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AIM: To evaluate the clinicopathological and computed tomography (CT) and magnetic resonance imaging (MRI) findings of steatohepatitic hepatocellular carcinoma (SH-HCC). MATERIALS AND METHODS: Clinicopathological and radiological features were evaluated in 20 patients with SH-HCC. The diagnosis of SH-HCC was made histologically if the tumour had four of the following five characteristics: steatosis (>5% tumour cells), ballooning, Mallory-Denk bodies, interstitial fibrosis, and inflammation. All patients underwent dynamic CT and MRI. CT and MRI images were reviewed for morphological features including tumour size, presence, and distribution of fat, and patterns and degree of contrast enhancement. RESULTS: Obesity, hypertension, and history of heavy alcohol intake were common clinical findings observed in 10 (50%), 13 (65%), and 11 (55%) of the 20 patients, respectively. Steatosis and steatohepatitis were pronounced in the background liver in 12 (60%) and 10 (50%) patients, respectively. SH-HCC was moderately differentiated in 18 patients (90%) and well differentiated in two (10%). Pathologically, steatohepatitic features were diffuse in 12 (60%) of the 20 tumours and focal in eight (40%). Tumour size and the percentage of intratumoural steatosis were not correlated (r=0.17, p=0.47). On CT, 16 (80%) patients showed arterial phase enhancement and delayed washout. On MRI, 16 (80%) of 20 tumours showed prominent fatty deposition (10 diffusely, six focally) with arterial phase enhancement. CONCLUSIONS: SH-HCC is likely to show prominent fatty deposits with arterial phase enhancement on CT and MRI. A hypervascular lesion with prominent fatty change should raise the diagnostic suspicion of SH-HCC.

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We present an experimental and theoretical study of the 2D dynamics of electrically charged nanoparticles trapped under a free surface of superfluid helium in a static vertical electric field. We focus on the dynamics of particles driven by the interaction with quantized vortices terminating at the free surface. We identify two types of particle trajectories and the associated vortex structures: vertical linear vortices pinned at the bottom of the container and half-ring vortices traveling along the free surface of the liquid.

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The pathobiology of alopecia areata (AA), one of the most frequent autoimmune diseases and a major unsolved clinical problem, has intrigued dermatologists, hair biologists and immunologists for decades. Simultaneously, both affected patients and the physicians who take care of them are increasingly frustrated that there is still no fully satisfactory treatment. Much of this frustration results from the fact that the pathobiology of AA remains unclear, and no single AA pathogenesis concept can claim to be universally accepted. In fact, some investigators still harbour doubts whether this even is an autoimmune disease, and the relative importance of CD8(+) T cells, CD4(+) T cells and NKGD2(+) NK or NKT cells and the exact role of genetic factors in AA pathogenesis remain bones of contention. Also, is AA one disease, a spectrum of distinct disease entities or only a response pattern of normal hair follicles to immunologically mediated damage? During the past decade, substantial progress has been made in basic AA-related research, in the development of new models for translationally relevant AA research and in the identification of new therapeutic agents and targets for future AA management. This calls for a re-evaluation and public debate of currently prevalent AA pathobiology concepts. The present Controversies feature takes on this challenge, hoping to attract more skin biologists, immunologists and professional autoimmunity experts to this biologically fascinating and clinically important model disease.

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BACKGROUND: We have previously reported several trichoscopic (dermatoscopic) characteristics, such as black dots, 'exclamation-mark' hairs, broken hairs, yellow dots and clustered short vellus hairs as being useful clinical indicators for alopecia areata (AA). 'Coudability hairs', which are normal-looking hairs tapered at the proximal end, have been previously reported as another sign of AA. AIMS: To use trichoscopy to evaluate coudability hairs as a clinical indicator for the disease activity of AA and a substitute-marker for the hair-pull test. METHODS: Trichoscopic examinations of hair loss and perilesional areas on the scalps of 100 East Asian patients with AA were performed using a dermatoscope. Using Spearman's rank-order correlation coefficient by rank test, we examined the correlations of scores between coudability and AA disease activity, severity or duration and other trichoscopic features, and then evaluated the coudability score as a surrogate-marker for the hair-pull test. RESULTS: Coudability scores correlated positively with AA disease activity, hair-pull tests, short duration, black dots and exclamation-mark hairs, and correlated negatively with short vellus hairs. CONCLUSIONS: Coudability hairs, more closely perceived by trichoscopy, are useful-markers for disease activity in AA and provide a surrogate-marker for the hair-pull test.

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Since acne formation is a multistep process accelerated by androgens, we examined whether a new anti-acne antibiotic roxithromycin (RXM) may act as anti-androgen using transient transfection assays in human skin fibroblasts. The result showed no significant effect of 0.5, 1 and 5 microg/ml RXM on 10(-9) M R1881-induced androgen receptor (AR) transcriptional activity. While the cotransfection of exogenous ARA55, a novel AR coactivator, increased AR transactivation up to 2.59-fold, this increase was attenuated by 5 microg/ml RXM to 64.7%. Semiquantitative RT-PCR results showed that 0.1 mM H(2)O(2) treatment increased ARA55 mRNA expression level, indicating that reactive oxygen species increase the expression of ARA55 in skin. These results suggest that RXM may serve as anti-androgen only in the hypersensitive state to androgen, but not in the physiological state, through modulating end-organ hypersensitive condition to androgen possibly involving the pathway from reactive oxygen species to ARA55.

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A 69-year-old Japanese man suffered from bronchial asthma, atrial fibrillation, general fatigue, high fever, and weight loss of about 5 kg within a month. He also had intermittent claudication, a tingling feeling in his fingers and toes, and an ulcer on his toe. His laboratory data revealed leukocytosis with absolute eosinophilia. The patient was treated with predonisolone 30 mg daily. Although the ulcers healed once, the lesions recurred with tapering predonisolone. The patient visited us because of the ulcer on his toe. Physical examination showed a 2 cm ulcer surrounded by slight erythema on his right fourth toe. Magnetic resonance angiography detected tapering stenosis of the medium-sized arteries in both legs. A biopsy from his myocardium showed the infiltration of eosinophils into the myocardium. The neuron conduction rate of his lower leg was slower than that of the normal control, demonstrating mononeuritis. From these findings, we diagnosed this patient as Churg-Strauss syndrome.

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A 65-year-old Japanese man presented with itchy purpuric lichenoid papules of six months' duration on his legs and buttock. A topical glucocorticoid ointment was not effective. The biopsy specimen histologically showed a dense lichenoid infiltration of lymphocytes and histiocytes into the dermoepidermal junction; red blood cells were seen in the infiltration. Based on the clinical and pathological findings, we diagnosed this case as lichenoid purpura of Gougerot-Blum. The lesions disappeared when the diltiazem hydrochloride that he had been taking was discontinued.

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An 81-year-old woman presented with a round erythematous macule with keratotic scales on her left hand. The skin specimen histologically showed hypergranulosis and apoptotic keratinocytes in the epidermis with lichenoid infiltration of lymphocytes. Parakeratosis seen in the hyperkeratotic cornified layer indicated lichen planus-like keratosis, as distinguished from lichen planus. Direct immunofluorescence study revealed the linear deposition of IgM in the basement membrane zone; IgG, IgA and C3 were not detected.

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We here reported a case of an 82-year-old man with double involvement of extramammary Paget's disease in the genitalia and axilla. Physical examination revealed erythema and reddish tumors on the pubic area and scrotum and irregular-shaped erythema on the left axilla. The skin biopsy sample from the genital area showed Paget's cells in the epidermis and upper dermis. The specimen from the left axilla showed Paget's cells scattered in the epidermis but not in the dermis.

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Since detection of androgen receptor (AR) expression in keratinocytes by immunostaining is controversial, we investigated whether keratinocytes can act as androgen target cells using transient transfection assays. Chloramphenicol acetyltransferase (CAT) assays for the endogenous AR transcriptional activity in HaCaT keratinocytes indicated that DHT (10(-9)-10(-8) M) can induce less than 1.5-fold of mouse mammary tumor virus CAT, which is quite low, compared with 38-fold induction by 10(-7) M 1,25-dihydroxyvitamin D(3) of P450cc24-CAT. Furthermore, this low DHT-mediated induction could not be enhanced by the AR co-activators, ARA70 or ARA55. Western blotting analysis indicated that HaCaT and normal keratinocytes do not express AR protein. Transfection of exogenous AR into HaCaT keratinocytes, however, could install AR transcriptional activity, suggesting that HaCaT keratinocytes have all the necessary accessory factors for AR transcription activity. In conclusion, keratinocytes are unlikely to be target cells for androgen.

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A murine alpha4, identified in lymphocytes, binds to protein phosphatase 2A (PP2A). We found another murine alpha4-related gene (named alpha4-b) expressed selectively in the brain and testis. The alpha4-b transcript is expressed in the brain and testis, but is not detected in the spleen, thymus, bone marrow, liver, kidney, lung, heart or muscle. In-situ RNA hybridization analysis suggested that alpha4-b is expressed in most neuronal cells in the brain, but it is not expressed in the glial cells. The alpha4-b cDNA encodes a putative protein that is highly homologous (66% identity in amino-acid sequence) to the alpha4 molecule. The alpha4-b protein associates with the catalytic subunit of PP2A (PP2Ac), suggesting that the alpha4-b protein is involved in the regulation of phosphatase activity in neuronal cells.

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Activation of resting B cells requires an initial triggering of the B cell antigen receptor (BCR) and secondary stimuli through various cytokine receptors and B cell activation molecules including CD40. We found that activation of B cells through CD40 is selectively inhibited by an immunosuppressant drug, rapamycin. This effect of rapamycin on anti-CD40-mediated activation of B cells was observed using three different in vitro assays. Rapamycin suppressed the anti-CD40-induced proliferation of splenic B cells, suppressed differentiation to surface IgMhigh/IgDlow B cells, and inhibited an anti-CD40-mediated prevention of apoptosis induced by BCR cross-linkage of WEHI-231 cells. We next examined several known CD40 signal transduction pathways to identify the target of rapamycin in stimulated B cells. Rapamycin did not inhibit the activation of c-Jun N-terminal kinases (JNKs) induced by anti-CD40 stimulation nor the activation of immediate nuclear transcription factors of NF-kappaB. Therefore, rapamycin affects a novel element of the CD40 signal transduction pathway which influences the proliferation, differentiation, and prevention of apoptosis of B cells.

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The catalytic activity of the C subunit of serine/threonine phosphatase 2A is regulated by the association with A (PR65) and B subunits. It has been reported that the alpha4 protein, a yeast homolog of the Tap42 protein, binds the C subunit of serine/threonine phosphatase 2A and protein phosphatase 2A-related protein phosphatases such as protein phosphatase 4 and protein phosphatase 6. In the present study, we showed that alpha4 binds these three phosphatases and the association of alpha4 reduces the activities of these phosphatases in vitro. In contrast, PR65 binds to the C subunit of serine/threonine phosphatase 2A but not to protein phosphatase 4 and protein phosphatase 6. These results suggest that the alpha4 protein is a common regulator of the C subunit of serine/threonine phosphatase 2A and protein phosphatase 2A-related protein phosphatases.

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Human TR4 orphan receptor (TR4) can modulate the transcriptional activity of the reporter gene containing an AGGTCA direct repeat-hormone response element. Here we studied the potential role of TR4 in human HaCaT keratinocytes. Using a chloramphenicol acetyl-transferase reporter gene assay, it was shown that TR4 can suppress retinoic acid-induced transactivation by 47.3% in human HaCaT keratinocytes. Electrophoretic mobility shift assay indicated that this suppression may be due to TR4 binding with higher affinity to the retinoic acid response element than retinoid receptors. Western blot analysis further suggested that retinoic acid can increase the expression of TR4 protein in human HaCaT keratinocytes, indicating that TR4 acts as a negative feedback modulator for retinoic acid action. Interestingly, TR4 expression is increased in normal human keratinocytes when substituting a low calcium medium with a high calcium medium. Together, our data suggested, for the first time, that an orphan receptor, such as TR4, may play an important part in retinoid-mediated signaling pathways in human keratinocytes, providing a new insight into keratinocyte biology.

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