 g in weight and 8.5x5x3 cm in size. Post operative course was uneventful. The echocardiography is useful for diagnosis of the left atrial myxoma. The left atrial myxoma should be operated when it is diagnosed how the patient is advanced age. The septal-superior exposure gives a good operative field.

Age of Onset↗

[An improved assay for plasma tissue factor activity].

We developed an improved assay for measuring tissue factor activity in plasma with chromogenic substrate (S-2765) which is highly sensitive to factor Xa. In the ordinary assay with S-2222, it was required to prepare the euglobulin fraction of plasma and to heat it, while the improved assay required 20-fold-diluted plasma with Owren's barbital buffer (pH 7.35). The absorbance at 405nm on a colorimeter and human placental tissue thromboplastin preparation (HPT; Thromborel S, Behringwerke AG) was regressed on a semilogarithmic curve. The mean value obtained by this assay for normal subjects was 15.8 +/- 16.4 micrograms/ml HPT (mean +/- 2SD). A correlation of tissue factor activities assayed by the present method and the ordinary method was 0.62. Our data suggest that this improved assay is a useful method for measuring the plasma tissue factor activity.

Adult↗

[Cardiac operation of the cases associated with malignant tumor].

Twelve cases of malignant tumor (mean age 64 years) underwent the cardiac operation. The procedure of cardiac operations were 10 coronary artery bypass grafting and 2 mitral valve replacement. The detail of malignant tumors were 4 gastric cancer, 3 colon cancer, 3 lung cancer, 1 esophageal cancer and 1 lip cancer. The cardiac operations followed the operations of malignant tumor in 4 cases and the cardiac operations were followed by the operations of malignant tumor in 7 cases. The former cases did not recur the tumor from 10 to 30 months follow up period. The all latter cases survived except 1 case from 1 month to 21 months. Our management for the cases associated with malignant tumor and cardiac diseases as next. We perform the cardiac operation for the case whose life expectancy is longer than 1 year. We perform the cardiac operation before the operation of malignant tumor. We perform the operation for malignant tumor as soon as the patient had recovered from the cardiac operation. We would not perform any adjuvant therapy before completion of the operation for the heart and tumor.

Aged↗

Hemostatic studies in patients with carbohydrate-deficient glycoprotein syndrome.

The carbohydrate deficient glycoprotein (CDG) syndrome is a newly described disorder characterized by impaired glycosylated molecules. It has been reported that transient stroke-like episodes appear in half of the patients. We performed hemostatic studies on three CDG syndrome patients belonging to two unrelated families. The most characteristic findings were decreases in antithrombin III (AT III), protein C and alpha 2 plasmin inhibitor to nearly half normal levels. Protein S was reduced in two (siblings) patients. Isoelectric focusing of AT III in native plasma revealed decreased intensity of the major band and increased intensity of a minor cathodal band. These minor AT III molecules were considered to lack an oligosaccharide sidechain. A 12-year-old girl defective not only for AT III but also protein C and protein S developed disseminated intravascular coagulation accompanied by arterial thrombosis in her left hand following dyspnea associated with bronchial asthma. These findings suggest that thrombotic predisposition in patients with CDG syndrome is due to decreased levels of major coagulation inhibitors, particularly as a result of impaired glycosylation of AT III.

Adolescent↗

Low density, but not high density, C6 glioma cells support dorsal root ganglion and sympathetic ganglion neurite growth.

Accumulating evidence suggests that an inhibitory influence of the environment on growth cones plays a crucial role in development and regeneration of neuronal projections. Oligodendrocyte-associated neurite growth inhibiting substance is one of the most extensively studied molecules. Molecular biological studies, however, remain slow in progress. Although finding clonal cells that express such factors would facilitate the analysis of inhibitory influences on neurite growth, few cell lines have been reported to express neurite growth inhibitor. We therefore investigated the possibility of a clonal glial cell line to differentiate and express inhibitory or non-permissive features for neurite outgrowth in culture. We chose the C6 glioblastoma cell line and examined neurite extension from chick dorsal root ganglion (DRG) explants. Neurites from embryonic day 9 DRG extensively grew on C6 cells that were cultured at low cell density, while they failed to grow on C6 cells cultured at high density, even in the presence of nerve growth factor in high concentrations. Membrane extract from high density C6 cells, when used as culture substratum, was less permissive for neurite outgrowth compared to extract from low density cells. Treatment of the membrane extract derived from high density C6 cells with trypsin made it less non-permissive for neurite growth. These results suggest that C6 cells are induced to express a non-permissive property for neurite outgrowth by culturing them at high density.

Animals↗

The effects of calcium antagonists and prostaglandin E1 on isolated canine coronary arterial tension.

The effects of calcium antagonists (nifedipine, nicardipine, diltiazem, and verapamil) and prostaglandin E1 (PGE1) on the tension of isolated canine coronary arterial strips were studied. In a solution containing 20 mEq/L of K+, 127 mEq/L of Na+, the tension was increased by 500-1,000 mg with 4 mEq/L of Ca2+. This increase in tension was suppressed by Ca-antagonists and PGE1 dose-dependently. Nifedipine 10(-5) M, nicardipine 3 x 10(-7) M, diltiazem 3 x 10(-6) M, and verapamil 3 x 10(-6) M completely suppressed the increased tension. The maximal suppression of the tension produced by PGE1 was about 40% at 10(-10) M. In 20 mEq/L K+ solution (0 mEq/L Ca2+, 37 degrees C), the reduction of the Na+ concentrations from 127 mEq/L to 12 mEq/L increased the tension by 50 to 100 mg. This increase in tension was not suppressed by Ca-antagonists or PGE1. In conclusion, this study demonstrated that Ca-antagonists and PGE1 suppressed an increase in the tension caused by Ca2+ but did not suppress an increase in the tension caused by Na+ reduction.

Alprostadil↗

Effects of vinconate and pentobarbital against postischemic alterations in spirodecanone binding sites in the gerbil brain.

We investigated the effects of vinconate and pentobarbital against the alterations in spirodecanone binding in the gerbil striatum and hippocampus 5 h and 7 days after 10 min of cerebral ischemia, using receptor autoradiography. Vinconate and pentobarbital were given intraperitoneally 10 and 30 min prior to ischemic insult, respectively. The spirodecanone binding in vehicle-treated gerbils subjected to ischemia was unchanged in the brain 5 h after recirculation, compared with that in sham-operated animals. Seven days after ischemia, a significant elevation in the spirodecanone binding was observed in the striatum and the stratum radiatum of the hippocampal CA1 sector and the hippocampal CA3 sector of the vehicle-treated animals. Other regions showed no significant change in the binding. Vinconate and pentobarbital showed no significant change in the striatum and hippocampus 5 h after ischemia. However, the administration of vinconate inhibited a significant elevation in the spirodecanone binding in the lateral striatum and the stratum radiatum of hippocampal CA1 sector 7 days after ischemia. Pentobarbital also prevented a significant elevation only in the lateral striatum. A histological study revealed that cerebral ischemia caused severe neuronal damage in the lateral striatum and hippocampal CA1 and CA3 sectors. However, ischemic neuronal damage was not observed in the dentate gyrus. An immunohistochemical study also showed that numerous reactive astrocytes were evident in the hippocampus, particularly in the hippocampal CA1 sector, 7 days after ischemia. The present study demonstrates that cerebral ischemia can cause a conspicuous elevation in spirodecanone binding in the striatum and hippocampus. They also suggest that the postischemic elevation in the spirodecanone binding is partly prevented by treatment with vinconate and pentobarbital. These results suggest that the postischemic elevation in spirodecanone binding sites may reflect expression of reactive astrocytes.

Animals↗

[Surgical repairs of anomalous pulmonary venous connection to superior vena cava and right atrial junction].

We recently encountered a case of total anomalous pulmonary venous connection (TAPVC, Darling Ib) and 3 cases of partial anomalous pulmonary venous connections (PAPVC) to the superior vena cava. We surgically treated these 4 cases by different procedures which were selected according to the morphological features of individual cases. In the case of TAPVC (Darling Ib), we created a right atrial wall flap, according to the method of Vargas, so that the blood from the abnormal pulmonary vein could pass the left atrium via the superior vena cava and atrial septal defect. In 3 cases of PAPVC, we modified some techniques of right atrial incision and closure by suturing. Through these surgical procedures, none of the 4 patients developed postoperative stenosis of the pulmonary venous pathway or arrhythmias. Various surgical procedures have been reported for the treatment of anomalous pulmonary venous connection, an anomaly involving direct connection of the pulmonary vein to the superior vena cava or to the right atrial junction of the superior vena cava. However, the incidence of postoperative stenosis or obstruction of the pulmonary venous pathway or postoperative sick sinus syndrome has been high with these procedures.

Adult↗

[Evaluation of a latex agglutination assay method for the determination of plasmin/alpha 2 plasmin inhibitor complex].

We evaluated a latex agglutination assay method for concentration of plasmin/alpha 2 plasmin inhibitor complex (PPI) developed recently. The latex reagent consisted of two kinds of latex particles, one was coated with monoclonal antibody against plasmin (JIPPI-3) and another coated with monoclonal antibody against modified alpha 2 plasmin inhibitor (JIPPI-50). A correlation of concentrations of PPI between this method and ordinary EIA kit was very good (r = 0.969). Within-run precision of latex agglutination reagent also was good. The concentrations of PPI in plasmas of 40 in 43 normal subjects were 0-0.8 microgram/ml and others were 0.8-1.6 microgram/ml. Plasma levels of PPI were markedly elevated in patients with DIC. In addition, half of the patients with malignant tumors or liver diseases had increased levels of PPI. 16 of 32 cases with selected diseases (18 malignant tumors, 4 liver diseases, 2 infectious diseases, 2 cerebral contusions, 6 others) showed abnormal levels in PPI (> or = 0.8 microgram/ml) during several days preceding the elevation of FDP. It suggested that PPI could reflect fibrinolysis earlier than FDP. This latex agglutination assay is a simple and rapid method, and specific for the determination of PPI concentration as well as EIA method. We conclude that this assay method is very convenient for clinical use.

Antifibrinolytic Agents↗

Changes of spirodecanone binding in the gerbil hippocampus after cerebral ischaemia.

Using quantitative receptor autoradiography, spirodecanone binding was evaluated in the gerbil hippocampus 1 h-1 month after cerebral ischaemia of 10 min. The spirodecanone binding was unaffected in the hippocampus up to 48 h after ischaemia. Thereafter, increased binding was found in the stratum radiatum of hippocampal CA1 sector 7 days and 1 month after ischaemia. Other hippocampal regions showed no significant alterations in the spirodecanone binding. A histological study revealed that the hippocampal CA1 sector was severely damaged 7 days and 1 months after ischaemia. These results demonstrate that spirodecanone binding sites are located on interneurones or glial cells in the hippocampal CA1 sector.

Animals↗

Segregation of cerebrorubral and cerebellorubral synaptic inputs on rubrospinal neurons of fetal cats as demonstrated by intracellular recording.

Cerebrorubral and cerebellorubral inputs are localized to distal dendrites and somata of red nucleus neurons in adult cats, respectively. To examine if this segregation is established early in development, we performed intracellular recording from rubrospinal neurons of fetal cats aged from embryonic day 58 to 65. Stimulation of the contralateral cerebellar nuclei evoked excitatory postsynaptic potentials (EPSPs). EPSPs were also induced by stimulation of the ipsilateral pericruciate cortext but they were much slower in time course and smaller in amplitude compared to cerebellar ones. We suggest that cerebrorubral and cerebellorubral synapses are segregated on soma-dendritic membrane of rubrospinal neurons early in development.

Animals↗

Effect of pentobarbital on postischemic SCH 23390 and rolipram binding in gerbil brain.

We investigated the postischemic alterations in dopamine D1 receptor and Ca2+/calmodulin independent cyclic adenosine monophosphate (cyclic AMP) selective phosphodiesterase in gerbils and examined the effect of pentobarbital on these alterations. [3H]SCH 23390 and [3H]rolipram, respectively, were used to label dopamine D1 receptor and Ca2+/calmodulin independent cyclic-AMP selective phosphodiesterase. Transient cerebral ischemia was induced for 10 min, and pentobarbital (40 mg/kg) was administered intraperitoneally 30 min prior to ischemia. 5 h after ischemia, [3H]rolipram binding decreased significantly in the striatum and hippocampus, whereas no significant change was found in [3H]SCH 23390 binding. 7 days after ischemia, however, there was a marked reduction in both [3H]SCH 23390 and [3H]rolipram binding in the striatum and hippocampus, where histological neuronal damage was found. Pentobarbital significantly ameliorated postischemic decreases in [3H]rolipram binding both 5 h and 7 days after recirculation in most areas studied. Furthermore, this drug significantly prevented postischemic reduction in [3H]SCH 23390 binding (only) 7 days after ischemia. These results suggest that alteration of cyclic AMP selective phosphodiesterase is more sensitive at an earlier stage after ischemic insult than that of dopamine D1 receptors. Our results also demonstrate that pentobarbital reduces the alteration in [3H]SCH 23390 and [3H]rolipram binding after cerebral ischemia.

Animals↗

Kinetic and circular dichroism studies of enzymes adsorbed on ultrafine silica particles.

Negatively charged ultrafine silica particles (average diameter 20 nm) were used as support materials for adsorption immobilization of porcine trypsin, horseradish peroxidase, and bovine catalase under various conditions, and the changes in the enzyme activities and the circular dichroism (CD) spectra of these enzymes upon adsorption were measured. Since the light scattering intensity of the ultrafine particles was very low, the activities and the CD spectra of the enzymes adsorbed on the particle surfaces could be measured. The enzymes adsorbed at pH around and above their isoelectric points (pI) showed high activities. On the other hand, the enzymes adsorbed at pHs below their pI had significantly diminished activities and showed large CD spectral changes upon adsorption. The extent of CD spectral changes in the enzymes upon adsorption correlated very closely with that of the activity reduction. Therefore, the conformational changes in enzymes upon adsorption are one of the important factors that reduce the activities of adsorbed enzymes. These results demonstrate that the ultrafine particles are not only a novel support for enzyme immobilization but also are helpful for the molecular understanding of the immobilized enzymes.

Adsorption↗

Individual corticorubral neurons project bilaterally during postnatal development and following early contralateral cortical lesions.

The corticorubral projections in adult cats are primarily uncrossed. However, early in development and after early unilateral lesions of the sensorimotor cortex, crossed corticorubral projections are also observed. The present study was performed to disclose (1) whether the crossed projections originate from neuronal subpopulations different from those producing uncrossed ones and (2) how the neurons that give rise to the crossed projections in the lesioned animals are related to those occurring in normal development. We injected fluorescent latex microspheres into the red nucleus of two groups of animals: (1) intact kittens at postnatal week 3 and (2) kittens that had received unilateral ablation of the cerebral cortex at this stage and were then allowed to survive for at least 4 weeks. Red fluorescing microspheres were injected on one side and green ones on the other. In both normal and lesioned kittens, a number of cells in the cortex were labeled as a result of the contralateral as well as the ipsilateral injections, and no difference in size or distribution was found between the cells labeled from contralateral and ipsilateral injections. More than half of the cells labeled from contralateral injections were double-labeled in both groups of animals. These results indicate that individual corticorubral cells project bilaterally in normal development as well as following unilateral lesions of the cortex. With respect to the cells producing crossed projections, they were similar in both laminar and regional distributions between the intact and lesioned animal, suggesting that the crossed projections arise from the same neuronal subpopulation before and after cortical lesions. This view was supported by sequential injections of the tracers, which indicated that cells normally projecting contralaterally maintained the crossed projection after the lesions. Taking into account our previous observations that growth and proliferation of crossed corticorubral axons took place in the red nucleus (Murakami et al. 1991a), it is likely that growth and proliferation of the axons in denervated targets play a major role in lesion-induced establishment of aberrant projections.

Aging↗

An electrophysiological study of a transient ipsilateral interpositorubral projection in neonatal cats.

We examined whether transient projections in the developing central nervous system of Mammalia form functional synapses on their target neurons, using transient ipsilateral interpositorubral (iIR) projection in kittens as a model system. Intracellular recordings were made from red nucleus (RN) neurons in 26 kittens aged 6-26 postnatal days (PD6-26). RN neurons were identified by monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by stimulation of contralateral nucleus interpositus (IN), and additionally by intracellular staining in a few cells. Sixty-nine out of 362 RN neurons responded to stimulation of the ipsilateral IN. Of the 69 cells, 25 showed depolarizing responses with relatively short latency (2.1-6.7 ms) in kittens up to PD20. Such responses were not observed in older animals. Varying stimulus strength revealed that the potentials were unitary. Paired-pulse facilitation of the potential was observed, suggesting that the depolarizations are EPSPs. Several lines of evidence were obtained suggesting that the EPSPs are evoked monosynaptically. They followed high-frequency stimulation up to 50 Hz, and their latencies remained constant with varying stimulus strength. The latencies of ipsilaterally induced EPSPs were always longer than those of contralateral ones, evidence consistent with the longer course of ipsilaterally projecting axons than that of contralateral ones (Song and Murakami 1990). The age of disappearance of the monosynaptic EPSPs, i.e., PD20, also corresponds roughly with that of the anatomically demonstrable iIR fibers (PD15-PD25; Song and Murakami 1990). It is thus concluded that the transient iIR fibers in kittens form functional synapses on RN neurons.

Animals↗

Changes of [3H]cyclic adenosine monophosphate binding in the gerbil brain following transient cerebral ischemia: an autoradiographic study and investigation of the effects of vinconate and pentobarbital.

We studied the alterations in binding of cyclic AMP as an indicator of particulate cyclic AMP-dependent protein kinase binding activity following transient cerebral ischemia in Mongolian gerbils and examined the effects of vinconate and pentobarbital against alterations in the binding. Animals were allowed to survive for 5 h and 7 days after 10 min of cerebral ischemia induced by bilateral occlusion of common carotid arteries. [3H]Cyclic AMP binding was significantly reduced in the hippocampus 5 h after ischemia, whereas the striatum showed no significant change in the binding. Seven days after ischemia, a severe reduction of [3H]cyclic AMP binding was noted in the dorsolateral striatum, hippocampal CA1 and CA3 sectors, and dentate gyrus. Intraperitoneal administration of vinconate (100 or 300 mg/kg) showed a significant elevation of [3H]cyclic AMP binding in the striatum, stratum pyramidale of hippocampal CA1 and CA3 sectors, and dentate gyrus 5 h after ischemia. By contrast, the intraperitoneal administration of pentobarbital (40 mg/kg) showed no significant alteration of [3H]cyclic AMP binding in most of these regions. However, vinconate and pentobarbital prevented a significant reduction of [3H]cyclic AMP binding in the dorsolateral striatum and stratum pyramidale of hippocampal CA3 sector 7 days after ischemia, although both drugs failed to prevent damage to the hippocampal CA1 sector. These results suggest that alteration in cyclic AMP binding may not be a major factor in causing ischemic neuronal damage.

Animals↗