[A case of insulin autoimmune syndrome with transient islet cell surface antibodies accompanied by liver cirrhosis].
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Biomedical subjects
Publications and source records attributed to S Satoh.
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The autoregulation of norepinephrine (NE) release mediated by presynaptic alpha and beta adrenoceptors on sympathetic nerve terminals in the heart of pentobarbital-anesthetized dog was studied. NE overflow elicited by left cardiac sympathetic nerve stimulation was determined from the coronary sinus blood, by using high-performance liquid chromatography with electrochemical detection. Intracoronary infusion of epinephrine (1,3 and 10 micrograms/min) into the left circumflex artery increased basal left ventricular dp/dt maximum (LV dp/dt max) and coronary sinus blood flow. The epinephrine infusion decreased coronary sinus output of NE (NE output) during left cardiac sympathetic nerve stimulation. Intracoronary infusion of isoproterenol (0.03, 0.1 and 0.3 microgram/min) increased the basal LV dp/dt max and coronary sinus blood flow, whereas the stimulation-induced increases in NE output, LV dp/dt max and coronary sinus blood flow were not altered by its infusions. Intravenous injection of IPS-339 (0.03, 0.1 and 0.3 mg/kg), a selective beta-2 adrenoceptor antagonist, diminished the stimulation-induced increases in LV dp/dt max and coronary sinus blood flow in a dose-dependent manner, whereas it did not decrease the stimulation-induced increase in NE output. Intracoronary infusion of yohimbine (10, 30 and 100 micrograms/min), a preferentially selective alpha-2 adrenoceptor antagonist, facilitated the stimulation-induced increases in NE output, LV dp/dt max and coronary sinus blood flow. There was no significant difference in the facilitation of the stimulation-induced increases in NE output, LV dp/dt max and coronary sinus blood flow between intracoronary infusion of both isoproterenol (0.1 microgram/min) and yohimbine (100 micrograms/min) and the infusion of yohimbine alone.(ABSTRACT TRUNCATED AT 250 WORDS)
The patient was a 27-year-old man who developed spastic quadriplegia and cerebral disorders. Initial signs were gait disturbance, spastic paraplegia, and sphincter disturbance; these occurred when he was 21. Upon autopsy, the white matter of the brain and spinal cord showed diffuse demyelination, and the adrenal glands and right testis were atrophic. Cytoplasmic striations seen by light microscopy and trilamellar inclusions seen by electron microscopy were found in ballooned adrenocortical cells. Trilamellar inclusions were also observed in macrophages of the affected cerebral white matter. Biochemical analysis disclosed a high ratio (0.27) of hexacosanoic acid (C26:0) to docosanoic acid (C22:0) in cerebrosides and sulfatides of the cerebrum. The histological features as well as the result of biochemical analysis were those of classical adrenoleukodystrophy. However, the time of the onset of clinical signs and the duration of the disease were different in the present case from classical adrenoleukodystrophy. The case presented here was diagnosed as adrenoleukomyeloneuropathy, which is a variant of adrenoleukodystrophy.
Thirty-one patients (23 adolescent, eight adult) underwent spinal fusions with Zielke instrumentation for idiopathic thoracolumbar and lumbar scoliosis. Their curves averaged 55.2 degrees. In most patients the length of fusion did not extend beyond the major curve. Correction of scoliosis was 82% in adolescents and 59% in the adults. The kyphotic component of the curves was corrected from an average of 21 degrees to 8 degrees. Correction of the spinal vertebra rotation was 46% in the adolescent patients. The tilt angle of the vertebra at the lower end of the curve was reduced significantly. The fusion rate was 93.5%. Two of the adult patients developed pseudarthrosis. Major complications were not encountered. The Zielke instrumentation system in the management of idiopathic thoracolumbar and lumbar scoliosis offers the advantages of a relatively good correction and minimal segment fusion.
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From 1978 to 1983, 54 consecutive patients with unstable degenerative spondylolisthesis were treated by medial facetectomies and posterolateral fusion with combined distraction and compression rod instrumentation. The average period of follow-up observation was 30 months. Twenty-five patients had a combination of disc herniation or instability, excluding olisthesis. Single-level fusion was performed in 29 patients, two-level in 23, and three-level in two. Preoperative low-back pain in 87.0% and sciatica in 66.7% were reduced to 7.5% and 5.6%, respectively, at follow-up treatment. Preoperative neurogenic intermittent claudication in 63.0% and neurogenic bladder in 11.1% disappeared completely in all patients at follow-up examination. The solid fusion rate was 96.3%. Difference between the values of %-slip and slip-angle before surgery and those at follow-up examination was not statistically significant. Rod breakage occurred in two patients with pseudarthrosis. The overall clinical results were satisfactory relief of clinical symptoms and regression of physical signs, with a high rate of solid fusion.
The effect of ventromedial-arcuate (VMH-ARC) nuclei lesions on plasma growth hormone (GH) response to human growth hormone-releasing factor (GRF, 1 microgram/kg b.wt., i.v.) was studied in conscious rats after they had received chlorpromazine (CPZ) or CPZ plus antiserum against somatostatin (ASS). When rats were pretreated with CPZ alone, there was no difference in basal plasma GH level between VMH-ARC lesioned rats and controls. The magnitude of plasma GH response to GRF in 5 out of 6 VMH-ARC lesioned rats exceeded that of controls. When the same observation was repeated using the same rats after they had received ASS and CPZ, basal plasma GH levels of controls were significantly higher than those of VMH-ARC lesioned rats, and the magnitude of the plasma GH response to GRF was augmented in both groups of rats. The plasma GH response to GRF was comparable between two groups, though the peak plasma GH response to GRF was slightly but significantly lower in VMH-ARC lesioned rats as compared to controls. Pituitary GH content was reduced significantly in VMH-ARC lesioned rats as compared to controls. The results demonstrate that the pituitary responsiveness to GRF does not appear to be altered significantly in rats bearing bilateral VMH-ARC lesions. In addition, the placement of electrolytic lesions in VMH-ARC regions causes reduced SS secretion into the hypophyseal portal vessels and leads to an augmentation of plasma GH response to GRF.
Angiotensin II markedly potentiated both PGE2 and PGI2 productions in the isolated dog renal arteries. This angiotensin II-induced response was significantly reduced by the treatments of EGTA and calcium antagonists such as verapamil, nifedipine and 8-(N,N'-diethylamino)-octyl-3,4,5,-trimethoxybenzoate (TMB-8). Calmodulin inhibitors, trifluoperazine and W-7 also inhibited the angiotensin II-induced PG productions while an inactive analogue of W-7, W-5 did not have any effect. The results suggest that angiotensin II may enhance the intracellular Ca2+ level through the influx of extracellular Ca2+ and then, calmodulin activated with Ca2+ will stimulate both PGE2 and PGI2 productions via its activation of phospholipase A2 in the dog renal arteries.
The effects of verapamil and isosorbide dinitrate (ISDN) alone or together on mechanical responses of the rabbit coronary artery and mesenteric vein, and the dog coronary artery have been investigated. Verapamil, in concentrations exceeding 10 nM consistently inhibited and at 10 microM, blocked the contraction evoked by excess concentrations of K in these tissues, but agonist-induced contraction was not modified by the presence or absence of Ca. In concentrations greater than 1 microM, verapamil depolarized the membrane by inhibiting the K-conductance of the membrane. ISDN had little effect on the rabbit coronary artery in concentrations below 10 microM. In contrast, in the rabbit mesenteric vein and dog coronary artery, ISDN in concentrations over 1 microM inhibited the contraction evoked by excess concentrations of K or by agonists. Species differences were apparent in the actions of ISDN on vascular tissues. When verapamil and ISDN were simultaneously applied to the rabbit mesenteric vein and dog coronary artery, the K-induced contraction was markedly inhibited by an amount exceeding that produced by the sum of the contractions evoked by the individual application of both agents. An enhanced vasodilating action induced by simultaneous applications of both agents indicates a possible clinical benefit for anti-anginal treatment.
We have developed a sensitive and nonradiometric assay of estradiol 2- and 16 alpha-hydroxylase activities using reverse-phase high-performance liquid chromatography with voltametric detector. The 2- and 16 alpha-hydroxylated estrogens produced by the incubation of estradiol with rat liver microsomes were initially separated into the catechol and phenolic fractions using a QAE-Sephadex A-25 borate column. The metabolites were detected in quantities as low as 0.5-1 ng using 3-methoxy-1,3,5(10)-estratriene-2,16 alpha,17 beta-triol or 4-hydroxyestrone 17-oxime as an internal standard. Apparent Km and Vmax of the 2- and 16 alpha-hydroxylases were 41.9 microM and 1.3 nmol/mg protein/min, and 82 microM and 480 pmol/mg protein/min, respectively.
We studied the effect of mitochondrial protein synthesis inhibitors on the neurotrophic action of the nerve stump in mice. The sciatic nerve was cut as close to, or as far from the extensor digitorum longus muscles as possible. At 2 and 3 days after denervation, depolarization in the resting membrane potential of muscles with long nerve stumps (14-16 mm) was significantly smaller than in muscles with very short (less than 2 mm) nerve stumps. Chloramphenicol (100 mg/kg, p.o.), erythromycin (4 micrograms/kg, i.p.), ethidium bromide, (10 micrograms/kg, i.p.) or acridine (10 micrograms/kg, i.p.), administered for 2 or 3 days after denervation, increased depolarization in the resting membrane potential of muscles with long nerve stumps; muscles with very short nerve stumps were not affected by these drugs. The administration of chloramphenicol and erythromycin resulted in an earlier increase in the depolarization than ethidium bromide and acridine. Activities of cathepsin B and L of lysosomal proteases in the nerve stumps were enhanced by nerve degeneration; they were not affected by the administration of chloramphenicol or ethidium bromide. We suggest that proteins synthesized in mitochondria of the nerve may participate in trophic actions.
Fifty-three cases of isthmic spondylolisthesis were treated with distraction rod instrumentation and posterolateral fusion with or without nerve root decompression, and they were followed for an average of 39 months. Thirty-one cases without neurologic deficit were treated with instrumentation and fusion only. In 22 cases of predominant sciatic pain with neurologic deficit signs, nerve root decompression and instrumentation with fusion were conducted. The results showed a 90.6% solid union rate with satisfactory clinical improvement. Realignment of the vertebral displacement such as reduction of olisthesis and widening of the olisthetic disc spaces was obtained to some extent. No serious complications were encountered.
A di-isopropyl phosphorofluoridate-sensitive endopeptidase activity against some minor components of heat-denatured alpha-casein was detected in the endoplasmic reticulum and Golgi body-rich fraction of spinach callus. The activity was not solubilized with 0.05% sodium deoxycholate, but with 0.5% sodium cholate. The activity was strongly inhibited by deoxycholate (0.2-0.5%), di-isopropyl phosphorofluoridate, p-chloro-mercuric benzoate, o-phenanthroline, NiCl(2), CuCl(2), and ZnSO(4), and moderately by phenylmethylsulfonyl fluoride, l-1-tosylamide-2-phenylethyl chloromethyl ketone, iodoacetic acid, ethylenediaminetetraacetate, and FeSO(4), and slightly by chymostatin. The inhibitory effect of o-phenanthroline was partially recovered with the addition of FeSO(4) and ZnSO(4).
The response of plasma renin activity (PRA) to stepwise reductions in renal arterial pressure (RAP) induced by suprarenal aortic constriction (SAC) or hydralazine (0.1-30 mg/kg i.v.), and the effect of indomethacin (5 mg/kg i.v.) or propranolol (1.5 mg/kg) s.c.) on the PRA response were examined in anesthetized rats whose right kidneys had been removed 6-7 days earlier. The stepwise reduction of RAP by SAC or hydralazine produced a steep increase in PRA when RAP was below approximately 100 mm Hg. Above this level, PRA was unaffected by changes in RAP. The SAC-induced increase in PRA was nearly abolished by indomethacin. On the other hand, propranolol failed to affect the SAC-induced increase in PRA. The hydralazine-induced renin release was remarkably suppressed by either indomethacin Or propranolol. These results suggest that SAC-induced renin release is mainly dependent on the prostaglandin system, whereas hydralazine-induced renin release is dependent on the prostaglandin and the adrenergic nervous system. We estimated the threshold pressure for increasing renin release is approximately 100 mm Hg.
The response of the urethra to intra-arterially administered autonomic agonists was studied in vivo by measuring the motility and pressure changes in female dogs. Phenylephrine produced shortening along the transverse axis with an increase in urethral pressure in a dose-dependent manner. Isoproterenol produced lengthening along the transverse axis with a decrease in urethral pressure. Both acetylcholine and dimethylphenylpiperazinium did not produce consistent patterns in urethral response. It seems that adrenergic drugs act predominantly on the circular muscle layer and cholinergic drugs act equally on both the circular and longitudinal muscle layers.
The characteristic of the antinociceptive effect of a tetrapeptide, Asn-Ala-Gly-Ala (NAGA), was examined. Intracisternal (i.cist.) administration of NAGA to mice produced dose-dependent and long-lasting antinociceptive effect as evaluated by the hot plate and tail flick methods. NAGA-induced antinociception was reversed by naloxone (2 mg/kg), reserpine (2 mg/kg X 2 d) and alpha-methyl-p-tyrosine (100 mg/kg). NAGA (10 microM) did not significantly affect the actions of opioid peptides on the electrically evoked twitches of the myenteric plexus-longitudinal muscle strips from the guinea-pig esophagus and strips of the mouse vas deferens. NAGA-induced antinociception was scarcely affected by p-chlorophenylalanine (PCPA, 300 mg/kg X 2 d) and methysergide (2 mg/kg). From the above results, it was suggested that the antinociceptive effect of NAGA may involve the participation of endogenous opioid peptides and endogenous catecholamines.