Frontal Fibrosing Alopecia: Role of Dermoscopy in Differential Diagnosis

Frontal fibrosing alopecia (FFA) is more common in postmenopausal women, but it can occur in younger women. Some authors consider FFA to be a distinct frontal variant of lichen planopilaris. From a clinical point of view, this relatively uncommon condition is characterized by progressive frontotemporal recession due to inflammatory destruction of hair follicles. Dermoscopy can be very useful, as the differential diagnosis between traction alopecia, alopecia areata, FFA and cicatricial marginal alopecia may be difficult. It is not clear whether or not treatment alters the natural history of the disease - the disease stabilized with time in most of the patients with or without continuing treatment. Here we report a case of a 50-year-old woman with FFA and discuss the relevance of dermoscopy in the differential diagnosis of this disease

concordance and time estimation of store and forward mobile teledermatology compared to classical face to face consultation

Smartphones have overcome the limitations of image quality seen in older devices and opened a new field of telemedicine called "mobile teledermatology". Technological advances and the need to reduce health service costs will strongly promote the development of telemedicine. For this reason, we evaluated the concordance be tween store-and-forward mobile teledermatology and the classical face-to-face dermatological visit. We also measured the time taken to submit a teleconsultation using a smartphone. Before conventional face-to-face visit, a final-year resident of the 3-year course for general practitioners collected medical history, took digital images of skin diseases with a smartphone and, measuring the time required to complete this operation, transmitted them to an expert teledermatologist. In 391 patients we obtained a concordance between face-to-face and store-and-forward diagnosis of 91.05% (Cohen κ coefficient = 0.906). On average only few minutes needs to be added to a no

CD4+CD25+ lymphocyte subsets in chronic graft versus host disease patients undergoing extracorporeal photochemotherapy.

Extracorporeal photochemotherapy (ECP) has been used successfully for the treatment of chronic Graft versus Host Disease (cGvHD). However, the mechanism by which ECP exerts its protective effects remains elusive. Some recent observations have suggested a possible role of certain subsets of T lymphocytes with immunosuppressive properties (T-regulatory cells) that coexpress CD4 and high levels of the interleukin-2 receptor chain: CD4+CD25+ T lymphocytes. We studied whether ECP affects the percentage of these cells in the peripheral blood of patients with cGvHD. The study population consisted of 14 patients with cGvHD refractory to systemic steroids. On enrolment in each cycle of ECP, patients underwent clinical examination, blood chemistry analysis and other instrumental procedures to document and assess involvement of the various organs and systems. For cytofluorimetric identification and phenotyping of CD4+CD25+ T lymphocytes, peripheral blood samples were collected in EDTA anticoagulant before ECP, after 48 hours, and after 6 and 12 months from the start of treatment. The 14 patients in this study received a total of more than 300 cycles of ECP, with only minor side effects. The clinical outcome was negative in 2 patients and positive in 12 patients. Within-subject analysis indicated that the percentage of CD4+CD25+ T lymphocytes before ECP and after 12 months of treatment was significantly increased. Our study confirms that changes in the percentage of CD4+CD25+ T cells induced by ECP could be a central aspect in the cascade of immune events leading to the immunological and clinical effects of this treatment in patients with cGvHD

Measurement of the stellar Ni 58 (n,γ) Ni 59 cross section with accelerator mass spectrometry

The Ni58(n,γ)Ni59 cross section was measured with a combination of the activation technique and accelerator mass spectrometry (AMS). The neutron activations were performed at the Karlsruhe 3.7 MV Van de Graaff accelerator using the quasistellar neutron spectrum at kT=25 keV produced by the Li7(p,n)Be7 reaction. The subsequent AMS measurements were carried out at the 14 MV tandem accelerator of the Maier-Leibnitz Laboratory in Garching using the gas-filled analyzing magnet system (GAMS). Three individual samples were measured, yielding a Maxwellian-averaged cross section at kT=30 keV of (σ)30keV = 30.4 (23)syst(9)stat mbarn. This value is slightly lower than two recently published measurements using the time-of-flight (TOF) method, but agrees within the uncertainties. Our new results also resolve the large discrepancy between older TOF measurements and our previous value

Hypertrophic Cardiomyopathy in Children: Pathophysiology, Diagnosis, and Treatment of Non-sarcomeric Causes

Hypertrophic cardiomyopathy (HCM) is a myocardial disease characterized by left ventricular hypertrophy not solely explained by abnormal loading conditions. Despite its rare prevalence in pediatric age, HCM carries a relevant risk of mortality and morbidity in both infants and children. Pediatric HCM is a large heterogeneous group of disorders. Other than mutations in sarcomeric genes, which represent the most important cause of HCM in adults, childhood HCM includes a high prevalence of non-sarcomeric causes, including inherited errors of metabolism (i.e., glycogen storage diseases, lysosomal storage diseases, and fatty acid oxidation disorders), malformation syndromes, neuromuscular diseases, and mitochondrial disease, which globally represent up to 35% of children with HCM. The age of presentation and the underlying etiology significantly impact the prognosis of children with HCM. Moreover, in recent years, different targeted approaches for non-sarcomeric etiologies of HCM have emerged. Therefore, the etiological diagnosis is a fundamental step in designing specific management and therapy in these subjects. The present review aims to provide an overview of the non-sarcomeric causes of HCM in children, focusing on the pathophysiology, clinical features, diagnosis, and treatment of these rare disorders

Dietary thiols: A potential supporting strategy against oxidative stress in heart failure and muscular damage during sports activity

Moderate exercise combined with proper nutrition are considered protective factors against cardiovascular disease and musculoskeletal disorders. However, physical activity is known not only to have positive effects. In fact, the achievement of a good performance requires a very high oxygen consumption, which leads to the formation of oxygen free radicals, responsible for premature cell aging and diseases such as heart failure and muscle injury. In this scenario, a primary role is played by antioxidants, in particular by natural antioxidants that can be taken through the diet. Natural antioxidants are molecules capable of counteracting oxygen free radicals without causing cellular cytotoxicity. In recent years, therefore, research has conducted numerous studies on the identification of natural micronutrients, in order to prevent or mitigate oxidative stress induced by physical activity by helping to support conventional drug therapies against heart failure and muscle damage. The aim of this review is to have an overview of how controlled physical activity and a diet rich in antioxidants can represent a “natural cure” to prevent imbalances caused by free oxygen radicals in diseases such as heart failure and muscle damage. In particular, we will focus on sulfur-containing compounds that have the ability to protect the body from oxidative stress. We will mainly focus on six natural antioxidants: Glutathione, taurine, lipoic acid, sulforaphane, garlic and methylsulfonylmethane