CD34-positive dendritic cells are an intrinsic part of smooth muscle hamartoma.
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Adult↗
Biomedical subjects
H Koizumi
Publications and source records attributed to H Koizumi.
Analysis of c-kit exon 11 and exon 17 of urticaria pigmentosa that occurred in monozygotic twin sisters.
Genomic DNA extracted from peripheral blood mononuclear cells of monozygotic twin patients with urticaria pigmentosa was investigated for mutations of proto-oncogene c-kit. Neither the patients nor their families had genomic mutations in exon 11 or exon 17 of c-kit. The patients did not have any systemic involvement or bone marrow abnormalities. There are indications that some genetic factors may participate in the pathogenesis of urticaria pigmentosa in monozygotic twins. In the present patients, factors other than genomic faults in exon 11 and exon 17 of c-kit may be responsible for the pathogenesis.
Adult↗
Bullous pemphigoid with permanent loss of the nails.
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Biopsy, Needle↗
A pilot study of electroencephalographic changes associated with ki.
OBJECTIVE: To measure changes in the electroencephalogram (EEG) of a ki master and ki recipients during ki emission. DESIGN: A 54-year-old, male ki master and three recipients were recorded with 21-channel digital EEG technique using the 10-20 electrode placement system. Ki recipients were three Caucasian females with no prior experience with ki practice. The ki master has practiced ki healing for more than 20 years. EEG recordings were obtained from the ki master and each recipient during baseline, direct healing ki emission, transtelephonic healing ki emission, and emission of fighting ki through the study subject to a third individual. EEG recordings were reviewed in a blinded fashion by a neurologist with no ki experience. RESULTS: No detectable EEG changes occurred during ki emission, either in the ki master or in the subjects. CONCLUSIONS: EEG may not be an appropriate objective instrument to measure ki activity, at least for moving-type ki.
Adult↗
Effects of mild hypothermia on the cortical release of excitatory amino acids and nitric oxide synthesis following hypoxia.
Studies concerning neurotransmitter release following cerebral hypoxia are scarce, and the effects of mild hypothermia on hypoxia-induced neurotransmitter release are unknown. The purpose of this study was to investigate changes in excitatory amino acid (EAA) concentrations and nitric oxide (NO) synthesis following cerebral hypoxia in rats, and the effects of mild hypothermia on both. Cerebral hypoxia (PaO2, 30-40 mm Hg) was induced in each rat for 60 min. Cerebral blood flow (CBF) was measured by laser-Doppler flowmetry, and the extracellular concentrations of EAAs and NO end-products (nitrite and nitrate) were measured by in vivo microdialysis in normothermic (37 degrees C) and hypothermic (32 degrees C) rats. In both groups, CBF showed modest increases during hypoxia and returned to baseline during reoxygenation. The EAA levels of the normothermic rats increased markedly after hypoxia induction and returned to baseline levels during reoxygenation. Hypothermia abolished these increases completely. The NO end-product levels under normothermic conditions declined slightly during hypoxia, and then increased transiently during reoxygenation. Hypothermia appeared to attenuate the NO end-product level and to delay the peak. When the relationship between glutamate and the NO end-products was examined on an individual-animal basis, glutamate release did not parallel NO synthesis. The results indicate that hypothermic neuroprotection during cerebral hypoxia may be attributable to the amelioration of damage by reduction of presynaptic EAA release. Although it is unclear from the present results alone whether endothelial NO synthase, neuronal NO synthase or both caused the elevation of the NO end-products during reoxygenation, it is possible that the attenuation and delay of the peak of the NO end-product level plays a role in protection from NO-induced neuronal damage.
Animals↗
Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levels in small intestinal mucosa of protein-malnourished mice.
We examined whether vitamin A improved mucosal immune depression in mice with wasting protein deficiency. In male C3H/HeN mice fed a semi-purified 1% protein diet for 2 wk, plasma retinol and immunoglobulin A (IgA) concentrations in the small intestinal mucosa were 50 and 55%, respectively, of those in mice fed a semi-purified 20% protein diet, (P < 0.05). Daily supplementation of 0.3 mg of retinyl acetate to protein-deficient mice for 2 wk increased the plasma retinol level to the value in the protein-sufficient mice. However, 1 mg/d of retinyl acetate was required to prevent the decline of the IgA level caused by the protein deficiency. Mice fed the low-protein diet had lower concentrations of IL-4 and IL-5 in the small intestinal mucosa and fewer IL-4- and IL-5-containing cells in the lamina propria (P < 0. 05). Retinyl acetate (1 mg) significantly restored the IL-5 level and the number of IL-4- and IL-5-containing cells. After immunization with 20 microg of cholera toxin (CT), the intestinal mucosa of protein-deficient mice contained significantly less CT-specific IgA than control mice. Treatment with 1 mg of retinyl acetate prevented the decline of anti-CT IgA level in the protein-deficient mice, improving their survival rate after an exposure to 0.1 mg of CT. These results suggest that large oral supplements of vitamin A may preserve mucosal IgA level during protein malnutrition, possibly by stimulating Th2 cytokine production and thereby, inducing resistance against infection.
Animals↗
MEG spatio-temporal analysis using a covariance matrix calculated from nonaveraged multiple-epoch data.
We propose a magnetoencephalographic (MEG) spatio-temporal analysis in which the measurement-covariance matrix is calculated using nonaveraged multiple epoch data. The proposed analysis has two advantages. First, a very narrow time window can be used for the source estimation. Second, accurate localization is possible even when the source activation has a time jitter. Experiments using auditory evoked MEG data clearly demonstrate these advantages.
Algorithms↗
Specific cutaneous lesions of the scalp in myelodysplastic syndrome with deletion of 20q.
We reported a specific skin lesion on the scalp in a patient with myelodysplastic syndrome (MDS), treated as refractory anemia with excess of blasts (RAEB). Histologically, a specimen from a nodule of the scalp consisted of a diffuse infiltration of atypical cells in the dermis and subcutaneous tissue. The patient died of acute leukemia 3 months later. Chromosomal examination of bone marrow cells revealed deletion of 20q and 21 trisomy. The specific cutaneous lesions in this patient were associated with acute transformation. The deletion of 20q and specific cutaneous lesions are regarded as signs of poor prognosis.
Biopsy, Needle↗
Nuclear factor kappa B mediates interleukin-8 production in eosinophils.
BACKGROUND: Recent reports indicate that in response to various stimuli, eosinophils produce a variety of cytokines (e.g. IL-8) which play pivotal roles in allergic inflammation. In that regard, the transcription factor, nuclear factor, Kappa B (NF-kappaB), is an important activator of tumor-necrosis-factor-alpha (TNF-alpha)-induced IL-8 gene expression in monocytes, lymphocytes and neutrophils. We therefore investigated the role played by NF-kappaB in cytokine production induced by stimulation of eosinophils with the proinflammatory cytokines, granulocyte-monocyte colony-stimulating factor (GM-CSF) and TNF-alpha. METHODS: Peripheral blood samples were obtained from human subjects with slight to moderate eosinophilia. NF-kappaB activation elicited by exposing cells to GM-CSF and/or TNF-alpha was investigated using immunohistochemistry and gel shift assays. To functionally assess the effects of NF-kappaB translocation, IL-8 production was also examined using an enzyme-linked immunosorbent assay. RESULTS: Stimulation of eosinophils with GM-CSF + TNF-alpha induced significant increases in the synthesis and secretion of IL-8 which were associated with translocation of NF-kappaB p50 into the nucleus. The binding of NF-kappaB to the DNA was verified by the gel shift assays. IL-8 production was significantly inhibited by N-acetyl-L-cysteine, FK506 and MG-132, inhibitors of NF-kappaB activation and translocation. CONCLUSION: On the basis of our findings, we conclude that activation and translocation of NF-kappaB plays a crucial role in the signal-transduction pathway leading to the synthesis and release of IL-8 by eosinophils.
Acetylcysteine↗
Malignant intravascular lymphomatosis associated with venous stenosis. Case report.
This 55-year-old man presented with malignant intravascular lymphomatosis, a rare vascular disorder of the central nervous system characterized by proliferation of malignant lymphoma cells. The clinical manifestations were focal neurological signs and progressive dementia. Angiography demonstrated stenoses of the cortical veins. Postmortem examination revealed infiltration of tumor cells into the lumen and vascular wall, although the stenoses were caused primarily by fibrin thrombi. To the authors' knowledge this is the first case of malignant intravascular lymphomatosis associated with venous stenosis.
Angiography, Digital Subtraction↗
[Detection of anti-nuclear antibodies in liver diseases by indirect immunofluorescence method and enzyme-linked immunosorbent assay].
Detection of anti-nuclear antibodies (ANA) is essential for diagnosing autoimmune diseases including autoimmune liver diseases. An indirect immunofluorescence (IIF) method with a cell line (HEp-2) derived from human laryngeal carcinoma has been used as a standard substrate. Recently, an enzyme-linked immunosorbent assay (ELISA) using multiple solid-phase antigens has been developed. We assayed sera from 272 cases of chronic liver diseases, 91 cases of healthy subjects and studied clinical significance of ANA. The sensitivity of IIF method in detection of ANA (fluorescence-ANA: FANA) and that of ELISA (ELISA-ANA: EANA) were 19.2% and 17.3% in chronic hepatitis B (CH-B), 16.7% and 17.3% in chronic hepatitis C (CH-C), 84.2% and 50.9% in primary biliary cirrhosis (PBC), 100% and 85.7% in autoimmune hepatitis (AIH) and 15.4% and 18.7% in healthy subjects. The sensitivity of EANA was considerably lower than that of FANA in PBC and AIH, but the sensitivity was the same in CH-C, CH-B, and healthy subjects. Because the solid-phase target antigens do not include nuclear antigen components recognized only by patients with PBC or AIH, ELISA can not detect all the species of ANA. This accounts for the low sensitivity of EANA in PBC and AIH. In conclusion, the current EANA is useful for screening of ANA, but FANA should be performed when PBC or AIH is suspected.
Antibodies, Antinuclear↗
Obesity and mild hyperinsulinemia found in neuropeptide Y-Y1 receptor-deficient mice.
To elucidate the role of neuropeptide Y (NPY)-Y1 receptor (Y1-R) in food intake, energy expenditure, and other possible functions, we have generated Y1-R-deficient mice (Y1-R-/-) by gene targeting. Contrary to our hypothesis that the lack of NPY signaling via Y1-R would result in impaired feeding and weight loss, Y1-R-/- mice showed a moderate obesity and mild hyperinsulinemia without hyperphagia. Although there was some variation between males and females, typical characteristics of Y1-R-/- mice include: greater body weight (females more than males), an increase in the weight of white adipose tissue (WAT) (approximately 4-fold in females), an elevated basal level of plasma insulin (approximately 2-fold), impaired insulin secretion in response to glucose administration, and a significant changes in mitochondrial uncoupling protein (UCP) gene expression (up-regulation of UCP1 in brown adipose tissue and down-regulation of UCP2 in WAT). These results suggest either that the Y1-R in the hypothalamus is not a key molecule in the leptin/NPY pathway, which controls feeding behavior, or that its deficiency is compensated by other receptors, such as NPY-Y5 receptor. We believe that the mild obesity found in Y1-R-/- mice (especially females) was caused by the impaired control of insulin secretion and/or low energy expenditure, including the lowered expression of UCP2 in WAT. This model will be useful for studying the mechanism of mild obesity and abnormal insulin metabolism in noninsulin-dependent diabetes mellitus.
Animals↗
Non-invasive assessment of language dominance with near-infrared spectroscopic mapping.
Hemispheric dominance for language is usually assessed by means of the Wada test where amobarbital is injected into the carotid artery. Recently, positron emission tomography and functional MRI have been used as non-invasive alternatives to this method. We have applied 24-channel near-infrared spectroscopic topography (NIRS) as another non-invasive method to detect the unilateral cerebral activation during a language task. We used 11 healthy volunteers and six patients with intractable epilepsy. A word-generation task was applied for 17 s, followed by an extinction/resting period of 60 s. In healthy volunteers, the inferior frontal region was activated on the side opposite to the subject's handedness in infancy. In the epilepsy cases, the activated side agreed with the dominance determined by the Wada test. Our results demonstrate that NIRS is a feasible non-invasive alternative to the Wada test.
Adult↗
Cis-urocanic acid attenuates histamine receptor-mediated activation of adenylate cyclase and increase in intracellular Ca2+.
UVB irradiation causes suppression of delayed hypersensitivity. Various photoreceptors and mediators of these changes have been proposed, one of which is cis-urocanic acid formed from the naturally occurring trans-urocanic acid in the epidermis on exposure to UV irradiation. The mechanism by which cis-urocanic acid alters the immune system is not fully clarified, but it acts through different mechanisms, perhaps via histamine or histamine-like receptors. Histamine stimulation of keratinocytes induces activation of adenylate cyclase leading to an accumulation of cyclic AMP and an increase in intracellular Ca2+. Thus we investigated the effects of cis-urocanic acid on these transmembrane signaling systems in keratinocytes. Normal human keratinocytes were cultured in serum-free KGM medium. Cyclic AMP was measured by radioimmunoassay. Alterations in intracellular Ca2+ in single living keratinocytes were measured using an inverted fluorescence microscope and an ARGUS-200/CA digital imaging system. Cis-urocanic acid itself did not induce adenylate cyclase activation in cultured normal human keratinocytes. Cis-urocanic acid inhibited histamine-induced cyclic AMP accumulation. It did not affect keratinocyte growth, and did not induce an increase in intracellular Ca2+, but did attenuate the histamine-induced increase in intracellular Ca2+ but not that induced by epinephrine. Cis-urocanic acid acts on keratinocytes via modulation of the effects of histamine.
Adenylyl Cyclases↗
Comparison of covariance-based and waveform-based subtraction methods in removing the interference from button-pressing finger movements.
A covariance matrix-based subtraction method has recently been proposed to remove interference using two MEG measurements: The first has both target and interfering activities and the second only has the interference. This paper compared covariance matrix-based subtraction with conventional waveform-based subtraction, which requires that the waveforms of interference be equal at every time point between the two measurements. Our analysis showed that covariance-subtraction only requires that the time-average of the squared intensity of interference be equal between the two measurements. As a result, the method is still effective when the onset of interference differs or even their measured waveforms differ between the two measurements. The covariance- and waveform-subtraction methods were both applied to remove the interference caused by response-button-pressing finger movements in auditory-evoked MEG measurements. The results of this application demonstrated the superiority of the covariance-subtraction method over the conventional waveform-subtraction method.
Algorithms↗
Nodular localized cutaneous amyloidosis: further demonstration of monoclonality of infiltrating plasma cells in four additional Japanese patients.
Nodular localized cutaneous amyloidosis (NLCA) is a disorder characterized by deposition of amyloid derived from immunoglobulin light chains. We used semi-nested polymerase chain reaction (PCR) to analyse archival paraffin-embedded sections from a previous patient and from four additional, previously reported patients with NLCA to determine whether involvement of monoclonal plasma cells is a universal feature of this condition. The semi-nested PCR analysis revealed one or two amplified bands, around 100-120 bp, for all five cases of NLCA, although the yields varied from case to case. These results suggest that clonal expansion of plasma cells in NLCA may occur locally.
Adult↗
Congenital onychodysplasia of the index fingers with anomaly of the great toe.
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Aged↗
Cis-urocanic acid down-regulates histamine-mediated activation of adenylate cyclase in the pig epidermis.
Urocanic acid (UCA), one of the skin's major components for absorbing UV radiation, is present naturally in the stratum corneum as a trans-isomer. On absorption of UVB radiation either in vitro or in the skin, UCA undergoes trans- to cis-isomerization in a dose-dependent manner. Although the mechanism by which cis-UCA suppresses immunity remains unelucidated, recent studies have indicated that cis-UCA appears to inhibit the induction of cyclic AMP in fibroblasts, which suggests that this molecule plays an active role in modifications to the skin. Here, we report that although neither trans-UCA nor cis-UCA increases cyclic AMP in the pig epidermis, cis-UCA actively down-regulates the increase of cyclic AMP induced by histamine. The effects of cis-UCA on the pig epidermis are revealed through the modulation of the effects caused by histamine. These findings suggest that in the pig epidermis, the initial biochemical and cellular event for UVB-induced immune suppression--that is, the step immediately following the isomerization of trans-UCA to cis-UCA--is down-regulation of cyclic AMP brought about by the activity of cis-UCA.
Adenylyl Cyclases↗