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La secreción mamaria en el varón es infrecuente y se encuentra altamente asociada a malignidad. Sin embargo, también puede ser debida a procesos benignos. Además de la exploración física, todos los pacientes se deben realizar un examen radiológico con mamografía y/o ecografía. Además, nosotros proponemos el uso de la mamografía con contraste en los casos de secreción mamaria sospechosa dado el alto valor predictivo negativo de esta técnica, lo que permite reducir el número de biopsias innecesarias. El objetivo de este artículo es realizar una revisión de los hallazgos por imagen de las causas más frecuentes de secreción mamaria en el varón tanto benignas como malignas. Asimismo, nos gustaría compartir nuestra experiencia con el uso de la mamografía con contraste en el estudio de esta patología.

El presente estudio pretende evaluar la utilidad de la elastosonografía por ondas de corte transversales (SWE) para la identificación de la sinovitis en pacientes con un historial de artritis dentro de un diagnóstico de una enfermedad reumatológica definida.

In the present study, the molecular mechanism underlying the up-regulatory effect of estradiol (E2) on mouse insulin receptor substrate-1 (IRS-1) promoter was investigated in CHO cells on which the same promoter had first been functionally characterized. The mouse IRS-1 promoter bears four consensus half Estrogen Responsive Elements (ERE) sequences and thirteen AP-1- and ten Sp1-binding elements. We performed molecular dissection of this promoter gene providing 3' different deleted constructs, containing the same AP-1 rich region with a progressively increased number of ERE half sites located downstream. None of these constructs was responsive to E2, while a downstream region (nt –1420 to –160) rich in GC elements was induced by E2. However, the latter region lost its intrinsic E2 responsiveness when the whole IRS-1 promoter was mutated for deletion in all four ERE half sites. Deletion analysis of the ERE half sites demonstrated that only ERE located at the position –1500 to –1495, close to the GC-rich region, was able to maintain the induced activatory effect of E2 on the IRS-1 gene. Electrophoretic mobility shift and chromatin immunoprecipitation assays identified the region containing the half ERE/Sp1 (nt –1500 to –1477) as the one conferring E2 responsiveness to the whole promoter. This effect occurs through the functional interaction between E2/ERα and Sp1.

In the present study, the molecular mechanism underlying the up-regulatory effect of estradiol (E2) on mouse insulin receptor substrate-1 (IRS-1) promoter was investigated in CHO cells on which the same promoter had first been functionally characterized. The mouse IRS-1 promoter bears four consensus half Estrogen Responsive Elements (ERE) sequences and thirteen AP-1- and ten Sp1-binding elements. We performed molecular dissection of this promoter gene providing 3′ different deleted constructs, containing the same AP-1 rich region with a progressively increased number of ERE half sites located downstream. None of these constructs was responsive to E2, while a downstream region (nt −1420 to −160) rich in GC elements was induced by E2. However, the latter region lost its intrinsic E2responsiveness when the whole IRS-1 promoter was mutated for deletion in all four ERE half sites. Deletion analysis of the ERE half sites demonstrated that only ERE located at the position −1500 to −1495, close to the GC-rich region, was able to maintain the induced activatory effect of E2on the IRS-1 gene. Electrophoretic mobility shift and chromatin immunoprecipitation assays identified the region containing the half ERE/Sp1 (nt −1500 to −1477) as the one conferring E2responsiveness to the whole promoter. This effect occurs through the functional interaction between E2/ERα and Sp1.

Mitogen-activated protein kinases (MAPKs) are evolutionary conserved enzymes playing a key role in the transduction of biological signals from cell surface receptors, through the cytoplasm, up to the transcriptional machinery in the nucleus. MAPKs are expressed by alveolar and airway vascular endothelial cells, as well as by bronchial epithelial cells, which actively participate in the inflammatory and immune processes characterizing many lung diseases. We have recently shown, in human pulmonary endothelial cells, that the synthetic glucocorticoid dexamethasone is able to inhibit the phosphorylation-dependent activation of MAPKs induced by oxidative stress and by the pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α. In primary cultures of human bronchial epithelial cells, our group has also demonstrated that budesonide, a topical corticosteroid widely used as inhaled anti-inflammatory therapy, exerts a potent inhibitory effect on transforming growth factor-β-induced activation of p38, which represents the MAPK subgroup mostly involved in inflammatory processes. Furthermore, other authors have detected an anti-inflammatory action of specific p38 inhibitors in some experimental models of pulmonary inflammation. Therefore, MAPK signalling pathways are emerging as very important, newly recognized targets of anti-inflammatory and immunoregulatory therapies, aimed in particular at controlling the pathogenic events underlying several lung diseases. In this regard, we think that our studies, together with those of other research groups, may contribute to better elucidate the molecular mechanisms responsible for the therapeutic effects of currently available anti-inflammatory agents, as well as to develop novel pharmacological strategies directly targeted at MAPK modulation.

The association between forearm bone mineral areal density (BMD) and dietary calcium, anthropometric characteristics, puberty, and physical activity was studied for the first time in 200 girls (aged 11-15 years) and 100 women (aged 20-23 years) living in Southern Italy.

To determine the late effects of treatment on thyroid function in children who survive acute lymphoblastic leukemia, we assessed plasma levels of thyroid hormones in 24 children (15 girls and 9 boys) who had received combination of chemotherapy along with 18–24 Gy of irradiation to the cranium. The children were aged between 1 and 10.5 years (mean 3.1) at diagnosis and thyroid status was investigated between 1.3 and 13 years (mean 6.8) after completion of therapy. Six children showed a low peak of plasma thyroid stimulating hormone (TSH), after stimulation with thyrotrophin-releasing hormone (TRH). Three children showed a low basal plasma TSH concentration. Serum levels of thyroxine (T4, fT4) and triiodothyronine (T3, fT3) were normal in all patients. The frequency of thyroid hypofunction (low peak response of TSH to TRH) was more common in children receiving 24 compared to 18 Gy cranial irradiation (50% vs 14%; odds ratio=7) and those who had completed therapy more than 5 years ago (31.3% vs 12.5%, odds ratio 3.18) although no significant association could be found (95%IC: 0.27–65.8 and 0.24–90 respectively). Because of the low mean age at diagnosis of our population no significant association could be found between children younger than 3 years of age at diagnosis and thyroid hypofunction (odds ratio = 0.14; 95%IC: 0.01–1.48). We conclude that treatment for acute lymphoblastic leukemia including cranial irradiation may lead to TRH/TSH dysfunction and therefore long term survivors should be followed for a long period after completion of therapy.

El músculo tensor de la fascia lata es una estructura muscular que forma parte de la porción lateral de la pelvis y del muslo proximal. Debido en parte a que la patología de este músculo no es bien conocida y descrita en la literatura. Por el contrario, la hipertrofia y la seudohipertrofia del músculo tensor de la fascia lata son hallazgos por imagen relativamente frecuentes que a menudo no se diagnostican y entran en un diagnóstico diferencial con patologías más complejas y peligrosas. En este artículo, nuestro objetivo es describir las características anatómicas y funcionales del músculo tensor de la fascia lata, profundizando en la descripción del músculo en radiología, su patología y un resumen de la literatura sobre el tema.

Several studies have investigated the possible relationship between fertility drugs and the risk of breast cancer. To provide further information on this issue, we analysed data from a case control study, conducted in Northern Italy between 1983 and 1991. Trained interviewers identified and questioned 3415 cases (women aged 23-74 years with histologically confirmed breast cancer) and 2916 controls (women aged 21-74 years admitted to the same hospitals for diseases other than malignant, hormonal or gynaecological conditions). Fifty (1.5%) cases and 53 (1.8%) controls reported any history of infertility; the corresponding multivariate odds ratios (OR) of breast cancer was 0.8 [95% confidence interval (CI) 0.5-1.1]. Sixteen (0.5%) cases and 11 (0.4%) controls reported ever using fertility drugs; the corresponding OR was 1.2 (95% CI 0.5-2.6). Allowance for potential confounding factors did not markedly modify these estimates. In conclusion, this study provides reassuring evidence on the absence of an association between fertility drug treatment and breast cancer risk.