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Biomedical subjects

M Shimojo

Publications and source records attributed to M Shimojo.

At least 19 recordsLinked to original sources
PubMed2004

Dynamic profile calculation of deposition resolution by high-energy electrons in electron-beam-induced deposition.

The effect of the accelerating voltage of incident electrons on the resolution of electron-beam-induced deposition was investigated by a dynamic Monte Carlo profile simulator which includes the electron scattering in the already grown deposit structure. By simulating the deposition at two different accelerating voltages of 20 and 200 kV with an idealistic zero-diameter incident probe on a bulk substrate, it was revealed that the smaller size structures were attainable by 200 keV than by 20 keV. The effect of the substrate was also argued by comparing the above results with the simulation results obtained for a point-like starting substrate. Surprisingly, the shapes of the deposits grown on bulk substrates were reproduced well by the simulations starting from point-like substrates indicating the small effect of the substrate on the shape of deposits.

Journal Article↗
PubMed2004

Application of transmission electron microscopes to nanometre-sized fabrication by means of electron beam-induced deposition.

Electron beam-induced deposition was carried out using a scanning transmission electron microscope with a field emission gun to fabricate nanometre-sized structures. A small amount of a metal-organic gas was introduced near the substrate in the microscope chamber, and focused electron beams were irradiated. Two- and three-dimensional structures were fabricated by scanning the beam position. The minimum line width of the freestanding structures was 8 nm at a constant gas flux used. This line width of 8 nm is considered to be achieved by employing a high accelerating voltage, which leads to a small probe size, and the optimum scanning speed.

Imaging, Three-Dimensional↗
PubMed2001

Role of zinc finger domains of the transcription factor neuron-restrictive silencer factor/repressor element-1 silencing transcription factor in DNA binding and nuclear localization.

The transcription factor neuron-restrictive silencer factor/repressor element-1 (RE-1) silencing transcription factor (NRSF/REST) contains nine zinc finger domains and binds to the DNA element, neuron-restrictive silencer element/repressor element-1. REST4, a C-terminally truncated form of NRSF/REST, contains the five N-terminal zinc fingers and binds weakly to DNA yet is transported into the nucleus. To study the contribution of zinc fingers 6-8 to DNA binding, each was mutated. A mutation in zinc finger 6 or 8 had little effect; however, mutation of zinc finger 7 diminished DNA binding. Mutations in any two of these zinc fingers eliminated DNA binding. The contribution of zinc fingers 2-5 to nuclear targeting was studied. Deletion of zinc finger 5 prevented nuclear targeting. Mutations in zinc finger 2, 4, or 5 did not abolish nuclear targeting. However, a zinc finger 3 mutation together with a zinc finger 2 mutation localized to the nuclear envelope. A zinc finger 3 mutation alone or in combination with a zinc finger 4 or 5 mutation produced a punctate nuclear distribution. These results suggest the presence of signals for nuclear targeting, for nuclear entry, and for release from the translocation machinery within zinc fingers 2-5 of REST4.

Base Sequence↗
PubMed2001

Role of (111)In-DTPA-pentetreotide scintigraphy in accurate diagnosis of neuroendocrine gastroenteropancreatic tumors.

Most gastroenteropancreatic neuroendocrine tumors contain high-affinity binding sites for somatostatin, and somatostatin-receptor scintigraphy has been introduced for the in-vivo evaluation of such tumors. We report two patients with gastroenteropancreatic neuroendocrine tumors, in whom it was quite difficult to localize the tumors by conventional techniques, and in whom we found that (111)In-DTPA-pentetreotide scintigraphy was useful for accurate information on tumor localization. In the first patient, who had gastrinoma, multiple tumors were shown in the gastrinoma triangle, but we could not clarify whether there were any tumors in the pancreatic body. The selective arterial secretin injection (SASI) test diagnosed that the gastroduodenal artery was the feeder of the gastrinomas, and (111)In-DTPA-pentetreotide scintigraphy with single-photon emission computed tomography indicated the absence of tumors in the pancreatic body. In the second patient, who had insulinoma, multiple liver tumors and a large mass in the hilum of the spleen were shown. (111)In-DTPA-pentetreotide scintigraphy was useful in determining that there was no secretion of insulin from the tumor in the hilum of the spleen. In conclusion, X-ray computed tomography is superior for detection of neuroendocrine tumors, because not all neuroendocrine tumors have somatostatin receptors; however, somatostatin receptor scanning, as well as the SASI test, may be useful for the surveillance of patients with known primary tumors, for monitoring patients with disseminated disease, and for following the treatment of these patients.

Adult↗
PubMed2001

Relationships between feeding and locomotion behaviors after central administration of CRF in chicks.

The effect of intracerebroventricular injection of corticotropin-releasing factor (CRF) on various behaviors in chicks was determined at 15-min intervals over a 30-min period. Food intake of chicks was significantly decreased, and pecking rhythm was significantly delayed by CRF during the first 15-min post-injection. The similar tendencies were observed in the second 15-min post-injection, but not significantly different. Stepping, as an indicator of locomotion, was not different at 15-min post-injection, but was increased by CRF, thereafter. These results suggest that CRF acts within the central nervous system to decrease food intake and increase locomotion in the chick.

Animals↗
PubMed2001

Expression of 11 beta-hydroxysteroid dehydrogenase isoenzymes in the human pituitary: induction of the type 2 enzyme in corticotropinomas and other pituitary tumors.

One of the defining biochemical features of Cushing's disease is a relative insensitivity to glucocorticoid (GC) feedback, but an analysis of the GC receptor has failed to detect any major abnormalities. However, two isoenzymes of 11 beta-hydroxysteroid dehydrogenase (11 beta HSD), either by converting cortisone (E) to cortisol (F) (type 1) or conversely by converting F to E (type 2), play an important prereceptor role in regulating corticosteroid hormone action at several sites. 11 beta HSD1 and -2 expression within the anterior pituitary gland itself may modulate GC feedback at an autocrine level, and we have speculated that this may be deranged in Cushing's disease. Detection of 11 beta HSD type 1 and 2 immunoreactive protein was performed using fluorescence immunohistochemistry. Double immunofluorescent studies were undertaken on normal pituitary to define the cellular localization of 11 beta HSD isoenzymes using antisera against GH, ACTH, LH, FSH, PRL, and S100, a nonhormonal marker of folliculo-stellate cells. In normal pituitary, positive staining for 11 beta HSD1-immunoreactive protein was observed in GH- and PRL-secreting cells and in folliculo-stellate cells; gonadotrophs, thyrotrophs, and ACTH-positive cells were negative. 11 beta HSD2 immunoreactivity was absent in all cell types. RT-PCR detected 11 beta HSD1 messenger ribonucleic acid (mRNA) expression in the normal pituitary; 11 beta HSD2 mRNA expression was also seen in most normal tissue. By contrast, in ACTH-secreting adenomas 11 beta HSD2 immunostaining was strongly positive in every case of corticotroph adenoma. 11 beta HSD1 immunoreactivity was also observed occasionally, but to a much lesser extent. In other pituitary tumors, both functional and nonfunctional, 11 beta HSD expression was variable in terms of isoenzyme mRNA and intensity of protein staining. The expression of 11 beta HSD1 (which generates F from E) in somatotrophs and lactotrophs suggests an autocrine role for this isoenzyme in the glucocorticoid regulation of pituitary GH and PRL secretion. 11 beta HSD2 expression is markedly induced in ACTH-secreting pituitary tumors and, by converting F to E, may explain the resetting of glucocorticoid feedback control in Cushing's disease.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2001

Pituitary apoplexy caused by luteinizing hormone-releasing hormone in prolactin-producing adenoma.

We report a case in which pituitary apoplexy developed shortly after an intravenous (i.v.) injection of luteinizing hormone-releasing hormone (LH-RH). A 56-year-old man with prolactin-producing pituitary tumor complained of severe headache, visual field loss and facial nerve palsy shortly after LH-RH test. Magnetic resonance image (MRI) revealed a hemorrhage in the pituitary adenoma. He showed dramatic improvement in his symptoms after decompression surgery. These findings suggest a causal relationship between the i.v. injection of LH-RH and pituitary apoplexy. Possible pituitary apoplexy should be kept in mind during pituitary testing.

Facial Paralysis↗
PubMed2000

Central bombesin inhibits food intake and the orexigenic effect of neuropeptide Y in the neonatal chick.

It is well known that central injection of bombesin (BN) suppresses feeding in mammalian and avian species, but the anorexigenic effect of central BN are still open with special reference to the chick. The dose response (0, 0.1 and 0.5 microg) of intracerebroventricular (ICV) injection of BN was examined in Experiment 1. ICV injection of BN inhibited food intake in a dose-dependent manner. Experiment 2 was done to determine whether BN interacts with the orexigenic effect of neuropeptide Y (NPY) in the neonatal chick. Central administration of NPY (2.5 microg) greatly enhanced food intake, but co-injection of BN (0.5 microg) suppressed food intake. The dose response of NPY (2.5 microg) co-injected with three levels of BN (0, 0.1 and 0.5 microg) was examined in Experiment 3. ICV injection of BN attenuated the hyperphagia by NPY in a dose-related fashion. It is suggested that central BN may interact with NPY for the regulation of feeding in the neonatal chick.

Animals↗
PubMed2000

Studies on the interaction of REST4 with the cholinergic repressor element-1/neuron restrictive silencer element.

REST4 is a neuron specific truncated form of the transcription factor REST/NRSE derived by alternative splicing. REST4 was previously shown to block the repressor activity of REST/NRSF by forming a hetero-oligomer, Shimojo et al. [Mol. Cell. Biol. 19 (1999) 6788-6795]. A series of deletion mutants have now been used to characterize REST4 in terms of its structure and DNA binding. REST4 was found to be O-glycosylated between between residues 87 and 152. Binding of REST4 to the cholinergic RE-1/NRSE was approximately 1/10 to 1/20 as strong as full length REST/NRSF. DNA binding was enhanced by deletion of the first 86 residues and was found to require all four of the C-terminal zinc fingers as well as a twelve amino acid sequence preceding the first of these zinc fingers. REST4 can form homo-oligomers, however only the monomer was found to bind to DNA. REST4 binds to the 3' sequence of the cholinergic NRSE suggesting an anti-parallel orientation of the protein to the DNA.

Alternative Splicing↗
PubMed2000

Central administration of alpha-melanocyte stimulating hormone inhibits fasting- and neuropeptide Y-induced feeding in neonatal chicks.

In the present study, the effect of intracerebroventricular (i.c.v.) administration of alpha-melanocyte stimulating hormone (alpha-MSH) on food intake of neonatal chicks was examined. In experiment 1, i.c. v. injection of alpha-MSH (0.04, 0.2 and 1 microg) significantly inhibited food intake of 3-h fasted chicks in a dose-dependent manner. In experiment 2, alpha-MSH strongly inhibited neuropeptide Y-induced feeding when neuropeptide Y (2.5 microg) and several doses of alpha-MSH were given simultaneously i.c.v. These results suggest that alpha-MSH plays an important role in the regulation of food intake of neonatal chicks.

Animals↗
PubMed2000

Brain-derived mast cells could mediate histamine-induced inhibition of food intake in neonatal chicks.

In the present study, the effect of intracerebroventricular (i.c.v.) administration of histamine on food intake of neonatal chicks was examined over 2 h. Histamine (100, 200 or 400 nmol, respectively) was injected in the lateral ventricle of 2-day-old chicks, and cumulative food intakes were measured. i.c.v. injection of histamine significantly inhibited food intake in a dose-dependent manner. In addition, compound 48/80, which causes degranulation of mast cells and release of histamine, or thioperamide, which is an antagonist of the histamine H3 autoreceptor and increases histamine release from histaminergic nerve terminals, was injected i.c.v. to clarify whether mast cell- or neuron-derived histamine in the central nervous system of chicks is essential to the feeding inhibition. Central administration of compound 48/80 inhibited food intake with a dose-dependent manner, but thioperamide had no effect on feeding. An inhibitor of mast cell degranulation, sodium cromoglycate, somewhat attenuated food intake inhibited by compound 48/80. These results suggest that brain-derived mast cells could be a major source of histamine in the inhibition of food intake of neonatal chicks.

Animals↗
PubMed2000

The somatosensory evoked magnetic fields.

Averaged magnetoencephalography (MEG) following somatosensory stimulation, somatosensory evoked magnetic field(s) (SEF), in humans are reviewed. The equivalent current dipole(s) (ECD) of the primary and the following middle-latency components of SEF following electrical stimulation within 80-100 ms are estimated in area 3b of the primary somatosensory cortex (SI), the posterior bank of the central sulcus, in the hemisphere contralateral to the stimulated site. Their sites are generally compatible with the homunculus which was reported by Penfield using direct cortical stimulation during surgery. SEF to passive finger movement is generated in area 3a or 2 of SI, unlike with electrical stimulation. Long-latency components with peaks of approximately 80-120 ms are recorded in the bilateral hemispheres and their ECD are estimated in the secondary somatosensory cortex (SII) in the bilateral hemispheres. We also summarized (1) the gating effects on SEF by interference tactile stimulation or movement applied to the stimulus site, (2) clinical applications of SEF in the fields of neurosurgery and neurology and (3) cortical plasticity (reorganization) of the SI. SEF specific to painful stimulation is also recorded following painful stimulation by CO(2) laser beam. Pain-specific components are recorded over 150 ms after the stimulus and their ECD are estimated in the bilateral SII and the limbic system. We introduced a newly-developed multi (12)-channel gradiometer system with the smallest and highest quality superconducting quantum interference device (micro-SQUID) available to non-invasively detect the magnetic fields of a human peripheral nerve. Clear nerve action fields (NAFs) were consistently recorded from all subjects.

Brain Mapping↗
PubMed2000

Dynamic brain topography of somatosensory evoked potentials and equivalent dipoles in response to graded painful skin and muscle stimulation.

The differential effects of painful stimulation of skin vs. muscle on the cerebral electrophysiology have been poorly described. This study examined the somatosensory evoked potentials (SEPs) and the associated dipole models of non-painful and graded painful electrical stimulation applied to the skin and muscle in 20 healthy subjects. With the psychophysical stimulus-response functions determined, the skin stimulation showed a steeper slope than muscle stimulation. For both types of stimulation, the SEPs indicated a similar temporo-spatial activation sequence: F4/N90-P4/P95, Fc2/N135, Cz/P250, Cz/P300, and Cz/N460. The SEP amplitudes increased significantly with the stimulus intensities in these components. The peak SEP latencies of skin stimulation were in general shorter than that of muscle stimulation. The SEP amplitudes to skin stimulation were significantly larger than those caused by muscle stimulation at every stimulus intensity level, except the early mid-latency component. In this case, muscle stimulation caused higher amplitudes over the contralateral parietal-frontal sites. For both types of stimulation, the topographic maps were quite similar. Equivalent dipole modeling revealed identical site parameters (<1.0 cm) between skin and muscle stimulation. However, the electrical skin stimulation did not correlate with the pain intensity. Pain intensity, in contrast, was uniquely associated with the Cz/P250 amplitudes for the muscle stimulation. It is concluded that non-nociceptive and nociceptive electrical stimuli applied to skin and muscle are processed in the common cerebral areas, but exhibit differential SEP effects.

Adult↗
PubMed2000

Brain dynamics of scalp evoked potentials and current source densities to repetitive (5-pulse train) painful stimulation of skin and muscle: central correlate of temporal summation.

Temporal summation is a potent central somatosensory mechanism and may be a major mechanism involved in e.g. neuropathic pain. This study assessed the long-latency somatosensory evoked potentials (SEPs) in response to trains of repeated painful electrical stimulation of human skin and muscle in order to investigate the cerebral representation of temporal summation. Forty series of stimuli were delivered at stimulus intensities corresponding to moderate pain levels in 20 young men. Each series consisted of a five-burst-pulses (1 ms) train delivered at 2 Hz, known to activate temporal summation, i.e. increased pain intensity during the series of stimuli. Grand mean averaged waveforms (31 ch. EEG) were obtained in response to the skin and muscle stimulation. In the "train" SEPs, the wave morphology was characterized by four peak components after the first stimulus (100 to 450 ms) and by three components after the fifth stimulus (2100-2145 ms). The latency was significantly prolonged for muscle stimulation only. The 3D topographic maps at the peak activation time (100, 140, 250, and 450 ms) showed clear reduction in the amplitudes and their spatial extent (P4/P100-Fc2/N100, POz/P140-Fc2/N140, Cz/P250, Cz/N460) betweenthe first and the fifth stimulus. The current source density (CSD) topology exhibited markedly differential patterns changing from the first to the fifth stimulus. For the skin stimulation, the fifth stimulus was associated with a distinct emergence of the frontal negativity source at Fc2 right frontal cortex. This was consistent across the 100,140, 250, and 450 peak components but was not even visible in the first stimulus. In the muscle, the fifth stimulus was associated with a marked reduction of the frontal positivity at contralateral F4 site in the early stages at 100 and 140 ms, and with a total disappearance of positive source at Cz. In summary, this study demonstrated a clear temporal summation of psychophysical ratings, reduction of the peak amplitudes in the last of the first stimuli, dissociation from simple amplitude increase of the cerebral responses to pain, and a concurrent transformation of the CSD patterns. This change in "rapid cortical dynamics" of short-term plasticity could be an important mechanism for wind-up and pain processing in the brain.

Adult↗
PubMed2000

Intracerebroventricular injection of mammalian motilin, melanin-concentrating hormone or galanin does not stimulate food intake in neonatal chicks.

1. Several neural peptides are known to stimulate feeding behaviour in mammalian species. The aim of this study was to elucidate whether central injection of mammalian motilin, melanin-concentrating hormone (MCH) or galanin stimulates feeding in the neonatal chick. 2. None of the peptides applied here enhanced the food intake of the chick. 3. It is suggested that motilin, MCH and galanin, at least those of mammalian origin, may not regulate feeding in neonatal chicks, when administered to the central nervous system.

Animals↗