Zabargad (St.John) Island: an uplifted fragment of Red Sea lithosphere

geochimica di una porzione di litosfera oceanica emergente nel Mar Ross

Oxidative Stress in Autism Spectrum Disorder

According to the United States Centers for Disease Control and Prevention (CDC), as of July 11, 2016, the reported average incidence of children diagnosed with an autism spectrum disorder (ASD) was 1 in 68 (1.46%) among 8-year-old children born in 2004 and living within the 11 monitoring sites’ surveillance areas in the United States of America (USA) in 2012. ASD is a multifaceted neurodevelopmental disorder that is also considered a hidden disability, as, for the most part; there are no apparent morphological differences between children with ASD and typically developing children. ASD is diagnosed based upon a triad of features including impairment in socialization, impairment in language, and repetitive and stereotypic behaviors. The increasing incidence of ASD in the pediatric population and the lack of successful curative therapies make ASD one of the most challenging disorders for medicine. ASD neurobiology is thought to be associated with oxidative stress, as shown by increased levels of reactive oxygen species and increased lipid peroxidation, as well as an increase in other indicators of oxidative stress. Children with ASD diagnosis are considered more vulnerable to oxidative stress because of their imbalance in intracellular and extracellular glutathione levels and decreased glutathione reserve capacity. Several studies have suggested that the redox imbalance and oxidative stress are integral parts of ASD pathophysiology. As such, early assessment and treatment of antioxidant status may result in a better prognosis as it could decrease the oxidative stress in the brain before it can induce more irreversible brain damage. In this review, many aspects of the role of oxidative stress in ASD are discussed, taking into account that the process of oxidative stress may be a target for therapeutic interventions. © 2020, Springer Science+Business Media, LLC, part of Springer Nature

Proximal Splenic Artery Embolization In Blunt Splenic Trauma

Proximal embolization of the splenic artery (PSAE) has recently been reported for traumatic splenic injury. The suggested mechanism of action entails a decrease in the splenic blood pressure without ischemia due to collateral blood supply. The main complications of selective embolization are continuous bleeding, splenic infarcts and splenic abscesses. The main complications of observation alone are continuous bleeding and formation of splenic pseudoaneurysms. Our aim was to assess the efficacy of PSAE in the cessation of bleeding without formation of pseudoaneurysms, and the outcome of the spleen after such intervention. A prospective observational study of all patients undergoing PSAE for traumatic splenic injury in our institution over a 33-month period. Clinical and Doppler sonographic examinations were performed to assess cessation of bleeding, splenic blood flow, and formation of splenic pseudoaneurysms, infarcts or abscesses. During 33 months, 11 patients with blunt abdominal trauma and tomographic evidence of either high grade or actively bleeding splenic injuries were treated by PSAE. During follow-up, no patient underwent surgery or repeated embolization. Preserved blood flow was found on Doppler sonography in 82% of the patients and no pseudoaneurysms were demonstrated. A perisplenic collection was found in one patient and responded well to percutaneous drainage. Proximal embolization of the splenic artery for severe splenic injury is highly successful in cessation of bleeding while preserving splenic architecture. There were minimal complications in this series demonstrated by clinical and Doppler examinations