21 research outputs found

    Benign dermatoses of the male genital areas: A review of the literature

    Get PDF
    The male genitalia are a common site of dermatoses. Patients with penile diseases often delay or avoid medical care due to anxiety and embarrassment. In this narrative review, we describe some of the main benign dermatoses localized to male genital, focusing on their epidemiology, clinical and dermoscopic features, as well as available therapies

    Dermoscopic clues in Pagetoid reticulosis Woringer-Kolopp type

    No full text
    we present the case of a 66 years-old male patient who presented a lesion on the left arm, appeared eight months before. The lesion was well circumscribed with a diameter of 15mm x 20mm and had the aspect of a hyperkeratotic scaly plaque, mildly pruritic. Dermoscopy showed structurless with pinkish area in the central area of the lesion and segmental brown radial lines at 1-3 o'clock, and a large scaly circular peripheral border with some linear vessel

    Drug induced longitudinal melanonychia and transverse muerhcke's lines.

    No full text
    We describe the case of a 60 years old woman, who came to our attention in November 2017. She was worried about a "dark line" which had recently developed on the second finger nail of the right hand. The patient had a medical history of infiltrating ductal carcinoma of the breast and she had received in the Spring of 2017 six courses of adjuvant chemotherapy with Docetaxel and Cyclophosphamide, later in October 2017 she had started a hormonal therapy with Letrozole. This article is protected by copyright. All rights reserved

    Autophagy and amyotrophic lateral sclerosis: The multiple roles of lithium

    No full text
    In a pilot clinical study that we recently published we found that lithium administration slows the progression of Amyotrophic Lateral Sclerosis (ALS) in human patients. This clinical study was published in addition with basic (in vitro) and pre-clinical (in vivo) data demonstrating a defect of autophagy as a final common pathway in the genesis of ALS. In fact, lithium was used as an autophagy inducer. In detailing the protective effects of lithium we found for the first time that this drug stimulates the biogenesis of mitochondria in the central nervous system and, uniquely in the spinal cord, it induces neuronogenesis and neuronal differentiation. In particular, the effects induced by lithium can be summarized as follows: (i) the removal of altered mitochondria and protein aggregates; (ii) the biogenesis of well-structured mitochondria; (iii) the suppression of glial proliferation; (iv) the differentiation of newly formed neurons in the spinal cord towards a specific phenotype. In this addendum we focus on defective autophagy as a "leit motif" in ALS and the old and novel features of lithium which bridge autophagy activation to concomitant effects that may be useful for the treatment of a variety of neurodegenerative disorders. In particular, the biogenesis of mitochondria and the increase of calbindin D 28K-positive neurons, which are likely to support powerful neuroprotection towards autophagy failure, mitochondriopathy and neuronal loss in the spinal cord

    Autophagy and amyotrophic lateral sclerosis: The multiple roles of lithium

    No full text
    In a pilot clinical study that we recently published we found that lithium administration slows the progression of Amyotrophic Lateral Sclerosis (ALS) in human patients. This clinical study was published in addition with basic (in vitro) and pre-clinical (in vivo) data demonstrating a defect of autophagy as a final common pathway in the genesis of ALS. In fact, lithium was used as an autophagy inducer. In detailing the protective effects of lithium we found for the first time that this drug stimulates the biogenesis of mitochondria in the central nervous system and, uniquely in the spinal cord, it induces neuronogenesis and neuronal differentiation. In particular, the effects induced by lithium can be summarized as follows: (i) the removal of altered mitochondria and protein aggregates; (ii) the biogenesis of well-structured mitochondria; (iii) the suppression of glial proliferation; (iv) the differentiation of newly formed neurons in the spinal cord towards a specific phenotype. In this addendum we focus on defective autophagy as a "leit motif" in ALS and the old and novel features of lithium which bridge autophagy activation to concomitant effects that may be useful for the treatment of a variety of neurodegenerative disorders. In particular, the biogenesis of mitochondria and the increase of calbindin D 28K-positive neurons, which are likely to support powerful neuroprotection towards autophagy failure, mitochondriopathy and neuronal loss in the spinal cord
    corecore