[Treatment programs for patients with substance-induced mental disorders].
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Biomedical subjects
Publications and source records attributed to K Endo.
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Patients with parietal lesions may fail to adjust the orientation of their hand to that of a target object, or may make errors in judging the orientation of a bar. This suggests that the parietal cortex has a function in the discrimination of the orientation of objects. In this study we investigated the responses of axis-orientation-selective neurons in caudal intraparietal (CIP) area to stereoscopic stimuli. Among the characteristics we investigated responses to the length and thickness of objects, sensitivity to binocular disparity, and position invariance in depth. Computer generated stereoscopic stimuli were presented to the monkey on a 70 inch screen. Most of the neurons responded better to long or narrow stimuli. All neurons which were orientation selective only in the frontal plane were not disparity sensitive. Most of the neurons which were orientation selective in the sagittal or horizontal plane were sensitive for binocular disparity. The majority of these neurons had wide receptive fields and their responses were position-invariant. These results suggest that the axis-orientation-selective neurons in CIP area encode the orientation of the longitudinal axis of objects in 3-dimensional space.
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PURPOSE: To characterize with scanning electron microscopy (SEM), the morphology of adhesive interfaces that had been functioning in an oral cavity for several years. MATERIALS AND METHODS: Cavities were prepared in vivo in caries-affected primary molars under local anesthesia. After removal of the entire carious lesion, the cavity was restored with a dentin adhesive system (Scotchbond Multi-Purpose). After several yrs, as the successor permanent teeth erupted, the resin-filled teeth were extracted. Then, the extracted resin-restored primary molars were cross-sectioned perpendicular to the adhesive interface using a low speed diamond saw and then polished for SEM examination. RESULTS: Morphological changes, such as digestion of the collagen fibrils and deterioration of the bonding resin and hybrid layer, were observed at the interface of the oral environment specimens. The results of this study demonstrated that degradation of resin-dentin bond structures appeared to occur in the human oral environment over time.
PURPOSE: To characterize resin-dentin bond structures of three adhesive resin systems using fractographic analysis to measure the area of failure at the fractured surface. MATERIALS AND METHODS: Flat dentin surfaces were ground perpendicular to the long axis of the tooth. The prepared dentin surfaces were treated by one of three adhesive resin systems (Mac Bond II, One-Step, and Single Bond). The samples were sectioned perpendicular to the adhesive interface to produce a square bar-shaped specimen (adhesive area: 0.9 mm2) using a diamond saw. A micro-tensile test was then conducted at a crosshead speed of 1.0 mm/min. The mean tensile bond strengths were statistically compared using one-way ANOVA and Fisher's PLSD test (P< 0.05). The fractured surfaces of all specimens were examined using SEM and the area of failure was measured using an image analyzer on SEM microphotographs. RESULTS: No significant differences in tensile bond strength were observed between Single Bond (62.1+/-18.2 MPa) and One-Step (53.8+/-13.1 MPa) (P > 0.05). However, the bond strength of Mac Bond II (36.5+/-13.7 MPa) was significantly lower than that of One-Step or Single Bond (P< 0.05). At the fractured surface, except for the cohesive failure of the bonding resin and resin-based composite, different failure patterns were observed for each resin system as follows: the failure of the hybrid layer and demineralized dentin was observed in the two wet bonding systems (One-Step and Single Bond) and of the hybrid layer but not the demineralized dentin in the self-etching primer system (Mac Bond II). The results demonstrated that the integrity of the hybrid layer depends on the adhesive system.
The Japan Society for Quality in Health Care (JSQua) created "Standards for the Evaluation of Hospital Infection Control Policies and Procedures, the First Version" in 1998 and carried out third-party surveys. Through the experience of those surveys, we revised the standards and created a second version in 1999. The surveyors felt that in using the second version of the standards it would be easier to evaluate the quality of hospital care and that these standards would be more widely applied.
Purpose: To specify the cues for the discrimination of orientation in depth in axis orientation selective (AOS) neurons.Method: We analyzed the responses of AOS neurons in the monkey caudal intraparietal sulcus (cIPS) region using binocular disparity stimuli generated by stereoscopic 3 D computer graphics.Result: Most AOS neurons (20/27) were sensitive to binocular disparity and showed tuning to the orientation of a slit in the sagittal plane with orientation disparity cues. For 12 neurons we also used an array of discs or dots instead of slits to eliminate orientation disparity. Half of the neurons (6/12) responded better to the slits than to the discs or dots, suggesting that they were sensitive to orientation disparity. Five neurons (5/12) responded equally well to the discs or dots suggesting that they were more sensitive to the gradient of horizontal disparity than to the orientation disparity.Conclusion: Both orientation disparity and disparity gradient were likely to be integrated in the cIPS area to represent axis orientation of an object in space.
The IAP (inhibitor of apoptosis) family of anti-apoptotic proteins regulates programmed cell death. Of the six known human IAP-related proteins, XIAP is the most potent inhibitor. To study the mechanistic effects of XIAP on DNA damage-induced apoptosis, we prepared U-937 cells that stably overexpress XIAP. The results demonstrate that XIAP inhibits apoptosis induced by 1-[beta-d-arabinofuranosyl]cytosine (ara-C) and other genotoxic agents. XIAP had no detectable effect on ara-C-induced release of mitochondrial cytochrome c and attenuated cleavage of procaspase-9. In addition, we show that ara-C induces the association of XIAP with the cleaved fragments of caspase-9 and thereby inhibition of caspase-9 activity. The results also demonstrate that ara-C induces cleavage of procaspase-3 by a caspase-8-dependent mechanism and that XIAP inhibits caspase-3 activity. These results demonstrate that XIAP functions downstream of procaspase-9 cleavage as an inhibitor of both proteolytically processed caspase-9 and -3 in the cellular response to genotoxic stress.
Rab GDP dissociation inhibitor alpha (Rab GDIalpha) is a regulator of the Rab small G proteins implicated in neurotransmission, and mutations of Rab GDIalpha cause human X-linked mental retardation associated with epileptic seizures. In Rab GDIalpha-deficient mice, synaptic potentials in the CA1 region of the hippocampus displayed larger enhancement during repetitive stimulation, which was apparently opposite to the phenotype of Rab3A-deficient mice. Furthermore, the Rab GDIalpha-deficient mice showed hypersensitivity to bicuculline, an inducer of epileptic seizures. These results suggest that Rab GDIalpha plays a specialized role in Rab3A recycling to suppress hyperexcitability via modulation of presynaptic forms of plasticity.
Genes of the IL-1 family encode three different peptides, IL-1alpha, IL-1beta, and IL-1Ra, respectively. IL-1 operates through IL-1RI, and is involved in airway inflammation in asthmatic subjects, whereas IL-1Ra appears to be a specific competitive inhibitor of IL-1. All genes are on chromosome 2q12-21 where genomewide searches have identified linkage for asthma. To test whether variants of IL-1 relate to asthma, we conducted a genetic association study in a Japanese population. We show that the A2 allele of IL1RN (encoding IL-1Ra) associates with nonatopic asthma [OR = 5.71, 95% CI: 1.63-19. 8, Pc = 0.007]. Both atopic and nonatopic asthmatics with the A2 allele had significantly lower serum IL-1Ra levels in both types of asthmatics. Peripheral blood cells from asthmatics with A2 alleles, however, produced as much IL-1 as did those with A1 homozygotes. Since Th1 and Th2 cytokines differentially regulate the ratio between IL-1beta and IL-1Ra, these findings suggest that dysregulation of IL-1beta/IL-1Ra, probably due to interaction between epithelium and immuno-competent cells in the airway, is important in asthma inflammation.
A unique protein of 23 kDa (Jf23) was found in the tarsus of the female swallowtail butterfly, Atrophaneura alcinous. Jf23 has 38% identity with a bilin-binding protein, which was found in the cabbage butterfly, Pieris brassicae, and which has two consensus sequences in common with the members of the lipocalin family, suggesting that it is a binding protein for lipophilic ligands. Western blot analysis showed that Jf23 was expressed only in the female, and not in the male. Electrophysiological response of the female tarsi was stimulated by methanolic extract of their host plant, Dutchman's pipe (Aristolochia debilis). The stimulated response was depressed by the presence of Jf23 antiserum. These results suggest that Jf23 is one of the chemosensory signaling proteins, which plays one or more roles in female butterfly oviposition.
We here cloned a cDNA encoding STAM2, a new member of the STAM family, which contains an SH3 domain and ITAM. STAM2 like STAM1 is associated with Jak2 and Jak3, and involved in the signaling for DNA synthesis and c-myc induction mediated by IL-2 and GM-CSF. Co-expression of the SH3 deletion mutants of STAM1 and STAM2 induces an additive effect on suppressing DNA synthesis upon stimulation with IL-2 and GM-CSF, suggesting that STAM1 and STAM2 exhibit compensatory effects on the signaling pathways downstream of Jak2 and Jak3 upon stimulation with GM-SCF and IL-2, respectively.
We evaluated peripheral nerve regeneration across an 80-mm gap using a novel artificial nerve conduit. The conduit was made of a polyglycolic acid (PGA)-collagen tube filled with laminin-coated collagen fibers. Twelve beagle dogs underwent implantation of the nerve conduit across an 80-mm gap in the left peroneal nerve. In four other dogs used as negative controls, the nerve was resected and left unconnected. Histological observation showed that numerous unmyelinated and myelinated nerve fibers, all smaller in diameter and with a thinner myelin sheath than normal nerve fibers, regrew through and beyond the gap 12 months after implantation. The distribution of the regenerated axonal diameters was different from that of the normal axonal diameters. Compound muscle action potentials, motor evoked potentials, and somatosensory evoked potentials were recorded in most animals 3 months after implantation. Peak amplitudes and latencies recovered gradually, which indicating the functional establishment of the nerve connection with the target organs. In addition to the ordinary electrophysiological recoveries, potentials with distinct latencies originating from Aalpha, Adelta and C fibers became distinguishable at the 6th lumbar vertebra following stimulation of the peroneal nerve distal to the gap 12 months after implantation. The pattern of walking without load was restored to almost normal 10-12 months after implantation. Neither electrophysiological nor histological restoration was obtained in the controls. Our nerve conduit can guide peripheral nerve elongation and lead to favorable functional recovery across a wider nerve gap than previously reported artificial nerve conduits.
Protein kinase C (PKC) mu is a novel member of the PKC family that differs from the other isozymes in structural and biochemical properties. The precise function of PKCmu is not known. The present studies demonstrate that PKCmu is cleaved during apoptosis induced by 1-beta-d-arabinofuranosylcytosine (ara-C) and other genotoxic agents. PKCmu cleavage is blocked in cells that overexpress the anti-apoptotic Bcl-x(L) protein or the baculovirus p35 protein. Our results demonstrate that PKCmu is cleaved by caspase-3 at the CQND(378)S site. Cleavage of PKCmu is associated with release of the catalytic domain and activation of its kinase function. We also show that, unlike the cleaved fragments of PKCdelta and theta, overexpression of the PKCmu catalytic domain is not lethal. Cells stably expressing the catalytic fragment of PKCmu, however, are more sensitive to apoptosis induced by genotoxic stress. In addition, expression of the caspase-resistant PKCmu mutant partially inhibits DNA damage-induced apoptosis. These findings demonstrate that PKCmu is cleaved by caspase-3 and that expression of the catalytic domain sensitizes cells to the cytotoxic effects of ara-C and other anticancer agents.
We reported that pyridoxal phosphate (PAP), a coenzyme form of vitamin B6, strongly inhibits activities of cathepsin B and weakly inhibits those of cathepsins S, K, and C in vitro. Either intraperitoneal injection or peroral administration of medication doses of vitamin B6 in the diet caused dose-dependent inhibition of hepatic cathepsins B, L, S, and C, and the inhibition was exhibited much more significantly in the case of a high protein diet than in a low protein diet. Administration of vitamin B6 induced the suppression of immune responses against ovalbumin (OVA) mediated by helper T lymphocyte type-2, based on the suppression of antigen processing by cathepsin B inhibition, as in the case of CA-074 administration, a cathepsin B specific inhibitor. Ovalbumin-dependent production of immunoglobulins IgE, IgG1 and interleukin IL-4 was suppressed by administration of medication doses of pyridoxal (PA) or pyridoxine (PI), while the production of IgG2alpha and interferon (INF)-gamma mediated by helper T lymphocyte type 1 was not changed. Administration of medication doses of vitamin B6 caused the inhibition of intracellular cathepsin B activity due to suppression of the functions of helper T lymphocyte type-2.
Hepatic endogenous hydrogen peroxide (H(2)O(2)) in bile of selenium-deficient rats (SeD) was for the first time found using the electron spin resonance (ESR) spin-trap technique, and the relationship between glutathione peroxidase (GPX) activity and H(2)O(2) amount is discussed. Normal rats and four groups of rats fed a selenium-deficient diet with different feeding periods were examined. The results showed that the GPX activity decreased depending on the feeding period with the selenium-deficient diet and that the hepatic endogenous H(2)O(2) amount in the bile of the rats fed the selenium-deficient diet for the longest period (a week before birth to 8 weeks old) was drastically higher than those in other groups of rats (P < 0.005). We found that generation of H(2)O(2) due to the decrease in the GPX activity has a threshold value. The results suggest that an exposure to selenium deficiency for long term will cause oxidative stress.
The inclusion behavior of gaseous guest molecules in a solid apohost, an orthogonal anthracene-bis(resorcinol)tetraol (1), was investigated with a quartz-crystal microbalance (QCM). Compound 1 forms crystals composed of molecular sheets bound together by an extensive hydrogen-bonded network. An apohost of 1 was cast onto a QCM and the binding of gaseous guest molecules was followed as a function of time by observing the decrease in the oscillation frequency, which is directly related to the increase in mass. Ethyl acetate and methyl ethyl ketone were significantly included into the apohost, whereas benzene and cyclohexane were simply adsorbed onto the surface of the solid; all these guests have similar vapor pressures at 25 degrees C. On the other hand, a host analogue 2, a tetramethoxy derivative of 1, barely included these guest molecules. The inclusion amount and the rate of inclusion of ethyl acetate or methyl ethyl ketone showed a drastic increase above a threshold concentration of guests in the gas phase. Thus, the structure of the apohost changed cooperatively in order to bind guest molecules above the threshold guest concentration. This cooperativity of the binding behavior was kinetically analyzed.
We investigated the neuroendocrine regulation of the development of seasonal morphs in a bivoltine race (Daizo) of the silkmoth, Bombyx mori, by decerebration, the transplantation of brain-suboesophageal ganglion (Br-SG) complexes and the injection of active neuropeptides. When brains were removed from fresh pupae destined to develop into summer morphs (SD pupae) by embryonic and larval exposures to short days at low temperature, the pupae developed into autumn or intermediate morphs. However, in pupae destined to develop into autumn morphs (LD pupae), the operation did not show an effect on seasonal morph development. Br-SG complexes were excised from fifth-instar LD and fifth-instar SD larvae 2 days after larval ecdysis and were transplanted into the abdomen of SD larvae of the same age. The Br-SG complexes of LD larvae, but not the Br-SG complexes of SD larvae, shifted the host's seasonal morph development toward the autumn morph. Furthermore, when treated with crude pupal SGs extract and diapause hormone (DH), fresh SD pupae developed into autumn or intermediate morphs, respectively. Possibly the development of seasonal morphs in the silkmoth, B. mori, is regulated by a novel function of DH. Alternatively, DH may act on the imaginal wing disks at an earlier stage than on the ovaries.