Biomedical subjects
Publications and source records attributed to M Kitahara.
For neurotological research we designed a soundproof pressure chamber in which pressure can be adjusted +/- 1000 mmH2O at the rate of less than 100 mmH2O per second. Noise in the chamber can be maintained under 30-35 dB while pressure is kept at a given level.
Hearing is assumed to be altered during or immediately after a change in atmospheric pressure, although this has not been tested experimentally. We used a soundproof pressure chamber to examine the effect of alterations in atmospheric pressure on hearing in 26 normal healthy subjects. The subjects were placed in the soundproof pressure chamber in a supine position and instructed to actively equilibrate middle ear pressure or to abstain from doing so. When the pressure was changed to +/- 500 mmH2O at 33 mmH2O/s the results were as follows: When subjects did not equilibrate middle ear pressure, air conduction at low frequency tones increased more than bone conduction. The degree of deterioration in hearing was greater when the chamber pressure was increased (descent) than where pressure was decreased (ascent). When the subjects equilibrated middle ear pressure, little change in the levels of air or bone conduction was observed. Most of the deterioration in bone conduction was considered to reflect functional loss due to increased stiffness and damping of the sound transmission mechanism.
We used a soundproof pressure chamber to examine how the changes in atmospheric pressure as experienced in daily life reduces bone conduction in a total of 48 normal adults. The subjects were given special ear plugs that connected external auditory canal to the pressure gauge and a small pump located outside the chamber, and were instructed not to swallow, to avoid active opening of the Eustachian tube. The chamber pressure was increased (or decreased) to +/- 500 mmH2O at a rate of 33 mmH2O/s. Then pressure in the external auditory canal was increased (or decreased) gradually after the chamber pressure had reached +/- 500 mmH2O, to equilibrate the pressure across the ear drum. Bone conduction did not recover the level before increase (or decrease) in the chamber pressure. We conclude that at least a minor part of the deterioration in bone conduction after changes in the chamber pressure was caused by displacement of the round window membrane.
Because of Eustachian tube controls middle ear pressure to maintain the best hearing level, we tested the equilibration capacity of the Eustachian tube by measuring hearing levels in a soundproof pressure chamber. The number of swallows to recover normal hearing after the chamber pressure reached -200 mm H2O (an index of equilibration capacity for the static pressure differences across the eardrum) was less than 9 in normal subjects. The worst level of hearing and the time required to recover normal hearing from the beginning of alteration in the chamber pressure to -700 mm H2O (indexes of equilibration capacity for dynamic pressure differences across the eardrum) were 0-17 dB and within 120s in normal subjects. It was difficult to determine definitive normal ranges of the equilibrium capacity of the Eustachian tube when positive pressure was applied.
Using a soundproof pressure chamber, we performed Békésy air conduction audiometry at 1000 Hz under the following pressure conditions: 1) from atmospheric pressure (AP) to 200 mmH2O below AP, 2) AP to 200 mmH2O above AP, 3) AP to 700 mmH2O below AP, and 4) AP to 700 mmH2O above AP. In conditions 1) and 2), the patient was instructed not to swallow until the pressure change was complete, then to swallow once every 15 seconds. The number of swallows required for hearing to return to the baseline level was counted. In conditions 3) and 4), the patient was told to swallow as many times as possible both before and after completion of the pressure change; maximum hearing level and the time needed for return to the baseline level were measured. Although all except one of the seven patients with suspected tubal dysfunction showed normal results with catheter insufflation and tympanometry, six of the seven showed abnormality and one reported the disappearance of ear stuffiness after the ventilation capacity test. We concluded that this test is useful not only for the diagnosis of tubal dysfunction but also as a possible therapy for aiding adaptation to changing environmental pressure.
The application of pressure to the middle ear changes the normal inner ear pressure in animal experiments. In this study we tested the effect of exposure to under- or overpressure on hearing in a total of 78 normal ears (40 subjects) in a soundproof pressure chamber. [After exposure to underpressure, a 10 dB or more gain in 3 ears and loss in 2 ears for at least one of the test frequencies was observed in 38 ears. After exposure to overpressure, a 10 dB or more gain in 5 ears and loss in 1 ear for at least one of the test frequencies was observed in 40 ears.] The characteristics of transferred inner ear pressure during a series of exposures to underpressure seemed to be similar to those during exposures to overpressure.
In the last 15 years, a pressure chamber able to generate negative air pressure has been used to treat patients with Menière's disease. In this study we sought to clarify whether the underpressure chamber can be used to diagnose Menière's disease. We studied 45 ears from patients with neurotological diseases. The subjects were placed supine in a soundproof pressure chamber. The pressure was first decreased to -500 mmH2O, and after 5 min to -700 mmH2O. The pressure was kept at this level for another 5 min and then increased to 0 mmH2O. This procedure was done three times in succession. While the chamber pressure was below 0 mmH2O, the subjects were instructed to abstain from actively equilibrating middle ear pressure. When the chamber pressure was raised to 0 mmH2O, they were instructed to equilibrate middle ear pressure, and if necessary Politzerization or catheterization of the Eustachian tube was done. As a result, hearing was improved after this procedure only in patients with Menière's disease (50%) and/or cochlear Menière's disease (32%) in which endolymphatic hydrops was suspected.
Hearing in patients with Menière's disease improved when they were treated in an underpressure chamber. In this study 46 patients with neurotological diseases, including 32 cases of Menière's disease, were tested in an overpressure chamber. As a result, hearing in 32% of the patients with Menière's disease improved, although this was lower than the 50% rate of improvement in Menière's disease patients tested in an underpressure chamber.
Global balance of inner and middle ear pressure is controlled by the cerebrospinal fluid inside and the atmospheric pressure outside. The cochlear and vestibular aqueducts and the Eustachian tube, connected by a one-way communication, provide a fine control over inner and middle ear pressure.
Local cerebral lesions may cause depression of function in remote areas of the brain presumably by a transneural mechanism. This has been called "diaschisis". In the present study, regional brain blood flow in hypertensive right putaminal hemorrhage was studied in 33 patients (mean age, 55 year; 22 men, 11 women) to investigate the relationship between the degree in damage of the original lesions and "diaschisis". The hematoma was treated conservatively in 8 patients, aspirated stereotaxically in 9 patients, and evacuated through craniotomy in 16 patients. The regional blood flow in bilateral motor cortices and bilateral cerebellar hemispheres was measured by a single photon emission CT with N-isopropyl-p- [123 I] iodo-amphetamine intravenous injection, and was evaluated by the RI count on early image/the decay-corrected RI count on delayed image (E/D). The regional brain blood flow was measured for 29 to 35 days from the onset. There was a negative correlation between the degree of the extension to the internal capsule and the regional blood flow of the right motor cortex and the bilateral cerebellar hemispheres. There was also a negative correlation between the volume of the hematoma and the regional blood flow of the right motor cortex and the bilateral cerebellar hemispheres. The regional blood flow of the left motor cortex correlated with neither the degree of the extension to the internal capsule nor the volume of the hematoma. On the other hand, there was a positive correlation in the regional blood flow between the bilateral motor cortices.(ABSTRACT TRUNCATED AT 250 WORDS)
Local cerebral lesions may cause depression of function in remote areas of the brain presumably by a transneural mechanism; it has been called "diaschisis". In the present study, to investigate the relationship between motor function and "diaschisis" regional brain blood flow in hypertensive right putaminal hemorrhage was studied in 33 patients (mean age, 55 years; 22 men, 11 women). The hematoma was treated conservatively in 8 patients, aspirated stereotaxically in 9 patients, and evacuated through a craniotomy in 16 patients. The regional blood flow in the right motor cortex and the left cerebellar hemisphere was measured by a single photon emission CT with N-isopropyl-p- (123 I) iodo-amphetamine intravenous injection method, and was evaluated by the RI count on early image/the decay-corrected RI count on delayed image (E/D) value. The time during which regional brain blood flow was measured ranged from 29 to 35 days from the onset. There was a positive correlation between the grade in the motor function in the subacute stage and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. There was also a positive correlation between the Barthel index in the chronic stage (mean follow-up periods: 40 months) and the regional blood flow in the right motor cortex and the left cerebellar hemisphere. The results of the present study suggest that in right putaminal hemorrhage the flow reduction in areas remote from the primary lesion, i.e., "diaschisis", may reflect not only the degree of functional abnormalities of the internal capsule, but also the possibility of functional recovery.
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A 20-year-old man received 60 Gy of radiation therapy after partial removal of craniopharyngioma. The patient had been well and follow-up CT scans did not show any aggravation for 16 years. Since his activity gradually diminished, he underwent an MRI at the age of 36 which revealed an abnormal mass on the corpus callosum. The mass lesion progressively enlarged thereafter, and was diagnosed as anaplastic astrocytoma by a stereotactic biopsy. He was treated with interferon, however, died at the age of 37. Review of literature disclosed 19 other cases of glioma following radiation therapy for sellar/parasellar tumors. Characteristic features of these cases included 1) lowness of age compared to common glioma cases, 2) tendency to be malignant, 3) tendency to occur in areas where significant doses of radiation had been received previously.
BACKGROUND: A 12-year-old girl with intractable retroperitoneal paraganglioma experienced increased appetite, acne, obesity, "moon face," and enlargement of the clitoris during the course of the tumor. Plasma cortisol, serum testosterone, and dehydroepiandrosterone sulfate (DHEA-S) levels were increased to 34.1 micrograms/dl, 2.0 ng/ml, and 6.628 ng/ml, respectively. Adrenocorticotrophic hormone (ACTH) levels were not increased, and results of dexamethasone suppression tests were negative. Her condition was diagnosed as Cushing syndrome with virilism. Plasma cortisol levels were increased to a level of 107.1 micrograms/dl before death. METHODS: Tumor samples were obtained at the time of autopsy. The concentrations of cortisol, androgens, ACTH, and catecholamines were assayed in the tumor extracts. The indirect immunoperoxidase procedure was performed on fixed tissues for cortisol, DHEA-S, testosterone, and ACTH. RESULTS: Extracts of the tumor masses contained steroid hormones: the amount of immunoreactive cortisol was 1.64 micrograms/g wet weight; the amount of immunoreactive testosterone was 25.60 ng/g wet weight; immunoreactive DHEA-S, 579.00 ng/g wet weight; and immunoreactive ACTH, 891.00 pg/g wet weight in the metastatic mass of the lung. Immunohistochemically, immunoreactive cortisol, testosterone, and DHEA-S were detectable in the tumor cells. The adrenal gland was atrophic. CONCLUSIONS: The patient is the first reported with malignant paraganglioma with the capacity to produce cortisol, androgens, and ACTH.
The cytotoxicity of monoterpenes, percutaneous absorption enhancers, to cultured human skin cells was investigated in order to quantitatively estimate their skin damage. A neutral red bioassay with epidermal keratinocytes and a contraction test of collagen gel in which dermal fibroblasts were cultured were employed for evaluating the cytotoxicity of terpenes. In the neutral red bioassay, keratinocyte proliferation was inhibited on the addition of terpenes, and cell survival remarkably decreased with an increase in the concentration of terpenes fed into the culture well. When the fibroblasts were cultured in a collagen gel matrix, the lattice of collagen contracted as the cells grew. Therefore, the application of cytotoxic agents brings about an inhibition of collagen gel contraction induced by the fibroblasts. Strong inhibition was observed in the cases of hydrocarbons in terpenes, and the inhibition was dependent on the concentration of these compounds added in the culture medium. The cytotoxicity of terpenes was compared with the skin damage evoked by the application of terpenes in rats in vivo. As a result, it was considered that the skin irritation caused by terpenes was predictable to a certain extent by means of the cytotoxic study of cultured human skin cells.
We studied the mechanisms of hypolipidemic effects of NIP-200 (3,5-dimethyl-4,6-diphenyltetrahydro-2H-1,3,5-thiadiazine- 2-thione), a potent hypolipidemic compound, in cholesterol biosynthesis in the liver, cholesterol absorption in small intestine, and cholesterol catabolism and excretion in rats. NIP-200 did not reduce cholesterol biosynthesis and had no effects on cholesterol absorption in the small intestine. In the cholesterol catabolism and excretion, NIP-200 induced increases in cholesterol and bile acids levels in the bile and acidic steroids in the feces, and it enhanced cholesterol 7 alpha-hydroxylase activity in the liver. These results suggest that NIP-200 increases the synthesis of bile acids as a result of the activation of cholesterol 7 alpha-hydroxylase, the rate-limiting enzyme in the conversion of cholesterol to bile acids. Therefore, it is considered that one of the probable mechanisms of the serum total cholesterol lowering action of NIP-200 involves the enhancement of catabolism and excretion of cholesterol in the liver.
A patient with an enhancing, completely intracanalicular mass on MRI was presented. He had noticed progressive hearing loss in the left ear with tinnitus. Neurological examination revealed no abnormality except decreased hearing in the left ear. There were no other cranial nerve or cerebellar signs. An audiogram revealed profound hearing loss on the left ear with no ability of speech discrimination. Brainstem auditory evoked response was absent on the left. MRI enhanced with gadolinium-DTPA demonstrated an intracanalicular enhancing lesion on the left which was presumed to be an intracanalicular acoustic neurinoma. The patient underwent a left suboccipital craniectomy. The eighth cranial nerve appeared normal in the cerebellopontine angle cistern, and was swollen and discolored in the internal auditory canal. It was removed piecemeal. The patient remained deaf in the left ear postoperatively. Histopathologically, the lesion consisted of edematous nerve fiber and inflammatory cells, but no tumor cell was present within the specimen. The patient was diagnosed as having neuritis. The clinical time course of symptoms in our patient was not unusual for an acoustic neurinoma. It seems that the distinction between an intracanalicular acoustic neurinoma and other lesions cannot be made on basis of MR imaging alone. All available imaging modalities should be considered before a definitive surgical procedure is undertaken.
For the elucidation of the mechanism of membrane stabilization by vitamin E, the effects of alpha-tocopherol and its model compounds on either retinol-induced hemolysis of rabbit erythrocytes or the permeability and fluidity of liposomal membranes have been studied. Retinol-induced rabbit erythrocyte hemolysis has been found not to be caused by the oxidative disruption of erythrocyte membrane lipids initiated by retinol oxidation, but rather to arise from physical damage of the membrane micelle induced by penetration of retinol molecules. In suppressing hemolysis, alpha-tocopherol was more effective than other naturally occurring tocopherols. alpha-Tocopheryl acetate, nicotinate, and 6-deoxy-alpha-tocopherol were more effective than alpha-tocopherol itself. The inhibitory effects of alpha-tocopherol model compounds having side chains with at least two isoprene units or a long straight chain instead of the isoprenoid side chain were similar to those of alpha-tocopherol. These data suggest that for protection of membranes against retinol-induced damage, the hydroxyl group of alpha-tocopherol is not critical, but rather the chroman ring, three methyl groups on the aromatic ring, and the long side chain are necessary. To verify the mechanism of the inhibitory effect on hemolysis, not only the effect of vitamin E and its model compounds on the membrane permeability and fluidity, but also the mobility of alpha-tocopherol molecule in membranes has been investigated using bilayer liposomes as the model membranes. Addition of alpha-tocopherol to membranes produced a greater decrease in the permeability and fluidity of rat liver phosphatidylcholine liposomes compared with egg yolk phosphatidylcholine liposomes. In dipalmitoylphosphatidylcholine liposomes, however, alpha-tocopherol was less effective, that is, the more unsaturated the lipids, the more they interact with alpha-tocopherol. 2,2,5,7,8-Pentamethyl-6-chromanol with no isoprenoid side chain and phytol without the chromanol moiety had no effect. The measurement of 13C NMR relaxation times revealed that the mobility of methyl groups on the aromatic ring of alpha-tocopherol in membranes is significantly restricted. In contrast, the methyl groups at positions 4'a and 8'a on the isoprenoid side chain have high degrees of motional freedom in the lipid core of membranes. Furthermore, it was found that alpha-tocopherol in membranes interacts with chromate ions added as potassium chromate outside the membranes, resulting in an increase in membrane fluidity. These results are compatible with those of the inhibitory effect on retinol-induced erythrocyte hemolysis. On the basis of the results obtained here, a possible mechanism for membrane stabilization by vitamin E is proposed.