Biomedical subjects
Publications and source records attributed to Y Handa.
A case of calcified chronic subdural hematoma was presented. This patient was a 51-year-old man, who had a dizzy spell with headache and vomiting. He was examined by MR study as well as CT scan. The operation was performed and the calcified subdural hematoma was removed safely. MR study is very useful for the preoperative evaluation.
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A multi-channel functional electrical stimulation (FES) system for the restoration of hand function of the quadriplegic is described. The system is composed of a personal computer NEC PC-880lmkII, peripheral electronic circuits and two kinds of sensors, i.e. an analog displacement sensor for volitional control (channel 1) and a logical sensor (high pitch sound or head switch, channel 2). Combination of the two channel signals allow three major function: 1) designation of the desired prehension pattern among cylindrical grasp, key grip and parallel extension grip; 2) selection of the operation status--'start', 'proportional control', 'hold', 'stop'--and, 3) volitional control which can be controlled by the shoulder movement. In the clinical application, Caldwell-Reswick type multistrand stainless steel percutaneous electrodes were used. In this FES system, standard multi-channel stimulation patterns were obtained from electromyographical analysis of joint movement of the upper extremities in normal subjects which gave us precise information about a role of each muscle during various kinds of motion. Such stimulation patterns have enabled us to restore motor function of the paralyzed upper extremities for activities of daily living (ADL).
The intramural fluid circulation of the cerebral arterial wall was investigated using horseradish peroxidase (HRP) as a tracer which was injected intravenously or intracisternally in dogs with or without subarachnoid haemorrhage (SAH). In the control dogs, the endothelial barrier function was confirmed for intravenous HRP, whereas the intracisternal HRP passed freely through the interstitial spaces of the adventitia and media to reach the intima within a few minutes. However, on the 5th day after SAH the barrier function of the intima for intravenous HRP was lost. In addition, there was a marked decrease in the amount of HRP reaching the intima when injected intracisternally. The intercellular space appears to be the main route for leakage of HRP into the subendothelial layer from the arterial lumen. Obstruction of the interstitial space in the adventitia by blood elements may be the cause of the disturbed intramural circulation of cerebrospinal fluid. These results suggest that this disturbance in the intramural circulation of the cerebral arterial wall plays a role in the development and/or progression of delayed cerebro-arterial narrowing after SAH.
Eighteen barbituric acid (BA) derivatives and three structurally related chemicals (non-BA-derivatives) were tested for their potency in supporting survival of functional hepatocytes from adult rats in primary culture. Of the 18 BA derivatives, nine drugs showed excellent maintenance effect on hepatocyte survival and function. Although four BA derivatives were also effective, their potency was relatively lower. The remaining five BA derivatives and three structurally related chemicals exhibited no maintenance effect. Thus, a correlation was found between the BA derivative structure and the potency for supporting hepatocyte survival in primary culture. The dose response curves of hepatocyte survival were generally biphasic in shape, as a function of BA derivative concentration. The optimum concentrations for observing the morphological and biochemical effects of the BA derivatives differed from each other. The maintenance of hepatocytes was attained only in the continuous presence of the BA derivatives in the medium. The nine excellent BA derivatives efficiently prevented hepatocytes from morphological degeneration which was observed in the control cultures. The surviving hepatocytes in the presence of these BA derivatives showed higher albumin secretion and retained higher basal levels of tyrosine aminotransferase (TAT) activity for at least 2 weeks in primary culture, as compared with control. Furthermore, the addition of dexamethasone (10 microM) caused a 2- to 4-fold induction of TAT activity for at least 2-weeks in primary culture.
Ten barbituric acid (BA) derivatives were synthesized and tested for their potency for supporting survival of functional hepatocytes from adult rats in primary culture. Of the 10 BA derivatives, 7 compounds (C-2, 3, 4, 5, 6, 9, and 10) efficiently supported hepatocyte survival for at least 2 wks in primary culture. Especially C-5, 6, and 9 showed excellent efficiency for such action. The optimum concentrations of the BA derivatives for observing the morphological and biochemical effects differed from each other. The maintenance of hepatocytes was attained only in the continuous presence of the BA derivatives in the medium. The morphologic features of hepatocytes surviving in the presence of the BA derivatives resembled those of hepatocytes 24 h after inoculation. The surviving hepatocytes secreted remarkably large amounts of albumin into the culture media. Tyrosine aminotransferase (TAT) activity was higher in the 1-wk-old cultures treated with C-5, 6, and 9 than in the freshly isolated hepatocytes. The addition of dexamethasone (10 microM) caused a 1.7 to 2.1-fold induction in TAT activity. The basal levels of TAT activity and the induction rates increased in the cultures treated with C-5 and 6 from Week 1 to 2 of primary culture.
Barbiturates are often utilized clinically in circumstances in which elevated intracranial pressure is expected. In this study, the mechanism of action of barbiturates was examined in dogs with intracranial hypertension induced by injecting autogenous incubated blood into the chiasmatic cistern. Intracranial pressure and systemic blood pressure were continuously monitored. A single bilateral administration of powdered pentobarbital (2 mg and 0.4 mg) in experimental animals and solid d-glucose (2 mg) in control animals was given into the posterior hypothalamus, pontine reticular formation, or medullary reticular formation when intracranial pressure reached 20-30 mmHg after the blood injection--usually in 3-6 h. The increased intracranial pressure following the experimental subarachnoid hemorrhage was always associated with either intracranial pressure irregularities or concomitant blood pressure variations, suggesting the presence of vasomotor instability. Administration of both 2 mg and 0.4 mg of pentobarbital into the medulla caused a significant (P less than 0.01) decrease of the intracranial pressure to 44 and 65% of control and stabilization of the intracranial pressure irregularities, whereas pentobarbital given at the other sites did not. The blood pressure was also decreased significantly (P less than 0.01) to 80 and 88% of control and the blood pressure variations were stabilized in animals after administration of pentobarbital into the medulla, whereas in those given pentobarbital at the other sites, it was not. The results suggest that, in the presence of elevated intracranial pressure following experimental subarachnoid hemorrhage, the mechanisms of action of barbiturates in reducing the intracranial pressure may result from alleviation of cerebral vasomotor instability by depression of the vasomotor center of the medulla.
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Plateau waves reflect both dilatation of the cerebral vessels and an increase in the cerebral blood volume under increased intracranial pressure (ICP). They are often associated with changes in arterial blood pressure (BP) and respiration, suggesting a role of the brain stem in their development. In experiments conducted on dogs in which intracranial hypertension was induced by occluding the neck veins, the authors stimulated the brain-stem reticular formation in the medulla oblongata and caudal pons to identify the brain sites that produce plateau-like responses. A rise in ICP was observed following stimulation of most areas of the brain stem and was associated with changes in arterial BP, cerebral perfusion pressure (CPP), cerebral blood flow (CBF), respiration, and pulse rate. The stimuli delivered to the medial reticular formation of the caudal medulla caused an arterial depressor response, a decrease in CPP and CBF, suppressed ventilation, and bradycardia; these responses were similar in many respects to plateau waves observed in clinical practice and almost corresponded to the depressor region of the vasomotor center. It is hypothesized that the medullary depressor area may play a role in eliciting cerebral vasomotor reaction concerned with the development of plateau waves in a state of increased ICP.
The effect of complete clot removal at times from 48 to 96 hours after subarachnoid hemorrhage (SAH) on the development of chronic cerebral vasospasm was evaluated to determine whether there is a critical point after which clot removal is ineffective in preventing vasospasm. Thirty cynomolgus monkeys were randomized to one of five groups: sham-operated group, clot removal at 48 hours after SAH (48-hour group), clot removal at 72 hours after SAH (72-hour group), clot removal at 96 hours after SAH (96-hour group), and clot placement only (clot group). Standard microsurgical techniques were used to dissect bilaterally the major cerebral arteries free of arachnoid. An autologous blood clot averaging 4.2 gm was placed around the vessels in the subarachnoid space of the monkeys in the 48-hour, 72-hour, 96-hour, and clot groups. Physiological saline was instilled into the subarachnoid space of the sham-operated animals. Animals in the clot-removal groups underwent surgical clot removal at the determined times for each group. Two animals in each of the sham-operated and clot groups were subjected to reoperation at each of 48, 72, and 96 hours after SAH. The incisions were reopened and then simply reclosed. Neurological status, angiographic cerebral vessel caliber, and physiological status were evaluated before and 7 days after SAH induction. There were no significant neurological deficits in the sham-operated, 48-hour, or 72-hour groups. Two animals in each of the 96-hour and clot groups showed deterioration in level of consciousness developing on Day 4 or 5 after SAH induction. All the major cerebral arteries of the animals in the clot and 96-hour groups showed significant vasospasm (p less than 0.01) on Day 7. Animals in the 72-hour group had significant vasospasm (p less than 0.05) of the internal carotid and middle cerebral arteries but not the anterior cerebral arteries. There was no significant vasospasm (p greater than 0.05) in any of the cerebral arteries in the 48-hour group. Severity of vasospasm paralleled the duration of contact between the blood clot and the cerebral vessels. Evacuation of the subarachnoid hematoma later than 48 hours after SAH resulted in no significant reduction in the degree of chronic cerebral vasospasm. It is suggested that clot removal at early operation is likely to be useful only if it is performed within 48 hours of SAH.
Two cases are reported in which the abdominal catheters slipped into the scrotum through the unobliterated processus vaginalis.
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A case is reported in which an aneurysm on the anterior communicating artery calcified during the time course of 17 years. A ring-like calcification was demonstrated in plain skull films as well as CT scans. Carotid angiograms showed that the aneurysm grew a little bit bigger for 17 years. The aneurysm was coated because of the calcified aneurysm.
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After treatment with 1.5 mM phenobarbital (PB) for about 2 months, non-tumorigenic rat liver epithelial-type cell lines (6F-7 and 6G-5), which were initiated by 3'-methyl-4-dimethyl-aminoazobenzene (3'-Me-DAB) in primary culture, showed an increase in plating efficiency, growth in soft agar and production of tumors in syngeneic animals. However, the PB-untreated control cells exhibited neither growth in soft agar nor production of tumors. Gamma-glutamyltranspeptidase (GGT)-positive (6F-7-cl-7) and negative (6F-7-cl-8) colonial clones, which were derived from 6F-7 cells, were also treated with 1.5 mM PB for about 2 months. The growth of GGT-positive 6F-7-cl-7 cells was not suppressed but rather stimulated by PB at 1.5 mM, whereas that of GGT-negative 6F-7-cl-8 cells was severely inhibited. Furthermore, the PB-treated 6F-7-cl-7 cells produced tumors in syngeneic animals, but the PB-treated 6F-7-cl-8 cells produced no tumors. The spontaneous cell line 6A-6, which was derived from the 3'-Me-DAB-untreated primary liver cell culture and was GGT-negative, did not exhibit tumorigenicity after treatment with 1.5 mM PB for the same period of time as described above. In conclusion, PB treatment efficiently and rapidly promoted the 3'-Me-DAB-initiated cells to a malignant state.
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