No abstract

Timing of activity along the Yammuneh segment (Lebanon–Syria) of the Dead Sea Fault Zone and its northward continuation is still a subject of controversy. Our field structural analysis and observations on radar, Landsat and digital elevation model imagery of the Homs region (Syria) are of concern for Plio-Quaternary tectonics of the whole northern part of the Dead Sea Fault Zone. We show in this paper that the northern Dead Sea Fault Zone has remained active since the onset of the Homs basalts at c . 6 Ma. Continuing movement in Recent times is indicated by the occurrence of Quaternary pull-apart structures and offset of active ravines along the fault. The Homs basalts are related to the distinct oval-shaped Shin volcanic edifice, of which the long axis trends NW. The volcano was fed through NW-striking tension fractures, which now form dykes and volcanic ridges. These patterns are consistent with a NE–SW extension that occurred c . 6 Ma ago. The northwestern end of the Shin volcano is left-laterally displaced c . 20 km, yielding a c . 3.3 mm a −1 mean rate of relative movement between the Arabian and African plates. In the northern part of the Dead Sea Fault Zone, the overall trace of the main active Dead Sea Fault Zone is not a single transform but forms an irregular plate boundary composed of transform fault and collision belt segments. Fine-grained mylonite developed in the fault corridor may have favoured aseismic deformation in the Shin volcano area.

No abstract

Immune dysfunction is widely regarded as one of the central tenants underpinning the pathophysiology of diabetes mellitus (DM) and its complications. When discussing immunity, the role of neutrophils must be accounted for: neutrophils are the most abundant of the circulating immune cells and are the first to be recruited to sites of inflammation, where they contribute to host defense via phagocytosis, degranulation, and extrusion of neutrophil extracellular traps (NETs). NETs are composed of DNA associated with nuclear and cytosolic neutrophil proteins. Although originally reported as an antimicrobial strategy to prevent microbial dissemination, a growing body of evidence has implicated NETs in the pathophysiology of various autoimmune and metabolic disorders. In these disorders, NETs propagate a pathologic inflammatory response with consequent tissue injury and thrombosis. Many diabetic complications—such as stroke, retinopathy, impaired wound healing, and coronary artery disease—involve these mechanisms. Therefore, in this review, we discuss laboratory and clinical data informing our understanding of the role of NETs in the development of these complications. NET markers, including myeloperoxidase, citrullinated histone H3, neutrophil elastase, and cell-free double-stranded DNA, can easily be measured in serum or be detected via immunohistochemical/immunocytochemical staining of tissue specimens. Therefore, NET constituents potentially constitute reliable biomarkers for use in the management of diabetic patients. However, no NET-targeting drug is currently approved for the treatment of diabetic complications; a candidate drug will require the outcomes of well-designed, robust clinical trials assessing whether NET inhibition can benefit patients in terms of morbidity, quality of life, health expenditures, and mortality. Therefore, much work remains to be done in translating these encouraging pieces of data into clinical trials for NET-targeting medications to be used in the clinic.