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Biomedical subjects

M Miyazaki

Publications and source records attributed to M Miyazaki.

At least 1,081 records · Page 60Linked to original sources
PubMed1976

Further studies on the reduction of vitamin A content in the livers of rats given polychlorinated biphenyls.

Further investigations on the reduction of vitamin A content in the liver of rats fed a 0.1% PCB diet were conducted. The first experiment, in which rats were fed a 0.1% PCB diet for 8 weeks and vitamin A in the liver was determined at 2-week intervals, suggested that a significant decrease of vitamin A in the liver might occur within 2 weeks of PCB ingestion. In the second experiment a significant reduction of vitamin A content per gram of liver, but not per whole liver, in rats fed a 0.1% PCB diet was observed on the 3rd day of PCB ingestion, and then on the 6th day the difference between the control group and the PCB-fed group became much more remarkable. But thereafter no further reduction was seen, indicating a lower limit of vitamin A concentration in the liver of rats fed PCB. It was found that retinol binding protein in the serum of rats fed the 0.1% PCB diet decreased to one-half that of the control group on the 10th day of PCB ingestion, suggesting also a marked reduction in serum vitamin A level. Another experiment revealed that a decrease in hepatic vitamin A occurred even at low PCB levels, but serum phospholipid did not respond at all to any PCB level examined until 7 days after PCB ingestion began. The mechanisms of sensitive response of vitamin A in the animals fed PCB are briefly discussed.

Animals↗
PubMed1976

[Massive epistaxis from intracranial extradural aneurysm of the internal carotid artery associated with head injury (author's transl)].

Severe epistaxis following head injury occur from damage to the anterior ethmoidal or sphenopalatine arteries. However, the more massive, life-threatening posttraumatic epistaxis is that arising from ruptured aneurysm, arteriovenous fistula, or tear of the intracranial extradural portion of the internal carotid artery. The authors had opportunities to treat successfully 3 cases of massive delayed epistaxis from the aneurysm of this site following closed head injury. Case 1. A 23-year-old man was injured in a motorcycle accident on April 19, 1968 and taken to an emergency hospital, where the findings were semicomatose state, profuse bleeding from the left nostril and oral cavity, and laceration above the left eye associated with fracture of the left sphenoid. Since regaining consciousness he was blind in the left. Slight localized protrusion of the cavernous portion of the left internal carotid was shown by angiography, which was performed on the next day (Fig. 1). Three days later, he was transfered to Toyokogyo Hospital. On April 29, he had sudden severe epistaxis. The nasal bleeding recurred massively 6 times over 2 months, requiring the replacement of more than 8000 cc of blood. Sixty days after the trauma, carotid angiography demonstrated an large aneurysm arising from the left internal carotid (Fig. 2). The authors were consulted on this occasion. Intra- and extracranial trapping of the internal carotid artery associated with muscle embolization (Jaeger's operation) was performed (Fig. 3). Postoperative course was uneventful except occurrence of temporary diabetes insipidus. Case 2. This 59-year-old man was admitted to our clinic on November 7, 1970, Because of posttraumatic recurrent massive epistaxis. Thirty-seven days before admisstion, he was hitted by a car and lost consciousness. Profuse nasal bleeding occurred immediately after the accident. Despite skin lacereation above the right eye, visual acuity was not distrubed and no fracture line was found. Two weeks after the injury, he had sudden massive bleeding from the right nostril. The epistaxis recurred 5 times over 3 weeks. Carotid angiography revealed an aneurysm arising from the right internal carotid (Fig. 4). The internal carotid was gradually occluded at the cervical level without any neurological complication. Case 3. A 33-year-old man was referred to our department on October 7, 1974, complaining of recurrent profuse bleeding from the oral cavity. About 2 months prior to admission, he fell from the fourth floor on the street and became comatose. Several fracture lines of the frontal bones were found on skull film. Thirty-six days after the accident, sudden severe epistaxis occurred. Massive bleeding from the oral cavity repeated every 7 to 10 days. Visual acuity was lost within 10 weeks. III and VI cranial nerves palsy was found on the both sides. Carotid angiography demonstrated a small aneurysm of the left internal carotid (Fig. 5). Occlusion of the internal carotid at the cervical level stopped bleeding without further neurological deficit...

Adult↗
PubMed1976

[Quantitative measurement of the basilar arterial flow in the dog-electromagnetic flow-meter study of the extra-and intracranial arterial occlusion (author's transl)].

Recent advances in microneurosurgery have markedly improved the result of surgical treatment of aneurysm and arteriovenous malformation in the posterior cranial fossa. However, more precise study on hemodynamics of the vertebro-basilar system may be necessary for further progress in treatment of the vascular lesions. From this point of view, the authors studied the basilar arterial flow of the dog by means of an electromagnetic flow-meter and the flow probe which was specially devised by the authors. (1) The ratio of absolute value of the mean basilar flow to the total brain weight was calculated, and the flow rate was expressed in ml/100 g brain/min. Mean value was 7.1 ml/100 g brain/min under normocapnea. (2) The effect of occlusion of the common carotid, of the external carotid, of the intracranial internal carotid, and of the extracranial internal carotid on the basilar flow was less remarkable in this order. (3) Under normocapnea, occlusion of the unilateral common carotid artery produced 115% increase in the basilar arterial flow. Bilateral common carotid occlusion resulted in 312% increase of the flow, demonstrating a remarkable ability of compensation of the basilar artery through the circle of Willis and leptomeningeal anastomoses. Under hypercapnea, unilateral common carotid occlusion was followed by 81% increase in the basillar flow. Occlusion of both common carotids caused 230% increase in the basilar flow. Percent increase in the basilar flow after unilateral or bilateral common carotid occlusion under normocapnea was significantly larger than under hypercapnea (p less than 0.05 and p less than 0.01 respectively). It may be supposed that under normacapnea the increased basilar flow following bilateral common carotid occlusion may compensate the decrease in total cerebral blood flow due to carotid occlusion. However, the compensatory rise in the basilar flow under hypercapnea may be not enough to supply the dilated vascular bed in the carotid and basilar territories. There might be even a risk of deficiency of blood supply in the territory of the basilar artery, if the vascular resistance in the carotid area could become less than that in the basilar. The significance of CO2 inhalation therapy for ischemic cerebral lesion was discussed. (4) After the both common carotid arteries were occluded, the basilar aretry was clamped temporarily. Following release of basilar occlusion, reactive hyperemia was observed in the basilar flow. Magnitude and duration of the reactive hyperemia increased progressively depending on duration of the basilar occlusion to some extent. The phenomenon may be best explained by a progressive accumulation of vasodilating metabolities in the ischemic area. (5) Unilateral vertebral occlusion caused 37% decrease in the basilar flow. Bilateral vertebral occlusion resulted in reverse of the basilar flow, averaging 61% of the original value in flow rate. (6) Occlusion of the unilateral subclavian artery produced "subclavian steal phenomenon"...

Animals↗
PubMed1976

Differential mechanisms of increased alpha 1-fetoprotein production in rats following carbon tetrachloride injury and partial hepatectomy.

Possible differences in the mechanisms of increased alpha1-fetoprotein (AFP) production following carbon tetrachloride (CCl4) intoxication and partial hepatectomy were studied with 5-week-old rats at the time of sacrifice. The maximum level of serum AFP reached in 4 days after a single dose of CCl4 was much higher than that after partial hepatectomy, although the incorporation of [3H]thymidine into liver DNA increased nearly to the same extent by either of these treatments. In the remnant after partial hepatectomy, the DNA synthesis that was further accelerated by treatment with a lower dose of thioacetamide was not associated with any further increases of serum AFP levels. However, CCl4 given to partially hepatectomized rats had an additive effect on increased AFP levels. The increases of serum AFP concentrations in CCl4-injured rats had an additive effect on increased AFP levels. The increases of serum AFP concentrations in CCl4-injured rats were depressed by Mitomycin C given in vivo, whereas the increases in partially hepatectomized rats were not. Treatment with 8-azaguanine inhibited both increase of serum AFP levels, although the inhibition was much less or was insignificant in partially hepatectomized rats. These results suggest that existence of different underlying mechanisms of the increased AFP production for the two experimental conditions.

Animals↗
PubMed1976

Increased alpha1-fetoprotein production in rat liver injuries induced by various hepatotoxins.

Serum alpha1-fetoprotein (AFP) concentration in 5-week-old rats was measured by the radioimmunoassay technique after a single administration of various hepatotoxins. Marked elevation of serum AFP concentrations occurred in rats treated with carbon tetrachloride, thioacetamide, D-galactosamine, allyl alcohol, allyl formate, and ethionine in 4 days of these treatments. The increased production of AFP appeared to be correlated with the induction of liver glucose-6-phosphate dehydrogenase (G-6-PD) among biochemical parameters studied for hepatocellular injuries. However, the difference in time courses of the increase in liver G-6-PD activity and serum AFP level following CC14 treatment suggested that the increased production of serum AFP and the induction of G-6-PD in injured liver were caused by closely related but different mechanisms. Pretreatment of CC14-injured rats with N,N'-diphenyl-p-phenylenediamine or aminoacetonitrile was effective not only in lowering the increased level of serum AFP and liver G-6-PD but also in preventing liver cell necrosis and steatosis induced by CC14. Treatment with a lower dose of thioacetamide resulted in littel elevation of serum AFP and liver G-6-PD with a markedly increased incorporation of 3H-thymidine into liver DNA without any evidence of liver injury. On the other hand, the administration of ethionine, which caused little necrosis of liver cells, produced increase in both serum AFP and liver G-6-PD levels with an only small increase of hepatic DNA synthesis compared to those following thioacetamide as well as CC14. These results suggest that the elevation of serum AFP is not directly related to the stimulation of hepatic DNA synthesis. Some additional mechanisms of specific gene amplification for AFP, which is geared to hepatic injury per se, appear to play a major role in the increased AFP production in injured liver.

Aminoacetonitrile↗
PubMed1975

Developmental study of human visual and auditory evoked responses.

The present study investigated the development of visual evoked response by varying the physical factor of photic stimulus size and the psychological factor of age and the development of auditory evoked response was investigated on habituation trials, using the subjects of wide range in ages. The results showed that visual evoked response decreased in amplitude as a function of age and increased as a function of stimulus size and the auditory evoked response also decreased in amplitude as a function of age, while no prominent habituation of evoked response over the trial blocks was observed.

Adult↗
PubMed1975

[Electric thrombosis of the experimental aneurysm--effect of alteration in intraaneurysmal hemodynamics on thrombus formation and progress of thrombosis (author's transl)].

Electric thrombosis may be one of useful method to provide protection against re-bleeding from the intracranial aneurysm which cannot be obliterated by clipping or ligation of its neck without disturbing arterial circulation. However, a better method is required to make the aneurysm to be almost completely thrombosed within one or two hours and to avoide marked damage of its wall, dislodging of the formed thrombus and excessive thrombosis. In this report a method of electric thrombosis of the experimental aneurysm was studied, and effects of hematocrit value and alteration in intraaneurysmal hemodynamics on thrombus formation and progression of thrombosis were investigated. An aneurysm-like vein pouch of 6 to 9 mm in diameter and of 5 to 8 mm in height was made on the common carotid artery of the dog. One week later, patency of the "aneurysm" was confirmed on angiogram. An anodal electrode of a platinum needle of 0.2 mm in diameter was inserted into the "aneurysm" to place the tip of the needle approximately at the center of the sack. Two platinum plates of 3 mm in diameter and of 0.1 mm in thickness were used as the cathodes and were placed externnally on the aneurysm wall. Direct current of 3 mA was applied for 5 or 10 minutes, or current of 5 mA for 5 minutes. Intraaneurysmal pulsating jet and turbulent flows were reduced by occlusion or stenosis of the common carotid. Size of the thrombus immediately after passing current and further progress of thrombosis were evaluated on angiogram and also on plethysmogram of the "aneurysm". Hematocrit value of 45% or more was favorable in producing a thrombus. Although direct current of 3 or 5 mA was desirable to avoid injury of the "aneurysm" wall and to inhibit dislodging of the formed thrombus, only a small thrombus was produced around the anode. Simultaneous occlusion or stenosis of the carotid artery proximally to the "aneurysm" during application of the current markedly promoted thrombus formation. With current application for 5 minutes, 30 to 40% or more of "aneurysm" lumen was occupied by the thrombus in a half of the cases. When the thrombus had reached to approximately 40% of aneurysm "sack" 5 minutes after passing DC current, it progressed to 80% within the following one hour. The most favorable site of the anode for progression of thrombosis was the proximal wall (cardiac side) of "aneurysm". Proximal occlusion or stenosis of the carotid artery promoted remarkably also progress of thrombosis. Excessive thrombosis, dislodging or spontaneous resolution of the formed thrombus was not found throughout one month follow-up. Histologically, the thrombus was organized within one month and covered with the endothel extending from the parent artery.

Animals↗