Search PubMed⌕ Search

Biomedical subjects

F Murakami

Publications and source records attributed to F Murakami.

At least 109 records · Page 6Linked to original sources
PubMed1993

Westernized food habits and concentrations of serum lipids in the Japanese.

To investigate the association of westernized food habits and concentrations of serum lipids in the Japanese, we studied 1200 healthy Japanese living in Hiroshima prefecture and 1483 ethnic Japanese from Hiroshima prefecture living in the Hawaii Islands and Los Angeles. The nutritional assessments were made by the same dietitians. No major difference was observed in the total energy intake between the Japanese and the Japanese-Americans in both males and females. However, the intake of animal fat and simple carbohydrates (especially fructose) were markedly greater, and that of complex carbohydrates lower, in the Japanese-Americans compared with the Japanese. The mean serum cholesterol (CH), LDL-CH and serum triglyceride (TG) levels were significantly higher in the Japanese-Americans in both sexes. The mean HDL-CH concentration was similar between the two groups in males, but it was approximately 7 mg/dl higher in Japanese-American females. Using the 75 percentile values of CH and TG in the Japanese in Hiroshima, the frequency of WHO types IIa and IIb hyperlipidemia was about twice as high in the Japanese-Americans. These results suggest that westernized food habits in the Japanese include qualitative changes in animal fat, simple carbohydrate and complex carbohydrate diet rather than an increase in the total energy intake. These changes are associated with marked increases in the concentrations of serum CH and TG and increased prevalence of types IIa and IIb hyperlipidemia.

Adult↗
PubMed1993

Postischemic changes in the binding of excitatory and inhibitory neurotransmitters in the gerbil brain.

We performed receptor autoradiography to determine sequential changes in the binding of N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acidA (GABAA) 1 h to 1 month after 10 min of transient cerebral ischemia in the gerbil. [3H]MK-801 and [3H]muscimol were used to label NMDA and GABAA receptors, respectively. [3H]MK-801 binding showed no significant changes in the striatum and hippocampus at an early stage (1-24 h) after ischemia. Thereafter, [3H]MK-801 binding exhibited a significant reduction in the dorsolateral striatum, most of hippocampal CA1 sector and dentate gyrus 48 h or 7 days of recirculation. However, [3H]MK-801 binding progressively depressed in the hippocampal CA1 sector 1 month after ischemia, whereas other regions showed no significant alteration in the binding. By contrast, [3H]muscimol binding was unchanged in all brain areas throughout the recirculation period. A histological study also demonstrated that transient ischemia caused severe neuronal damage in the striatum and hippocampus. These results demonstrate that NMDA and GABAA receptors are relatively resistant to severe degenerative processes. Furthermore, our finding suggests that transient ischemia may induce long-term changes in the properties of survival neurons or interneurons especially in the hippocampal CA1 sector.

Animals↗
PubMed1993

Naloxone receptor binding in gerbil striatum and hippocampus following transient cerebral ischemia.

Receptor autoradiographic and histological techniques were used to investigate sequential alteration of naloxone receptors in the gerbil brain 1 h-7 days after transient cerebral ischemia. Transient ischemia was induced for 10 min. [3H]Naloxone binding showed a transient elevation in the striatum 1 h after ischemia, whereas the hippocampus revealed no significant alteration in the binding. Thereafter, no conspicuous alteration in [3H]naloxone binding was seen in the striatum and hippocampus up to 24 h after ischemia. However, a significant elevation in [3H]naloxone binding was found in the hippocampal region 48 h after ischemia. In contrast, the striatum showed no significant alteration in [3H]naloxone binding. Seven days after ischemia, a severe reduction in [3H]naloxone binding was seen not only in the dorsolateral striatum and hippocampal CA3 pyramidal cell layer, where irreversible neuronal damage was found, but also in the histopathological intact dentate gyrus. However, the hippocampal CA1 sector which was most vulnerable to ischemia, revealed no conspicuous alteration in [3H]naloxone binding. These results demonstrate that alteration of naloxone receptors precedes ischemic neuronal damage to the striatum and hippocampus. They also suggest that the damage between striatum and hippocampus may be produced with different processes.

Animals↗
PubMed1993

Neuroprotective effect of vinconate against postischemic alterations in binding of [3H]SCH 23390 in the gerbil brain.

1. We investigated alterations in dopamine D1 receptors in the striatum and hippocampus after transient cerebral ischemia in gerbils using [3H]SCH 23390 autoradiography. 2. We also examined the effect of vinconate against the alterations in dopamine D1 receptors after transient ischemia. 3. Transient ischemia was induced for 10 min, and vinconate (100 and 300 mg/kg) was given intraperitoneally 10 min before ischemia. 4. [3H]SCH 23390 binding showed no significant alterations in the striatum and hippocampus 5 hr after ischemia, whereas severe reduction in these areas was found after 7 days of recirculation. 5. Vinconate showed no significant alterations in [3H]SCH 23390 binding in the striatum and hippocampus except for a decrease in the hippocampal CA3 sector and dentate gyrus 5 hr after ischemia. By contrast, vinconate prevented a significant reduction in [3H]SCH 23390 binding in the striatum, hippocampal CA3 sector, hilus, and dentate gyrus 7 days after ischemia. 6. Vinconate inhibited lipid peroxidation in rat brain homogenates in a concentration-related manner. 7. These results indicate that free radicals generated from abnormal dopamine metabolism may play a key role in the development of ischemic brain damage. Furthermore, they suggest that vinconate prevents ischemic brain damage by inhibiting lipid peroxidation.

Animals↗
PubMed1993

Electron microscopic localization and expression on cultured cells of a novel surface-associated molecule in the rat central nervous system.

Subcellular localization and in vitro expression of a newly raised monoclonal antibody 374 antigen, which outlines a subset of neurons in various regions of the rat CNS, were studied. Electron microscopy revealed that the immunoreactivity is associated with the outer surfaces of neuronal subsets, the surfaces of glial cell processes facing such neurons and less frequently, with the Golgi apparatus and inner cell surfaces. The monoclonal antibody also stained part of the cytoplasm of a population of dendrites. In order to test whether the antigen originates from neurons, we examined the expression of the antigen in cultured cortical cells. Double immunofluorescence staining with neuron-specific enolase and glial fibrillary acidic protein revealed that the antigen is expressed on a subset of neuronal cells and to a lesser extent on glial cells. The antigen is considered to be expressed on the outer surface because the cells were stained by the monoclonal antibody irrespective of whether they were alive or fixed. The monoclonal antibody 374 antigen may be a novel neuronal surface molecule which plays a role in neuron-neuron or glial-neuron interactions in the CNS.

Animals↗
PubMed1993

Sandwich repair with two sheets of equine pericardial patch for acute posterior post-infarction ventricular septal defect.

A 74-year-old man, who had posterior post-infarction ventricular septal defect, was treated successfully by early surgical repair with a sandwich technique involving two sheets of equine pericardial patch. In this technique the ventricular septal defect (VSD) was exposed through a trans-infarction approach. The inside patch covered the VSD and ventriculotomy from the inside. The outside patch generously covered the infarcted myocardium. The two patches completely sandwiched the infarcted myocardium including the VSD and ventriculotomy with eighteen interrupted sutures. This technique ensures strong fixation of the VSD, reducing the risk of bleeding and recurrence of VSD, and also maintains the proper shape and size of the left ventricle without the danger of ventricular aneurysm formation.

Aged↗
PubMed1993

Continuous retrograde cerebral perfusion for protection of the brain during aortic arch surgery.

Hypothermic circulatory arrest and selective cerebral perfusion for aortic arch surgery have been reported, but these procedures are of limited duration, require hazardous and complicated techniques and can cause clamp injury. Continuous retrograde cerebral perfusion (CRCP) is a new and simple technique for the protection of the brain during hypothermic circulatory arrest. We applied CRCP in 26 patients who underwent aortic arch surgery. Continuous retrograde cerebral perfusion was performed with a mean blood flow of 383 +/- 176, range 120-800, ml/min. The mean duration of CRCP was 63 +/- 15, range 32-92, min with the superior vena cava pressure at 15-42 mm Hg. No neurologic deficit was observed in 20 patients (90%) and only minor deficits in 2 out of the 22 cases without severe postoperative complications, allowing evaluation of the effectiveness of CRCP. Four patients had other severe complications, and the effectiveness of the method could not be evaluated. Continuous retrograde cerebral perfusion can be an excellent and safe technique which avoids clamp injury during aortic arch surgery.

Adult↗
PubMed1993

End-tidal CO2 changes under constant cardiac output during cardiopulmonary resuscitation.

OBJECTIVES: To evaluate a) whether end-tidal CO2 values change under constant cardiac output during cardiopulmonary resuscitation (CPR), and b) what factors are responsible for the change. DESIGN: A cohort study. SETTING: University research laboratory. SUBJECTS: Nine mongrel dogs. INTERVENTIONS: Ventricular fibrillation was electrically induced. After 2 mins, open-chest cardiac massage was initiated to maintain cardiac output at 0.2 L/min (23% of baseline cardiac output) by the measurement of blood flow with an electromagnetic flow probe on the ascending aorta. The cardiac massage was kept constant until 50 mins after the induction of ventricular fibrillation. MEASUREMENTS AND MAIN RESULTS: Before and during ventricular fibrillation, end-tidal CO2, minute volume of alveolar ventilation, and CO2 excretion were continuously monitored. Blood gases and oxygen saturation values were also measured in arterial and the mixed venous blood samples. CO2 content was calculated. After induction of ventricular fibrillation, end-tidal CO2 decreased and thereafter continued to increase until the end of the experiment. Two mechanisms may have contributed to the early reduction in end-tidal CO2. One mechanism is a further decrease in CO2 excretion compared with the reduction in alveolar ventilation and the other is an increase in alveolar deadspace (estimated from the increase in the difference between PaCO2 and end-tidal CO2). The subsequent increase in end-tidal CO2 was mainly due to a change in CO2 excretion. There are two hypotheses concerning the subsequent increase in CO2 excretion: the increase in pulmonary capillary blood flow (estimated from the change in the arteriovenous CO2 content gradient) and the increase in CO2 production itself. CONCLUSIONS: End-tidal CO2 changes under constant cardiac output during CPR. When end-tidal CO2 is used to estimate the effectiveness of the cardiac massage, this type of change must be recognized.

Animals↗
PubMed1993

[Etoposide/cis-platinum (CDDP) combined chemotherapy for ovarian cancer: evaluation of optimum schedule for CDDP administration in chronic continuous exposure of ovarian cancer cells to low-dose etoposide in vitro].

Combined chemotherapy with etoposide and cis-platinum (CDDP) is considered a second line regimen for refractory cases of ovarian cancer. In addition to the time-dependent cytocidal kinetic of etoposide, much attention has been paid to low-dose continuous administration of etoposide. In this study, ovarian cancer cells (SHIN-3) were continuously exposed to low-dose etoposide in vitro to determine the optimum schedule for CDDP administration. Etoposide concentrations of 1-3 micrograms/ml were used; per os administration of etoposide at 25 mg x 2/day has been shown to produce a continuous plasma concentration of etoposide of around 1 microgram/ml. The results were as follows: 1) The IC50 of CDDP after 72 hours of exposure was 8.0 micrograms/ml and that of etoposide after 114 hours was 3.0 micrograms/ml. 2) After 100 hours of exposure to 1 microgram/ml of etoposide, cell cyclic phase analysis showed cells predominantly in G2/M phase arrest. 3) After 24-hour administration of CDDP, it was more than 24 hours before a cytocidal effect was observed. 4) During continuous exposure of SHIN-3 to etoposide (1 microgram/ml) for 6 days, CDDP was added on the 1st, 3rd, and 5th days. The largest ratio of growth inhibition with combined treatment to that with CDDP alone was attained on the 5th day. We conclude that, in combination regimens using low-dose continuous etoposide, CDDP should be added after etoposide administration is begun.

Administration, Oral↗
PubMed1993

[A case of acute hemorrhagic gangrenous acalculous cholecystitis with bile peritonitis during anti-coagulant therapy after coronary-artery bypass grafting].

Acute acalculous cholecystitis is a relatively rare complication occurring after surgery on organs other than the bile duct system. It is often misinterpreted to be a post-operative symptom, and can progress into a very serious condition with high risk of mortality if gangrene and perforation develop. Its occurrence after open heart surgery is relatively rare. We experienced a case of acute hemorrhagic, gangrenous acalculous cholecystitis that developed after coronary-artery bypass grafting. The patient, a 78-year-old man, complained post-operatively of a right upper abdominal pain. The diagnosis of acute gangrenous acalculous cholecystitis was established on the basis of abdominal sonography and CT, and emergency operation performed was successful. Etiological factors in this case may have included post-operative stasis of bile, swelling of the gallbladder, hypotension during cardiopulmonary bypass, and post-operative anti-coagulant therapy administered after open heart surgery. These factors induced intracystic hemorrhage followed by sudden exacerbation, which resulted in gangrenous cholecystitis followed by perforative biliary peritonitis.

Acute Disease↗
PubMed1992

Developing corticorubral axons of the cat form synapses on filopodial dendritic protrusions.

Developing neurons transiently grow numerous spine- or filopodium-like dendritic protrusions (SLDPs). Electron microscopy on identified input and intracellular staining of postsynaptic cells were performed to gain insight into their significance. Newborn kitten-corticorubral axons, labelled with biocytin, commonly made synapses on SLDP, often multiply invaginated by the SLDPs. Correspondingly, intracellularly labelled kitten rubrospinal cells had numerous SLDPs. Taking into account that corticorubral synapses are largely formed on dendritic shafts in adult cats, it is likely that the SLDPs play some important role in the development of corticorubral synapses. We hypothesize that rubrospinal cells elongate SLDPs searching for corticorubral axons to form synapses.

Aging↗
PubMed1992

Plasticity of neuronal connections in developing brains of mammals.

Although mature nervous systems show substantial malleability following various surgical or environmental manipulations, developing brains show far more prominent plasticity, particularly in terms of morphological features. Neuronal circuits, for example, can be dramatically rewired following neonatal but not adult brain lesions. It remains unknown why neuronal circuits in developing brains show such remarkable plasticity. A number of anatomical and physiological studies suggest that there are transient projections in developing brains and they are eliminated by cell death and/or collateral elimination as development proceeds. This raises a possibility that aberrant projections observed following various surgical or environmental manipulations such as partial denervation, results from retention or stabilization of transient projections. However, evidence suggests that cell death does not play an important role in developmental fine-tuning of neuronal projections. Furthermore, although the elimination of axon collaterals takes place, individual neurons appear to elaborate axonal arbors in appropriate target areas, resulting in a net increase in the size of axonal arbor emerging from individual neurons. In accord with these observations, the number of synapses appear to increase during the period when axonal elimination proceeds. Taken together, reinforcement of appropriate projections rather than elimination of excessive connections plays a major role in developmental specification of neuronal connections. Appearance of aberrant projections after partial denervation may not be a consequence of disordered axonal growth, since they form topographic maps which precisely mirrors those for normal projections. They may be induced due to reinforcement of pre-existing neuronal connections rather than to construction of novel pathways. Observations of axonal morphology in denervated areas indicate that lesion-induced enlargement of projections is due to transformation of axonal morphology, from simple and poorly branched to multiply branched. Perhaps such simple and poorly branched axons in inappropriate target areas may represent ones in the course of elimination but they may serve as a source of sprouting when denervated. In other words, after total elimination of axons any surgical or environmental manipulation cannot induce enlargement of projections. The mechanisms underlying such modifiability of neuronal connections remains unclarified but possible participation of an activity-dependent competitive mechanism is discussed.

Animals↗
PubMed1992

Autoradiographic analysis of dopamine D1 receptors in the gerbil brain following transient cerebral ischemia.

1. We studied the postischemic time-course of dopamine D1 receptors in selectively vulnerable areas in the gerbil using receptor autoradiography. 2. [3H]SCH 23390 was used to label dopamine D1 receptors and transient cerebral ischemia was induced for 10 min. 3. [3H]SCH 23390 binding showed no significant alteration in selectively vulnerable areas at an early stage (1-24 hr) of recirculation. Thereafter, [3H]SCH 23390 binding showed a significant reduction in most selectively vulnerable areas 48 hr or 7 days of recirculation. The ventromedial striatum and dentate gyrus which were resistant to ischemia also exhibited a significant reduction in [3H]SCH 23390 binding. 4. Especially, marked reduction was noted in the dorsolateral striatum. However, this reduction in the dorsolateral striatum was not seen early in the recirculation prior to morphological neuronal damage. 5. The result suggests that transient cerebral ischemia can cause a severe reduction in dopamine D1 receptors in most selectively vulnerable areas. Furthermore, they suggest that dopamine D1 transmission is not always responsible for the evolution of ischemic brain damage. 6. These findings are discussed in relation to the mechanism of ischemic brain damage.

Animals↗
PubMed1992

[Effects of tiropramide hydrochloride on the isolated detrusor and intravesical pressure of the bladder in situ in rats].

The effects of tiropramide on the isolated detrusor and intravesical pressure of the bladder in situ in rats were compared with those of flavoxate, oxybutynin and terodiline. The IC50 values (x 10(-5) M) of tiropramide for carbachol (CCh)-, K+ (60 mM)-, Ba2+ (10 mM)-, and electrical stimulation-induced contractions were 3.6, 4.2, 5.8, and 2.9, respectively. The four antispasmodics used (2 and 4 mg/kg, i.v., each) abolished the rhythmic bladder contractions in situ in anesthesized rats. Of the four compounds, oxybutynin was most potent and no significant differences were observed between the inhibitory effects of tiropramide, flavoxate and terodiline. The administration of flavoxate (30 and 60 mg/kg) into the duodenum little influenced the rhythmic bladder contractions. Tiropramide, flavoxate, oxybutynin and terodiline (8 and 12 mg/kg, i.v., each) dose-dependently prolonged the time to the volume-evoked micturition reflex, and the activity of tiropramide was not statistically different from those of the other three antispasmodics. Under unilateral pelvic and bilateral hypogastric nerve transection, both of the contractions induced by electrical stimulation of the peripheral and central cut ends of the pelvic nerve were dose-dependently inhibited to the same extent by tiropramide and terodiline. These results suggest that the effects of tiropramide on the function of urinary bladder in rats may be mainly due to direct actions on the smooth muscle, and that tiropramide is more potent than flavoxate and less potent than oxybutynin and terodiline.

Animals↗
PubMed1992

Detection of uremic peaks in dogs by anion exchange high performance liquid chromatography.

Sera of dogs with gentamicin-induced uremia were analyzed by high performance liquid chromatography system with strongly basic macroreticular anion exchange resin. Satisfactory separation of peaks was achieved with good reproducibility after deproteinization of sera with trichloroacetic acid at a final concentration of 3%, confirming that the system was suitable for qualitative analysis of uremic serum. The chromatograms showed that the number of peaks and the peak area had relation to concentrations of serum urea nitrogen or creatinine and severity of uremia. Four peaks were selected as suspected canine uremic peaks with high correlation to serum creatinine concentrations which were hardly influenced by extrarenal factors. The results suggested that these four fractions might contain uremic toxins.

Animals↗
PubMed1992

[Automated assay method for protein C anticoagulant activity].

We developed an automated assay method for protein C anticoagulant activity to prolong the APTT measured with automated coagulation apparatus. The automated assay method required following three reagents. One was 0.025 mol/l calcium chloride solution. The other two were a protein C deficient plasma and a phospholipid plus protein C activator both of which constituted a recomposed protein C assay kit (BMY). 0-50% activities of protein C and clotting times were regressed on normal linear curve, while 25-150% activities and clotting times were regressed on logarithmic curve. The coefficients of variation were 2.9-3.4% (intra-assay) and 3.6-3.9% (inter-assay). A correlation of protein C activities between measured by automated assay method and by ordinary manual method was good (r = 0.954). Our data suggest that this automated assay is a useful method for measuring the protein C anticoagulant activities utilizing a coagulation apparatus.

Blood Coagulation Tests↗