Emergence of two superconducting phases (33 K and 40 K) and their relation to structural phase transitions in crystalline La2CuO4.011.
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Journal Article↗
Biomedical subjects
M Itoh
Publications and source records attributed to M Itoh.
Pressure dependence of phase-transition temperatures in oxygenated single-crystalline La2CuO4.035.
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Journal Article↗
Ultrasonography gives directly but noninvasively elastic characteristic of human tendon in vivo.
To obtain an insight into tendon elasticity during human movement, a real-time ultrasonography was applied to the contracting tibialis anterior muscle. The insertion point of fascicles onto the aponeurosis was clearly visualized, and its position relative to a fixed marker on the skin moved proximally (delta 1) according to the increasing dorsiflexion force (delta F) with a fixed ankle joint. Notably, the delta 1-delta F relationship in the tendon was found to be quadratic in nature (delta F = c delta 1(2); c = 1.48-2.24, r = 0.985-0.992, n = 9) as has been reported in the isolated tendon, although the delta F-delta 1 curves were slightly underestimated in comparison with the stiffness constant estimated from tendon architecture. This underestimation might be caused by changes in the height of the foot arch with the application of force.
Adult↗
Effects of hypophysectomy on soleus muscle fibers and spinal motoneurons in rats.
The fiber type distribution of the soleus muscle in male and female rats was investigated 4 weeks after hypophysectomy. Oxidative enzyme activity of the soleus motoneurons in the spinal cord was also examined by enzyme histochemical assay. In male rats, the total number of fibers in the soleus muscle was not changed after hypophysectomy, but the percentage of intermediate (INT) fibers (with intermediate adenosine triphosphatase activity following alkaline preincubation, and high succinate dehydrogenase and alpha-glycerophosphate dehydrogenase activities) was increased. All types of fibers in the soleus muscle of hypophysectomized rats showed high adenosine triphosphatase activity following acid preincubation. Oxidative enzyme activity of the motoneurons innervating the soleus muscle was not changed after hypophysectomy. Similar results were obtained in female rats. It is suggested that the increased percentage of INT fibers in the rat soleus muscle after hypophysectomy is due to a lack or reduced levels of growth hormones, and that the metabolic capacities of the muscle fibers and of the innervating motoneurons are affected independently by hypophysectomy.
Animals↗
Effects of hypobaric hypoxia on histochemical fibre-type composition and myosin heavy chain isoform component in the rat soleus muscle.
Histochemical fibre-type composition and myosin heavy chain isoform component in the soleus muscle were studied in normoxic rats at postnatal ages of 5, 10, 15, and 20 weeks and in rats exposed to hypobaric hypoxia (460 torr) for 5 weeks from postnatal ages of 5, 10, and 15 weeks. The increase in the percentage of type I fibres and the concomitant decrease in that of type IIa fibres in the soleus muscle of normoxic rats were observed until 15 weeks of age. On the other hand, no change in the fibre-type composition of the muscle during postnatal development was observed in hypoxic rats, irrespective of the age at which they were exposed to hypoxia. The changes in the myosin heavy chain isoform component (MHC I and MHC IIa) of the muscle during postnatal development and by hypoxia corresponded well with those in the muscle fibre-type composition. It is concluded that hypobaric hypoxia inhibits the growth-related shift of muscle fibre-types from type IIa to type I and of myosin heavy chain isoforms from MHC IIa to MHC I in the rat soleus muscle, and that there are no changes in the muscle fibre-type composition or the myosin heavy chain isoform component caused by hypoxia after the shifts in these parameters which occur during postnatal development are completed.
Aging↗
Safety and efficacy of intraperitoneal injection of etoposide in oil suspension in mice with peritoneal carcinomatosis.
We compared the safety and efficacy in mice with peritoneal carcinomatosis of two etoposide formulations: an aqueous solution (Etp-sol) and particles suspended in oil (the addition products of iodine and the ethyl esters of the fatty acids obtained from poppy-seed oil (Lipiodol) or sesame oil; Etp-oil). We also investigated tissue distribution of etoposide in rats treated with Etp-oil and Etp-sol. Etoposide was injected intraperitoneally at concentrations ranging from 52 to 392 mg/kg (increasing geometrically by a factor of 1.4). The 50% lethal dose (LD50), determined over a 2-week period of observation, was 135 mg/kg for Etp-oil and 108 mg/kg for Etp-sol. Autopsy findings included macroscopic intestinal bleeding, necrosis of the intestinal mucosa, and pulmonary congestion in mice from both treatment groups. In the efficacy trials. 10(6) P388 leukemia cells were transplanted into CDF1 male mice, and Etp-oil and Etp-sol were injected at doses of 20 mg/kg and 80 mg/kg. In the groups receiving the 20 mg/kg dose, 11 of 19 mice in the Etp-oil group survived to day 60 compared with 3 of 20 mice in the Etp-sol group. Toxicity-related deaths occurred in 1 of 20 mice treated with 80 mg/kg Etp-oil and in 8 of 20 mice treated with 80 mg/kg Etp-sol. No cancer-related deaths were associated with the 80 mg/kg dose in either treatment group. Our findings showed that the Etp-oil was associated with a lower toxicity and a higher efficacy than the Etp-sol. To evaluate tissue distribution, rats were injected intraperitoneally with 5 mg/kg body weight of Etp-sol or Etp-oil. The tissue distribution of etoposide was subsequently analyzed by high performance liquid chromatography. Compared with Etp-sol, Etp-oil delivered significantly greater amounts of etoposide and for a longer period to the omentum, taken as representative of the intraperitoneal tissue, and the etoposide concentration in blood plasma was increased more slowly and decreased more gradually.
Animals↗
Epidermal growth factor enhances repair of rat intestinal mucosa damaged by oral administration of methotrexate.
To examine the trophic effect of epidermal growth factor on the rat small intestine, we measured diamine oxidase and ornithine decarboxylase activities in intestinal mucosa injured by methotrexate. Methotrexate was infused orally via a gastric tube at a dose of 10 mg/kg per day on 3 successive days (days 1-3). Epidermal growth factor was injected intraperitoneally at a dose of 40 micrograms/kg per day on 4 successive days following methotrexate infusion (days 4-7). Methotrexate caused a marked decrease in diamine oxidase activity; this decrease returned to a normal level on day 13 in controls. In rats injected with epidermal growth factor, diamine oxidase activity began to recover earlier than in the controls, and returned to a normal level on day 11. Epidermal growth factor enhanced the increase of ornithine decarboxylase activity in mucosa injured by methotrexate. When the increase of ornithine decarboxylase activity was suppressed by alpha-difluoromethylornithine, epidermal growth factor failed to facilitate the repair of intestinal mucosa. These results indicate that epidermal growth factor enhances intestinal repair following methotrexate infusion, and that this effect is mediated, at least in part, by ornithine decarboxylase. It is proposed that epidermal growth factor can be used clinically as a means to enhance mucosal repair of the intestine after chemotherapy with methotrexate.
Administration, Oral↗
Validation of noninvasive quantification of rCBF compared with dynamic/integral method by using positron emission tomography and oxygen-15 labeled water.
This study proposes a new solution for the quantification of rCBF pixel-by-pixel using PET and 15O-H2O. The method represents an application of weighted integration that used PET image only, requiring no input function of arterial blood. It generates the rCBF image quickly and automatically. Simulation studies revealed that the calculation of rCBF was fairly stable as long as a relatively shorter scan frame time and longer scan time were selected. Calculated images of actual PET study by this method correlated significantly with those identified by the dynamic/integral method. Because this procedure could detect whole brain CBF change between different studies as accurately as by the dynamic/integral method, this procedure may be the most suitable for brain activation studies.
Cerebrovascular Circulation↗
The role of brain acetylcholine in phenol-induced tremor in mice.
The relation between phenol-induced tremor and brain acetylcholine levels, and the effects of cholinergic drugs on the tremor were investigated, using male ddY mice weighing 28-35 g. The magnitude of phenol-induced tremor was graded on a 4-point scale: 0, normal; 1, slight; 2, moderate; 3, severe, and acetylcholine levels were measured by high-performance liquid chromatography with electrochemical detection. The magnitude of tremor and the decrease in acetylcholine levels in the striatum and cerebral cortex induced by s.c. injection of phenol (50, 100, 200 mg/kg) were dose-dependent, and both showed parallel time courses. Intracerebroventricular (i.c.v.) injection of phenol (100 micrograms/mouse) caused a decrease in acetylcholine levels in the striatum but did not induce tremor. Intraperitoneal injection of pentobarbital (10 mg/kg), which inhibits the release of acetylcholine, weakened both the magnitude of the tremor and the decrease in acetylcholine levels induced by phenol (200 mg/kg), whereas i.c.v. injection of pentobarbital (120 micrograms/mouse) attenuated the decrease in acetylcholine levels induced by phenol, but did not affect the magnitude of the tremor. Intraperitoneal (20 mg/kg) or i.c.v. (60 micrograms/mouse) injection of mecamylamine further strengthened the tremor. Intraperitoneal (0.3 mg/kg) injection of physostigmine strengthened the tremor, while i.c.v. injection (1 microgram/mouse) caused a reduction in its magnitude. These results suggest that the tremor is caused directly by the phenol-induced increase in acetylcholine release in the peripheral nervous system (motor nerve endings), that the decrease in brain acetylcholine levels may be due to phenol-induced increases in acetylcholine release within the central nervous system, and that the resultant reduction in brain acetylcholine levels indirectly suppresses the tremor.
Acetylcholine↗
Nicotine stimulates pepsinogen secretion from guinea pig gastric chief cells in monolayer culture.
We evaluated the effects of nicotine on pepsinogen secretion in vitro, using a monolayer culture system of guinea pig gastric chief cells. Pepsinogen secretion was increased by above 5 mM nicotine in a dose-dependent manner, as was the elevation of intracellular free calcium concentration ([Ca2+]i). The pepsinogen secretion stimulated by 10 mM nicotine was inhibited by above 1 mM d-tubocurarine, a nicotinic receptor antagonist, but not by same concentrations of scopolamine hydrobromide monohydrate or pirenzepine, a muscarinic receptor antagonist. The elevation of [Ca2+]i induced by 5 mM nicotine was also reduced by 10 mM d-tubocurarine, but not by 10 mM pirenzepine. A calmodulin inhibitor, N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7), at the concentration of 10(-6) M and a myosin light-chain kinase inhibitor, 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-9), at concentrations above 10(-7) M also significantly blocked 10 mM nicotine-induced pepsinogen secretion. These finding indicate that nicotine directly stimulates pepsinogen secretion probably via nicotinic receptors on the gastric chief cells, and that the Ca(2+)-mediated messenger system, including calmodulin and myosin light-chain kinase, is involved in this event.
Animals↗
Phenotypical heterogeneity of testicular macrophages/dendritic cells in normal adult mice: an immunohistochemical study.
The distribution of macrophage/dendritic cell antigens was investigated immunohistochemically in frozen testis sections of normal A/J mice using a panel of rat monoclonal antibodies against murine macrophage/dendritic cell antigens (F4/80, BM8, MP23, MOMA1, MOMA2, M5/114, BMDM1 and NLDC145). Sections of lymphoid organs were employed as positive controls. Stained-macrophages/dendritic cells in the testicular interstitium were various in shape, such as irregular-, elongate-, round- or oval-shaped cytoplasm with short or long cytoplasmic protrusions, but, the most conspicuous morphology was irregular. The testicular macrophages/dendritic cells were subdivided into four types of cells by their localization; various-shaped cells associated with Leydig cells and other interstitial cells (Type I); stretched cells attached to the seminiferous tubular wall (Type II); stretched cells attached to the blood vessel wall (Type III); and stretched cells attached to the inner side of the testicular capsule (Type IV). Examination of the staining pattern of the various antibodies showed that the macrophage/dendritic cell antigens differed from each other in amount present and localization, indicating phenotypical heterogeneity of the testicular macrophages. Additionally, a few macrophages were identified in the testicular capsule and in the tubuli recti but never in the seminiferous tubules.
Animals↗
A quantitative study of the effects of prenatal X-irradiation on the development of cerebral cortex in rats.
Pregnant rats were exposed to a single whole body X-irradiation on day 15 of gestation at a dose of 1.0 Gy. The offspring showed microcephaly at 7 weeks of age. Their body weight, brain weight, cortical thickness and the numerical density of neurons and synapses in the somatosensory and visual cortex were examined. Significant decreases in cortical thickness in both somatosensory (25%) and visual (16%) cortex were observed. However, there were no significant changes in the numerical density of neurons and synapses, nor in synapse-to-neuron ratios in both cortical regions between control and X-irradiated groups. These results suggest that prenatal X-irradiation can decrease the number of neurons, and the neurons which survive X-irradiation proliferate and elaborate connections in a normal fashion. This is in contrast to the animals exposed to ochratoxin A, in which numerical density of neurons in the somatosensory cortex is increased, with normal numerical density of synapses, resulting in low synapse-to-neuron ratios. The discrepancy in the synapse-to-neuron ratios between the X-irradiation and ochratoxin A-treatment might derive from a different effect on the developing neurons.
Animals↗
Excitation and inhibition by cisapride of spontaneous and evoked electrical responses in smooth muscles of guinea-pig stomach.
In isolated circular smooth muscles of the guinea-pig stomach, cisapride depolarized the membrane, increased the amplitude and interval of slow waves, and enhanced the cholinergic excitatory junction potential, with no change in the nonadrenergic noncholinergic inhibitory junction potentials. Methysergide mimicked the excitatory actions of cisapride on junction potentials. Results showed that cisapride has dual actions on gastric muscles; excitation by facilitating the release of ACh possibly via 5-HT receptor blockade and also by depolarizing the smooth muscle membrane, and inhibition by reducing the frequency of slow waves, possibly by acting directly on the pacemakers.
Acetylcholine↗
Neuroleptic malignant syndrome in striatonigral degeneration.
A 6-year-old boy with striatonigral degeneration had an episode of neuroleptic malignant syndrome after an upper respiratory infection. Dantrolene treatment was successful. Some reports have demonstrated that anesthetic and antipsychotic agents lead to neuroleptic malignant syndrome in disorders of the basal ganglia. However, neuroleptic malignant syndrome attributable to a respiratory infection has not previously been reported. Our patient illustrates the potential morbidity of neuroleptic malignant syndrome in patients with striatonigral degeneration.
Child↗
Effects of mazindol in two patients with Prader-Willi syndrome.
Two patients with Prader-Willi syndrome, including gross obesity with food-related behavior and mild mental retardation, are presented. One patient was an 11-year-old girl with the diagnosis of development delay, hypoactivity, and waxy skin with normal female karyotype. The other patient was a 15-year-old girl with the diagnosis of abnormal chromosome 15. Obesity had been present since early childhood, and it was difficult for them to manage their weight control by means of diet and exercise therapy. With 24-week mazindol administration, they demonstrated marked improvement in weight control during the early period and improvement in pathologic behavior without side effects. Mazindol was given orally, 1.0-2.0 mg/day, in one or two daily doses. Mazindol may prove to be useful in the treatment of patients with Prader-Willi syndrome.
Adolescent↗
Sarcolemmal indentation in cardiomyopathy with mental retardation and vacuolar myopathy.
Muscle biopsies from three patients with cardiomyopathy, mental retardation and increased serum creatine kinase levels revealed scattered fibers with tiny intracytoplasmic vacuoles containing basophilic and acid phosphatase-positive material and slightly increased amounts of PAS-positive granules. These findings are consistent with those seen in the so-called lysosomal glycogen storage disease with normal acid maltase. In addition to the vacuoles, there were occasional folds or indentations in the sarcolemma which were connected to the membrane enclosing the vacuoles. These membranes were well demonstrated histochemically by the nonspecific esterase and acetylcholinesterase stains. On electron microscopy, most of the vacuoles were bounded by membranes with basal lamina. The vacuolar membrane stained positively with antibodies raised to dystrophin, dystrophin-associated glycoproteins, laminin and type 4 collagen, and it was identical to the sarcolemma and its basal lamina. Therefore, the membrane abnormality which causes sarcolemmal folding is probably critical to understanding the pathomechanism of this disease.
Adolescent↗
Positron emission tomography (PET) study of the alterations in brain distribution of [11C]methamphetamine in methamphetamine sensitized dog.
[11C]Methamphetamine ([11C]MAP) was synthesized by an automated on-line [11C]methylation system for positron emission tomography (PET) study. We newly produced a MAP sensitized dog by repeated MAP treatment and studied the brain distribution of [11C]MAP in the normal and the MAP sensitized dog. The maximal level of accumulation of [11C]MAP in the sensitized dog brain was 1.4 times higher than that in the control. No difference was found in the metabolism of MAP between the two conditions. The significant increase of [11C]MAP in the MAP sensitized brain indicates that subchronic MAP administration causes some functional change in uptake site of MAP.
Animals↗