Kazuo Maeda

Distribution of apoptosis-mediating Fas antigen in human skin and effects of anti-Fas monoclonal antibody on human epidermal keratinocyte and squamous cell carcinoma cell lines

Fast antigen is a cell surface protein that mediates apoptosis. Using immunohistological, flow cytometry and electron microscopic analyses, we investigated the expression of Fas antigen on various skin tissues, and on cultured SV40-transformed human epidermal keratinocyte cell line KJD and human skin squamous cell carcinoma cell line HSC. The Fas antigen was widely distributed in skin components such as the keratinocytes in the lower portion of the epidermis, epidermal dendritic cells, endothelial cells, fibroblasts, apocrine glands, eccrine sweat glands, sebaceous glands, some normal melanocytes and infiltrating lymphoid cells. It was also strongly expressed on the keratinocytes of lichenoid eruptions seen in lupus erythematosus and lichen planus, and on the spongiotic or acanthotic epidermis seen in chronic eczema, adult T-cell leukaemia/lymphoma (ATLL) and atopic dermatitis. Its expression was closely correlated with lymphoid infiltrating cells and it was strongly expressed in lymphoid neoplastic cells, particularly ATLL cells, and fibroblasts seen in dermatofibroma. However, the antigen was not detected on basal cell epithelioma cells, some malignant melanomas or any junctional naevi. The cell lines KJD and HSC strongly expressed the Fas antigen, and crosslinking of the Fas antigen by an anti-Fas monoclonal antibody induced apoptosis of these cell lines. These results indicate that the apoptosis-mediating Fas antigen may play an important role in normal skin turnover and cell differentiation, in immune regulation of skin tumours, and in the pathogenesis of various skin diseases.

Differentiation between physiologic and pathologic sinusoidal FHR pattern by fetal actocardiogram

Two cases of physiologic sinusoidal FHR pattern and one case of pathologic sinusoidal FHR pattern recorded on fetal actocardiograms are reported. The physiologic sinusoidal FHR patterns were recorded during periodic fetal respiratory movements and sucking movements. The physiologic sinusoidal FHR patterns were accompanied and synchronized with periodic fetal movement bursts. The pathologic sinusoidal FHR pattern observed in a case of severe fetal anemia due to massive fetal-to-maternal hemorrhage was not accompanied by any fetal movement bursts. It is suggested that with the use of fetal actocardiogram physiologic sinusoidal FHR pattern can be distinguished from pathologic sinusoidal FHR pattern.

Association of Vesiculobullous Eruptions with Mycosis fungoides

Mycosis fungoides (MF) is, on extremely rare occasions, associated with vesiculobullous eruptions. This report describes clinical, histological and immunohistochemical findings of a case of MF with vesiculobullous lesions. Characteristic features of our case included: bullous lesions evolving rapidly in 12-24 h with severe itch on erythematous and normal-appearing skin; a positive Nikolsky sign; an intraepidermal blister; direct and indirect immunofluorescence stainings were all negative with IgG, IgA, IgM and C3, and atypical lymphocytes in the infiltrates were of helper/inducer T cell type.

An Atlas of Fetal Central Nervous System Disease: Diagnosis and Management

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Heterogeneity of cutaneous T-cell lymphoma. Phenotypic and ultrastructural characterization of four unusual cases

This study characterized, by means of immunocytochemistry and electron microscopy, four cases of “unusual” cutaneous T‐cell lymphoma (CTCL) other than classical mycosis fungoids and Sézary syndrome. Cases 1, 2, and 4 were diffuse lymphoma of a pleomorphic type, and Case 3 was of a mixed type. Case 4 shared a feature common to pagetoid reticulosis. A fairly large number of inflammatory cells were seen in Cases 1, 3, and 4. Functionally, the neoplastic cells of Cases 1, 3, and 4 were of a helper/inducer T‐cell subset, whereas those of Case 2 were of a suppressor/cytotoxic T‐cell type. Epidermotropic cells with pagetoid growth in Case 4 failed to show these specific surface phenotypes, although they still retained pan T‐cell markers. Neoplastic large or intermediate‐sized cells revealed a marked difference in the development of cytoplasmic organelles and their nuclear profiles, ranging from a few simple indentations (Cases 2 and 3) to forms with many deep indentations (Case 1) and highly cleaved shapes (Case 4). All of these cells, however, possessed dense‐cored granules located in a portion of the cytoplasm. This study indicated the clinicopathologic and immunologic heterogeneity of CTCL, which may be classified, according to the reactivity with monoclonal antibodies and the fine structural features, into subtypes that correspond to functionally distinct subsets of T‐cells and their stages or types of differentiation.

Fetal behavior analyzed by ultrasonic actocardiogram in cases with central nervous system lesions

Abstract Aims: This study examined whether analysis of fetal behavioral states by monitoring fetal heart rate and movement using an actocardiogram (ACG), could provide prognostic information related to fetal central nervous system (CNS) lesions. Methods: The ACG simultaneously records fetal heart rate (FHR) and fetal movement bursts composed of spikes of ultrasonic Doppler signals. Durations of FHR accelerations and fetal movement bursts were measured manually. Five actocardiographic indices were studied in 12 fetuses with CNS lesions and in 14 normal pregnancies of 28–38 weeks. Results: Severity of the fetal CNS lesions was estimated from the acceleration/burst (A/B) duration ratio, which correlated with the rank of the sonographic fetal functional test in cases with CNS lesions. Severity of a fetal lesion may also be estimated by the regression equation of the A/B duration ratio and behavioral ranking. Conclusion: The severity of fetal CNS lesions may be estimated by quantitative analysis of ACG usings the measurement of A/B duration ratio to provide a prognosis. An ACG may demonstrate a loss of CNS control in cases with severe brain damage.

Origin of the long-term variability and acceleration of FHR studied for the prevention of cerebral palsy in fetal hypoxia and general insults

Abstract Aims: The development of fetal heart rate (FHR) variability and acceleration, and their loss in the hypoxic brain damage and cerebral palsy (CP) is investigated. Methods: FHR, movements in physiologic sinusoidal FHR and fetal movements were studied by actocardiogram. Results: Periodic fetal respiratory movements evoked moderate FHR variation similar to medium variability. Small fetal movements provoked FHR variability, and large fetal movement burst developed the acceleration. The brain centers should be midbrain for variability and acceleration. FHR variability and acceleration develop by the reaction of fetal brain to fetal movements. As severe organic fetal brain damage could develop through fetal hypoxia in the loss of variability, early delivery before the loss of variability will prevent infantile CP. As the abnormal FHR would be developed by fetal brain damage in non-hypoxic fetal insults, early delivery before the loss of variability could also prevent the brain damage in viral and bacterial infections.

Loss of FHR variability diagnosed by frequency analysis

Abstract Aims: To determine the loss of fetal heart rate (FHR) baseline variability by frequency analysis. Methods: The FHR tracings of 12 normal fetuses and others with various conditions, as well as flat FHR tracings of a late deceleration (LD) and anencephaly recorded with Doppler fetal monitors, were scanned and processed using fast Fourier transform (FFT) analysis. The ratio of the area under the low frequency spectrum divided by the area under the whole spectrum (La/Ta) and the peak power spectrum density (PPSD) were determined. Results: Long-term variability (LTV) measures >10 bpm revealed significantly more La/Ta and PPSD than LTV <10 bpm in normal FHR tracings. The La/Ta and PPSD were >15% and 60 bpm2/Hz, respectively, in representative values of normal FHR cases and in those of fetal respiration, hiccupps and non-reactive FHR, whereas those of the flat baseline of LD and anencephaly were <15% and 60 bpm2/Hz. Conclusion: Loss of baseline variability is diagnosed when the La/Ta ratio and PPSD are <15% and 60 bpm2/Hz, respectively, based on the FFT frequency analysis of the FHR baseline.

Immunohistochemical Characterization of Spitz's Nevus: Differentiation from Common Melanocytic Nevus, Dysplastic Melanocytic Nevus and Malignant Melanoma

Recently it has been reported that Spitzs nevus possesses a deranged melanogenesis with formation of the spherical melanosomes also seen in superficial spreading melanoma (SSM) and dysplastic melanocytic nevus (DMN). To characterize the nature of Spitzs nevus, immunohistochemical studies were carried out in 9 cases of this condition using monoclonal antibodies (MoAbs) which identify (a) human melanosome‐associated antigen (HMSA‐1 and HMSA‐2), (b) S‐100 protein (α and β subunits), (c) Leu‐7 (HNK‐1), (d) β2 microglobulin (B2MG), and (e) neuron specific enolase (NSE). In contrast to SSM and DMN, none of the 9 cases showed any significant reactivity with MoAbs HMSA‐1 and HMSA‐2. Similar to cutaneous malignant melanoma (CMM) and DMN, and unlike common melanocytic nevus (CMN), anti‐S‐100 protein α subunit MoAb reacted from moderately to intensely with Spitzs nevus, and anti‐S‐100 protein β subunit MoAb reacted weakly. Anti‐B2MG MoAb was reactive with 8 of 9 cases. Only one case showed cytoplasmic reactivity to anti‐Leu‐7 MoAb. Polyclonal NSE was found in 7 cases at varying intensities. Our immunohistochemical study indicates the distinct, benign neoplastic nature of Spitzs nevus which has immunoreactivities differing from those of CMM, DMN and CMN.

Preeclampsia is caused by continuous sympathetic center excitation due to an enlarged pregnant uterus.

Abstract Aims: To deduce the origin of preeclampsia characterized by hypertension and proteinuraia on the basis of results from animal studies and its therapeutic strategies. Methods: Sympathetic and parasympathetic zones of female non-pregnant rabbit brain were stimulated electrically with Kurotu’s electrodes. Systolic blood pressure, urine volume, and proteinuria were evaluated before and after the stimulation of autonomic zones. Results: Excitation, hypertension, urine reduction, cloudy urine, and proteinuria were observed following stimulation of the sympathetic zone. A stable state, low blood pressure, increased urine volume, and no proteinuria were observed following stimulation of the parasympathetic zone. Conclusion: Hypertension and proteinuria in preeclampsia are caused by continuous stimulation of the sympathetic nervous center in the hypothalamus through the innervation between the enlarged uterus and hypothalamus in the latter stages of pregnancy or in a complete hydatidiform mole. Future studies are needed to address the potential of pharmacological suppression of an overactive sympathetic nerve system.