[Pharmacokinetics and intraventricular therapy with methotrexate via Ommaya reservoir for central nervous system leukemia (author's transl)].
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Biomedical subjects
Publications and source records attributed to K Kitamura.
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In the previous report, the authors described a method obtaining numerical values of 'standard deviation (SD)' and deviation coefficient (DC) from printed out data of a brain CT slice picking up the basal ganglia. In the report, using these values, a possibility of numerical discrimination between normal and abnormal was also discussed. In the present investigation, it was attempted to apply admissible linear discriminant analysis to numerical diagnosis using SD value and DC value. From fifty normal scans and fifty abnormal ones of proved pathology, the admissible linear discriminant function, as below, was extracted, its misdiscriminant rate being 7.6% theroretically. S=-0.4248(SD)-6.4709 (DC) S larger than or equal to -11.447; normal, S < -11.447; abnormal. By this analysis, 98% of abnormal scans and 92% of normal scans were correctly judged without referring to analogue display and actual misdiscriminant rate was 5.0%. Furtermore, for the purpose of confirming reappearance of this result, another twenty normal scans and twenty abnormal scans were investigated by this method. Only one normal scan was judged uncorrectly and all abnormal scans were judged correctly. Accordingly misdiscriminant rate of this sample was 2.5%. It would be emphasized that this method was useful for screeing examination by CT, not only because the total discriminant rate was high, but also false negative rate was relatively low.
Difference in angles between horizontal section of Schaltenbrand & Bailey's atlas and horizontal section of CT based on Cantho-Meatal line is only 3.5 to 5.5 degrees. Therefore, the horizontal section of Schaltenbrand & Bailey's atlas can be utilized for analysis of the horizontal section of CT scan, because the basal ganglia are located approximately in the center of the cranial cavity. The lesions at the basal ganglia with superimposing technique utilizing the relation between horizontal section of Schaltenbrand & Bailey's atlas and analogue view of CT can be identified anatomically.
A case of aortitis syndrome (pulseless disease) associated with basilar aneurysm is reported. This patient was 52-year-old woman suffering from pulseless disease for past fifteen years. She was admitted to our hospital with severe headache, nausea and vomiting. Four vessel angiograms revealed an aneurysm of the basilar artery and occlusion of the right vertebral artery. The internal carotid artery in the left side and the subclavian artery in the right side were not demonstrated even by the serial aortography. As regard to the pathogenesis of cerebral aneurysms associated with aortitis syndrome, questions are in discuss whether the aneurysm is of congenital nature or the result of acquired arteriosclerosis due to aortitis syndrome. In addition, the rupture mechanism of basilar aneurysm associated with aortitis syndrome is discussed.
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Plasma and cerebrospinal fluid CEA determination was done in 97 patients with neurosurgical disorders. Elevated titres were found in 14 of 64 patients with brain tumours. CEA levels were elevated significantly in patients with metastatic brain tumours. Following treatment, the values fell in three patients with ependymoma, medulloblastoma, and unverified brain tumour. This study suggests that CEA levels may be of value in the differential diagnosis of primary and metastatic brain tumours, and useful in the evaluation of patients with brain tumours after treatment. CEA in the cerebrospinal fluid was absent in eight patients with brain tumours.
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Histopathology of a case of bilateral sensorineural hearing loss of abrupt (sharp cut) type is reported. While there was a 45 dB gap in threshold between 1,000 Hz and 2,000 Hz bilaterally, the patient had a good hearing at 1,000 Hz and lower frequencies. The patient was suffering from Takayasu's arteritis. Major histopathological findings were as follows: Almost complete loss of the outer hair cells from the basal end to 12 mm area in the left cochlea (length: 30.5 mm) and 13 mm in the right (length: 31.5 mm). The inner hair cell of the same region was also missing in the left cochlea, and to a lesser degree in the right. There was a clear separation between the normal and the pathological organ of Corti. Marked loss of the cochlear neuron was noted in the same region. Blood vessels within the cochlea and the internal auditory meatus were normal. Bilateral abrupt (sharp cut) type sensorineural hearing loss with unknown etiology is a group of inner ear disease due to abiotrophy of the organ of Corti and cochlear neuron. Disposition or hereditary factor possibly plays an important role in the development of hearing loss.
Three forms of alpha-glucosidase, I, II, and III, have been purified from the whole body extract of adult flies of Drosophila melanogaster in yields of 2.1, 5.3, and 6.7%, respectively. The purification procedures involved ammonium sulfate fractionation, Con A-Sepharose 4B affinity chromatography, DEAE-Sepharose CL-6B ion exchange chromatography, Sephacryl S-200 gel filtration, and preparative gel electrophoresis. Each purified enzyme showed a single band on polyacrylamide gel on both protein and enzyme activity staining. The molecular weights of alpha-glucosidases I, II, and III were estimated to be 200,000, 56,000, and 76,000, respectively, by gel filtration. SDS gels indicated that alpha-glucosidases II and III were each composed of a single polypeptide chain, whereas alpha-glucosidase I was composed of two identical subunits. Both alpha-glucosidases II and III hydrolyzed sucrose and p-nitrophenyl-alpha-D-glucoside (PNPG), but alpha-glucosidase I hydrolyzed PNPG to a much lesser extent than sucrose. For sucrose the pH optima of alpha-glucosidases I, II, and III were pH 6.0, 5.0, and 6.0 and the Km values were 13.1, 8.9, and 10 mM, respectively. For PNPG the pH optima of alpha-glucosidases II and III were pH 5.5 and 6.5 and the Km values were 0.77 and 0.21 mM, respectively.
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The effects of ACh on the smooth muscle cell membrane and mechanical property of the guinea-pig main coronary artery were observed by micro-electrode and isometric tension recording methods. 1. The membrane potential was low (--44 mV) and the membrane was electrically quiescent. Application of outward current pulse generated only a small graded response. The current--voltage relationship was linear for application of inward current pulses. 2. In low external Na or Cl solution the membrane was hyperpolarized. In external K solution of the 1.2--17.8 mM the membrane potential remained nearly the same; however increasing it to more than 29.5 mM depolarized the membrane. The maximum slope of depolarization was 42 mV per tenfold increase in external K. These results indicate that both Na and Cl equilibrium potentials were positive to the resting membrane potential. 3. ACh (greater than 10(-8) g/ml.) hyperpolarized the membrane, to a maximum of --67 mV with 10(-6) g ACh/ml. The dose--response relationship was sigmoidal, and the hyperpolarization was suppressed by atropine (10(-7) g/ml.). In external K of 1.2--29.5 mM, the application of 10(-6) g/ml. ACh hyperpolarized the membrane; this ACh-induced hyperpolarization was maximal in 1.2 mM-K (from --42.4 to --82.4 mV). When the hyperpolarization produced by 10(-6) g ACh/ml. was plotted against the external K concentration on a log scale, the relationship was linear above 1.2 mM-K and similar to that observed between the membrane potential and external K concentration between 29.5 and 118 mM in the absence of ACh. However, in a solution containing less than 1.2 mM-K, the amplitudes of ACh-induced hyperpolarization were reduced. 4. In Na- or Cl-deficient solution the membrane was hyperpolarized. The peak hyperpolarization to ACh was not modified by these changes in the ionic environments. It is concluded that ACh increases K permeability selectively in this muscle membrane. 5. To observe the reversal potential level of ACh-induced hyperpolarization, the effects of ACh were observed during the hyperpolarization and subsequent recovery of the membrane on rewarming the tissue following cold storage. When the membrane potential was high (less than --70 mV) ACh produced depolarization, but when it was low (greater than --70 mV) ACh produced hyperpolarization. The reversal potential level for ACh-induced potential change was about --70 mV. 6. Application of ACh (greater than 10(-8) g/ml.) evoked a mechanical response. The hyperpolarization of the membrane produced by ACh appeared coincidently with tension development. ACh also enhanced the amplitude of contracture produced by excess external K concentration. 7. It is concluded that ACh might increase K and Ca permeabilities of the membrane and release Ca from the intracellular store, thus causing hyperpolarization of the membrane and contraction.
The effects of acetylcholine (ACh), noradrenaline (NA) and isoprenaline (Isop) on the membrane and mechanical properties of smooth muscle cells of the pig coronary artery were investigated by micro-electrode, double sucrose gap and isometric tension recording methods. (1) The mean membrane potential was -51.4 mV and the membrane was electrically quiescent. Application of outward current pulse generated a graded response. The current-voltage relationship was linear for application of inward current pulses. The length constant of the tissue was 0.67 mm and time constant of the membrane was 290 msec. The tissue possessed cable-like properties. (2) ACh (10(-10) to 10(-5) g/ml.) did not change the membrane potential and membrane resistance, but NA and Isop hyperpolarized the membrane and reduced the membrane resistance. These actions of catecholamines, presumably mediated by beta-adrenergic receptors, were suppressed by propranolol but not phentolamine. (3) The minimum depolarization required to produce the contraction was 4 mV by excess extracellular K concentration and 6 mV by electrical displacement of the membrane potential. The amplitude of the contraction evoked by depolarization in excess K was consistently larger than that by the electrical displacement. The minimum concentration required to produce the contraction induced by ACh was 5 x 10(-9) g/ml. NA and Isop consistently suppressed the contraction evoked by excess extracellular K or by ACh. (4) When the tissue was immersed in Ca-free EGTA solution containing excess K or Ca-free EGTA Krebs solution, the time taken for Ca depletion from the intracellular store site was longer with depolarized membranes than that with polarized membranes. ACh evoked contraction, even after the tissue had lost the ability to produce contraction by excess extracellular K in Ca-free solution. (5) After the tissue had been immersed in Ca-free solution containing excess K for more than 4 hr, or Ca-free Krebs solution for more than 2 hr, application of Ca evoked the contraction. These effects of Ca were suppressed by application of catecholamines. The amplitudes of subsequent ACh-induced contraction in Ca-free excess K were not suppressed, while there was a suppression of the K-induced contraction in Ca-free Krebs solution. (6) It is concluded that the smooth muscle cell of the pig coronary artery possesses muscarinic and beta-adrenergic receptors. The former mainly activates the mechanical response without affecting the surface membrane while the latter modifies both membrane and mechanical properties.