A highly polymorphic minisatellite locus (KBMS2) in bovine.
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Animals↗
Biomedical subjects
M Morimoto
Publications and source records attributed to M Morimoto.
Chronic loss of glucocorticoids following adrenalectomy down-regulates the expression of glucocorticoid receptor mRNA in the rat forebrain.
In the negative feedback model, loss of endogenous glucocorticoids up-regulates the expression of glucocorticoid receptor mRNA. To elucidate further the effect of chronic lack of glucocorticoids on the expression of glucocorticoid receptor mRNA and protein, in situ hybridization and immunohistochemical methods were used to examine the long-term alteration of glucocorticoid receptor mRNA and its immunoreactivity in the forebrain of adrenalectomized rats. Constant lack of glucocorticoids resulted in marked decrease in the expression of glucocorticoid receptor mRNA and disappearance of glucocorticoid receptor immunoreactivity in many forebrain structures. In particular, in the suprapyramidal blade of the hippocampal granule cell layer and cerebral cortex, many cells showed almost no glucocorticoid receptor mRNA signals. These results suggest that long-term loss of endogenous glucocorticoids down-regulates the levels of glucocorticoid receptor mRNA, leading to reduction in the synthesis of glucocorticoid receptors in the rat forebrain. Therefore, the presence of endogenous glucocorticoids is vital to the continued expression of glucocorticoid receptor mRNA.
Adrenal Glands↗
In vivo induction of apoptosis in the thymus by administration of mycobacterial cord factor (trehalose 6,6'-dimycolate).
It is reported that some bacteria or bacterial components cause thymic atrophy via the apoptotic process. The present study demonstrated for the first time in vivo induction of apoptosis in the mouse thymus by mycobacterial cord factor (CF) (trehalose 6,6'-dimycolate). When 300 microg of purified CF from Mycobacterium tuberculosis was intravenously administered to BALB/c mice in the form of water-in-oil-in-water (w/o/w) emulsion, thymic atrophy and pulmonary granulomas were induced with a peak on day 7, whereas, in the form of liposomes, CF induced thymic atrophy on days 14 to 21 in parallel with the development of hepatic granulomas. Thymic atrophy resulted from the depletion of cortical lymphocytes via apoptosis as revealed by DNA fragmentation and karyorrhectic changes. In contrast, mycobacterial sulfatide (2,3,6,6'-tetraacyl trehalose 2'-sulfate) caused neither thymic atrophy nor granuloma formation. Compared to lipopolysaccharide-induced thymocyte apoptosis, CF (w/o/w)-induced thymocyte apoptosis developed more slowly, reached a maximum later, and lasted longer but was less intense. Although serum tumor necrosis factor alpha (TNF-alpha) levels in CF-treated mice were not significantly elevated, administration of anti-TNF-alpha antibody almost completely inhibited thymic atrophy and granuloma formation. Serum corticosterone levels were only slightly elevated by CF administration. The present results indicate that mycobacterial CF induces thymic atrophy via apoptosis, which is closely linked with granuloma formation.
Animals↗
Survival probability, delayed mortality, and relationship between short-term outcome and long-term survival after aneurysmal subarachnoid hemorrhage.
The long-term survival probability, causes of delayed mortality, and relationship between short-term outcome and long-term survival after aneurysmal subarachnoid hemorrhage were retrospectively studied in 106 patients followed up for longer than 5 years. The Kaplan-Meier cumulative survival probabilities at 1 month, 6 months, and 5 years were 85.9%, 79.2%, and 66.8%, respectively. Six months after the onset, 41 patients made a good recovery (GR) and 34 were moderately disabled (MD). On the last follow-up day, 64 had good outcome (GR or MD) and eight had died. In contrast, there were nine patients with poor 6-month outcome (severe disability or vegetative state), seven of whom died within 5 years. Five of these seven patients had experienced intraventricular hemorrhage (IVH) on admission. A total of 15 patients died beyond 6 months, five died of complications related to shunts. Six-month outcome is a predictor of long-term survival and delayed mortality. Improved long-term survival requires the development of better management for IVH, improved 6-month outcome, and careful follow-up of patients who undergo shunting.
Adult↗
Use of hepatic tumor index on color Doppler sonography for differentiating large hepatic tumors.
OBJECTIVE: Color flow patterns on Doppler sonography are nonspecific for differentiating various hepatic tumors. We previously reported that a tumoral peak systolic flow velocity of 0.40 m/sec or greater suggested a malignant hepatic tumor rather than a hemangioma. However, tumoral peak systolic flow velocity failed to differentiate hepatocellular carcinomas and metastatic tumors. In this study, we attempted to assess the value of the hepatic tumor index for differentiating hepatocellular carcinomas and other hepatic tumors. MATERIALS AND METHODS: Color Doppler sonography was performed in 80 patients with 108 hepatic lesions larger than 2.0 cm in diameter. The hepatic tumor index was calculated as the ratio of the tumoral peak systolic velocity to the peak systolic velocity of the right or left hepatic artery. RESULTS: Pulsatile color flow images were obtained in 42 of 48 hepatocellular carcinomas, 25 of 32 hepatic metastases, and 13 of 28 hemangiomas. The mean hepatic tumor indexes obtained from hepatocellular carcinomas, metastases, and hemangiomas were 1.14 +/- 0.37 (+/-SD), 0.63 +/- 0.22, and 0.60 +/- 0.17, respectively. The hepatic tumor indexes of hepatocellular carcinomas significantly exceeded those of metastases and hemangiomas (p < .01 in both cases). A hepatic tumor index equal to or greater than 1.0 was associated with 76% sensitivity, 92% specificity, and 82% accuracy in distinguishing hepatocellular carcinomas from hepatic metastases. In lesions with a tumoral peak systolic velocity of 0.40 m/sec or greater, a hepatic tumor index equal to or greater than 1.0 was associated with 91% sensitivity, 83% specificity, and 89% accuracy in distinguishing hepatocellular carcinomas from hepatic metastases. CONCLUSION: The hepatic tumor index on color Doppler sonography was useful in differentiating large hepatocellular carcinomas from hepatic metastases.
Adult↗
[Detection of microemboli in patients with extracranial carotid artery stenosis by transcranial Doppler sonography].
Embolism from a stenotic lesion of the extracranial internal carotid artery (ICS) is considered to be an important pathomechanism of cerebral infarction. The purpose of this study is to estimate the risk of cerebral infarction associated with microembolism in patients with ICS and thereby to determine the importance of TCD-detected microemboli in this condition. Seventy-one cases with more than 30% ICS and 10 cases without ICS were studied. TCD monitoring was carried out for an hour at the ipsilateral middle cerebral artery of each case using a 2-MHz pulse-wave transcranial Doppler device. High intensity transient signals were counted as microemboli. Microemboli were detected in 27 of 71 cases with ICS, but not in cases without ICS. Microemboli were detected more frequently in cases with 70% to 99% ICS (53.3%) compared with in cases with 30% to 69% ICS (12.5%). Cerebral infarctions were recognized in the ipsilateral hemisphere in 23 of 27 cases with microemboli (85.2%) by means of MRI. In contrast, cerebral infarctions were recognized only in 21 of 45 cases without microemboli (47.7%). These results suggest that a stenotic lesion of the extracranial internal carotid artery, especially high-grade stenosis, is a major source of cerebral embolism and that detection of microemboli by TCD is a useful tool capable of reliably assessing the risk of cerebral infarction due to ICS.
Aged↗
[Analysis of factors related to microemboli in cases with internal carotid artery stenosis].
Transcranial Doppler ultrasound (TCD) has been used to detect microemboli in cases with extracranial internal carotid artery stenosis. However, the mechanism causing microemboli has remained unclear. The purpose of this study is to clarify clinical characteristics and circumstances associated with the genesis of TCD-detected microemboli. Ninety-one cases with more than 30% stenosis of the internal carotid arteries were studied. TCD monitoring was carried out for an hour at the ipsilateral middle cerebral artery of each case using a 2-MHz pulse-wave transcranial Doppler device, and high intensity transient signals were counted as microemboli. Digital subtraction angiography, magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) were also performed in all cases. Microemboli were detected in 30 of 91 cases. Microemboli were significantly well detected in cases with a history of ischemic event and/or cerebral infarction recognized by MRI. Detection of microemboli had no relation to sex, age or clinical risk factors (hypertension, hypercholesterolemia, diabetes mellitus and smoke habituation). In contrast, detection of microemboli was significantly related to decrease in cerebral blood flow recognized by SPECT, severity of stenosis and wall irregularity of lesion recognized by angiography. Microemboli can be found in a significantly high percentage of these clinical conditions, which may be risk factors for embolic stroke caused by extracranial internal carotid artery stenosis.
Aged↗
[Detection of microemboli by transcranial Doppler sonography after carotid endarterectomy].
Transcranial Doppler sonography (TCD), a non-invasive monitoring technique, has potential for detecting microemboli caused by the extracranial internal carotid artery. Many previous reports have shown that TCD-detected microemboli may be a risk factor for stroke. The main purpose of this study is to verify whether microemboli cease after carotid endarterectomy (CEA). TCD monitoring was performed in 43 cases before and after CEA. TCD monitoring was carried out for an hour at the ipsilateral middle cerebral artery of each case using a 2-MHz pulse-wave transcranial Doppler device, and high intensity transient signals were counted as microemboli. Microemboli were detected preoperatively in 10 cases (23.3%). Microemboli were not detected in any case immediately after CEA, in either the subacute stage (from 14 to 21 days after CEA) or in the chronic stage (more than 3 months after CEA). In the acute stage (from 3 to 7 days after CEA), microemboli were detected in three cases (7.0%). The rate of TCD-detected microembolic was always significantly reduced after CEA. TCD monitoring can be helpful in assessing the effect of CEA for prevention of stroke by removing the suspected source of microemboli.
Aged↗
Mechanism of intracranial rebleeding in moyamoya disease.
Intracranial hemorrhage is the major catastrophic event in the natural course of Moyamoya disease, and outcome of the patients with rebleeding is very poor. However, the mechanism underlying intracranial rebleeding is not well elucidated. We retrospectively analyzed 15 patients who bled two times or more among 46 bled patients with Moyamoya disease. The results indicated that there were two different types in the manner of rebleeding. One group consisted of seven cases, which bled two times or more at the same site than the original bleeding site. In four of these seven cases, a ruptured aneurysm was identified at the distal part of collateral vessel or on the major vessel. In the other three cases, no source of bleeding was identified. In all of these cases, rebleeding occurred within 2 months after the initial insult except for one case. Another group consisted of eight cases, which bled repeatedly but at different sites from the initial bleeding site. In any of these cases, neither aneurysms nor other vascular abnormalities were identified. In all of these cases, rebleeding occurred more than 2 months after the initial bleeding. The present result indicated that intracranial bleeding might occur as a result of rupture of a tiny aneurysm at the periphery of collateral vessels. These aneurysms may be blown out after initial bleeding. When they persist after the event, they may rupture again in a fairly short interval. In other cases, bleeding occur at different sites from the initial site. They are considered to be a result of ruptured weak Moyamoya vessels which are forced to act as collateral pathways and are under unusually increased hemodynamic stress.
Adolescent↗
The alteration of glucocorticoid receptor-immunoreactivity in the rat forebrain following short-term and long-term adrenalectomy.
To examine the effect of short-term and long-term adrenalectomy (ADX) on the glucocorticoid receptor (GR) expression, we performed an immunohistochemical study on the rat forebrain. One day after ADX, the GR-immunoreactivity significantly decreased or disappeared in most forebrain structures, while relatively strong GR-immunoreactivity was still found within the hypothalamus especially in the arcuate nucleus (ARC) and the parvocellular paraventricular nucleus (PVN). Two weeks following ADX, GR-immunoreactive cells disappeared in many structures of the forebrain including most parts of hypothalamus while moderate GR-immunoreactivity was still observable in the ARC and PVN. More than 3 months after ADX, the rats still survived when they received replacement of corticosterone during the first 2 weeks following the operation. Moderate GR-immunoreactivity in the ARC and PVN of the hypothalamus was exhibited whereas no immunoreactive cells remained in the cerebral cortex, thalamus and other forebrain structures when these animals showed obvious cell death in the granule cells of the dentate gyrus, identified with the silver impregnation method for degenerating cells. Massive cell loss in this hippocampal region is an indicator of a complete ADX, in addition to the blood corticosterone level. These results demonstrate topographic differences of GR expression in the rat forebrain after ADX with only continuous immunoreactivity in the ARC and PVN of the hypothalamus, suggesting that some neurons in the ARC and PVN could keep active GR probably in order to maintain their survival after removing the adrenal gland.
Adrenalectomy↗
Role of aspartic acid 814 in the function and expression of c-kit receptor tyrosine kinase.
The c-kit receptor tyrosine kinase (KIT) is constitutively activated in three different types of neoplastic mast cell lines by naturally occurring mutations that result in substitutions of Val or Tyr for Asp814 in the phosphotransferase domain. In an effort to characterize the role of the Asp814 residue, we have investigated the properties of mutant KITs in which the Asp814 residue was deleted or mutated to a series of other amino acids. With the exception of rare instances, mutant KITs with substitutions of Asp814 were found to be constitutively phosphorylated on tyrosine and activated in the absence of the ligand, stem cell factor (SCF), whereas a deletion mutant lacking Asp814 (KITDel-Asp-814) did not exhibit tyrosine phosphorylation and activation even after treatment with SCF. In addition to constitutive activation, furthermore, both highly activated substitution mutants (KITVal-814 and KITTyr-814) and modestly activated substitution mutants (KITGly-814 and KITHis-814) were continuously degraded in the absence of SCF, whereas wild-type KIT (KITWild) required SCF stimulation to undergo degradation. These results suggested that the Asp814 residue may play a crucial role in regulating enzymatic activity and expression of KIT and that various types of mutations at the Asp814 residue may generate oncogenic protein with constitutive activation and degradation.
Amino Acid Sequence↗
2-[(2-Aminobenzyl)sulfinyl]-1-(2-pyridyl)-1,4,5,6-tetrahydrocyclopent[d]imidazoles as a novel class of gastric H+/K+-ATPase inhibitors.
Substituted 2-sulfinylimidazoles were synthesized and investigated as potential inhibitors of gastric H+/K(+)-ATPase. The 4,5-unsubstituted imidazole series 6-11 and the 1,4,5,6-tetrahydrocyclopent[d]imidazole series 12 were found to be potent inhibitors of the acid secretory enzyme H+/K(+)-ATPase. Structure-activity relationships indicate that the substitution of 2-pyridyl groups at the 1-position of the imidazole moiety combined with (2-aminobenzyl)-sulfinyl groups at the 2-position leads to highly active compounds with a favorable chemical stability. Other substitution patterns in the imidazole moiety result in reducing biological activities. 2-[(2-Aminobenzyl) sulfinyl]-1-[2-(3-methylpyridyl)]-1,4,5,6-tetrahydrocyclopent++ ++ ++ [d]-imidazole (12h, T-776) was selected for further development as a potential clinical candidate. Extensive study on the acid degradation of 12h indicates a mechanism of action different from that of omeprazole, the first H+/K(+)-ATPase inhibitor introduced to the market.
Animals↗
Constitutive activation of c-kit in FMA3 murine mastocytoma cells caused by deletion of seven amino acids at the juxtamembrane domain.
A peculiar point mutation results in constitutive activation of c-kit receptor tyrosine kinase (KIT) in three different tumor mast cell lines; ie, the HMC-1, P-815, and RBL-2H3. Because constitutive activation of KIT was also observed in the FMA3 mouse mastocytoma cell line, we investigated the molecular mechanism. Sequencing of the whole coding region of the c-kit showed that the point mutation found in HMC-1, P-815, and RBL-2H3 cells was absent in FMA3 cells and that the c-kit cDNA of FMA3 cells carried an in-frame deletion of 21 base pairs (bp) encoding Thr-Gln-Leu-Pro-Tyr-Asp-His at codons 573 to 579 at the juxtamembrane domain. The FMA3-type c-kit cDNA with 21 bp deletion was introduced into the IC-2 cell line, which was derived from murine cultured mast cells. IC-2 cells were dependent on interleukin (IL)-3 and did not express KIT on the surface. In IC-2 cells introduced with the FMA3-type c-kit cDNA, KIT was constitutively phosphorylated on tyrosines and activated. Moreover, the FMA3-type KIT was dimerized without the stimulation by stem cell factor (SCF), a ligand for KIT. The spontaneously dimerized FMA3-type KIT without SCF binding was not internalized even after the activation. IC-2 cells expressing the FMA3-type KIT grew in suspension culture without IL-3 and SCF and became leukemic in nude athymic mice. The deletion of seven amino acids at the juxtamembrane domain appeared to be a new activating mutation of KIT that might be involved in neoplastic growth of mast cells.
Amino Acid Sequence↗
Role of cytochrome P4502E1-dependent formation of hydroxyethyl free radical in the development of liver damage in rats intragastrically fed with ethanol.
We have previously shown that the treatment with diallyl sulfide (DAS) and phenylethyl isothiocyanate (PIC) of rats receiving ethanol in the alcohol tube-feeding model effectively suppressed the induction of cytochrome P4502E1 (CYP2E1) by ethanol. Here we report that rat treatment with DAS and PIC significantly decreased the trapping of hydroxyethyl free radicals in liver microsomes incubated in vitro with ethanol. Furthermore, these inhibitors also greatly reduced the production of hydroxyethyl radical-derived epitopes detectable in vivo in the liver of ethanol-fed rats. The action of DAS and PIC on the formation of hydroxyethyl radicals paralleled their inhibitory effect on lipid peroxidation as monitored using, respectively, liver malonildialdehyde (MDA) and plasma lipid hydroperoxide levels as well as by the titers of antibodies versus MDA adducts to proteins. Thus, these results indicated a link between the induction of CYP2E1 by ethanol, the formation of hydroxyethyl radicals and the stimulation of lipid peroxidation. The pathological scores in the livers of rats fed with ethanol plus or minus DAS and PIC also correlated with levels of hydroxyethyl radical-derived epitopes. Rats fed intragastrically with ethanol developed antibodies and the formation of these antibodies was greatly reduced by DAS and PIC. Taken together these results suggest that CYP2E1 plays an important role in the generation of hydroxyethyl radicals during chronic alcohol feeding and that ethanol-derived free radicals might play a role in the onset of liver injury in this model of alcohol administration.
Allyl Compounds↗
Supra- and infratentorial multiple cavernous angiomas in an infant: report with MR evaluation of an unusual case.
A rare case of multiple cavernous angiomas with repeated hemorrhages in a 9-month-old male infant is presented, together with sequential computed tomography (CT) and magnetic resonance (MR) images. The infant underwent hematoma evacuation for left cerebellar hemorrhage and his postoperative course was uneventful. The multiple cavernous angiomas receded gradually without any treatment except the hematoma evacuation. Two years following presentation, he continues to do well. To the authors' knowledge, this is the first report of multiple cavernous angiomas with brain stem involvement in an infant.
Brain Neoplasms↗
Ischemic colitis during interferon-alpha treatment for chronic active hepatitis C.
Between 1991 and 1994, at Hoshigaoka Koseinenkin Hospital, we treated 280 patients with chronic hepatitis C with interferon (IFN), and ischemic colitis occurred in two patients (0.7%) during the treatment. Melena appeared in case 1 in the 2nd month after the initiation of IFN-alpha treatment, and in case 2 in the 6th month. In both patients, longitudinal ulcerations in the descending colon were revealed by urgent colonoscopy, and these resolved within 2 weeks after discontinuation of the IFN treatment. It appears that ischemic colitis was associated with the IFN treatment, suggesting that attention should be paid to this possible complication.
Aged↗
Brain perfusion SPECT in neuro-Behçet's disease: discordance between Tc-99m-HMPAO and Tc-99m-ECD.
A patient with neuro-Behçet's disease was studied with both Tc-99m-HMPAO and Tc-99m-ECD brain perfusion SPECT during the same time period. In Tc-99m-HMPAO SPECT, focal high uptake was observed in the left basal ganglia where MRI depicted abnormal signal intensity. Conversely, Tc-99m-ECD SPECT did not show corresponding high uptake, but demonstrated rather low uptake in contrast to the Tc-99m-HMPAO SPECT. This case suggests that Tc-99m-HMPAO and Tc-99m-ECD may show discordant distribution in inflammatory brain disease such as neuro-Behçet's disease.
Adult↗
Distribution of glucocorticoid receptor immunoreactivity and mRNA in the rat brain: an immunohistochemical and in situ hybridization study.
The localization of glucocorticoid receptor (GR) immunoreactivity and mRNA in the adult rat brain was examined by light microscopic and electron microscopic immunohistochemistries, and in situ hybridization. For the purpose of detailed investigation of the distribution and comparison of GR immunoreactivities and mRNAs, specific polyclonal antibodies against a part of the transcription modulation (TR) domain of rat GR were used in the immunohistochemistry, whereas fluorescein-labeled RNA probes, complementary to the TR domain in the GR cDNA were used in the in situ hybridization. In the rat brain, GR immunoreactivity was predominantly localized in the cell nucleus, and the expression of GR mRNA was detected in the cytoplasm. GR-immunoreactive and GR mRNA-containing cells were widely distributed from the olfactory bulb of the forebrain to the gracile-cuneate nuclei of the medulla oblongata. The highest densities of GR-immunoreactive and mRNA-containing cells were observed in the subfields of cerebral cortex, olfactory cortex, hippocampal formation, amygdala, septal region, dorsal thalamus, hypothalamus, trapezoid body, cerebellar cortex, locus coeruleus and dorsal nucleus raphe. The distributional pattern of GR immunoreactivity in many regions was well-correlated with that of GR mRNA, but in the CA3 and CA4 pyramidal layers of the hippocampus, different localization was noted. The present study provides the groundwork for elucidating the role of GRs in brain function.
Animals↗