University of East Anglia

About: University of East Anglia is a education organization based out in Norwich, Norfolk, United Kingdom. It is known for research contribution in the topics: Population & Climate change. The organization has 13250 authors who have published 37504 publications receiving 1669060 citations. The organization is also known as: UEA.

Climatology of Cyclogenesis Mechanisms in the Mediterranean

Abstract: A general climatology of the main mechanisms involved in Mediterranean cyclogenesis is presented. A diagnostic study of both composite means and case studies is performed to analyze processes occurring in different seasons, and in different cyclogenetic regions within the same season. It is shown that cyclones that developed over the three most active areas in winter—the Gulf of Genoa, the Aegean Sea, and the Black Sea—are essentially subsynoptic lows, triggered by the major North Atlantic synoptic systems being affected by local orography and/or low-level baroclinicity over the northern Mediterranean coast. It is also suggested that cyclones in two, or all three, of these regions often occur consecutively, linked to the same synoptic system. In spring and summer, thermally induced lows become progressively more important, despite the existence of other factors, such as the Atlas Mountains contributing to lee cyclogenesis in northern Africa, or the extension of the Asian monsoon into the eastern ...

Cell envelope stress response in Gram-positive bacteria

Abstract: The bacterial cell envelope is the first and major line of defence against threats from the environment. It is an essential and yet vulnerable structure that gives the cell its shape and counteracts the high internal osmotic pressure. It also provides an important sensory interface and molecular sieve, mediating both information flow and the controlled transport of solutes. The cell envelope is also the target for numerous antibiotics. Therefore, the monitoring and maintenance of cell envelope integrity in the presence of envelope perturbating agents and conditions is crucial for survival. The underlying signal transduction is mediated by two regulatory principles, two-component systems and extracytoplasmic function σ factors, in both the Firmicutes (low-GC) and Actinobacteria (high-GC) branches of Gram-positive bacteria. This study presents a comprehensive overview of cell envelope stress-sensing regulatory systems. This knowledge will then be applied for in-depth comparative genomics analyses to emphasize the distribution and conservation of cell envelope stress-sensing systems. Finally, the cell envelope stress response will be placed in the context of the overall cellular physiology, demonstrating that its regulatory systems are linked not only to other stress responses but also to the overall homeostasis and lifestyle of Gram-positive bacteria.

TNF-alpha promotes fracture repair by augmenting the recruitment and differentiation of muscle-derived stromal cells.

Abstract: With an aging population, skeletal fractures are increasing in incidence, including the typical closed and the less common open fractures in normal bone, as well as fragility fractures in patients with osteoporosis. For the older age group, there is an urgent unmet need to induce predictable bone formation as well as improve implant fixation in situations such as hip joint replacement. Using a murine model of slow-healing fractures, we have previously shown that coverage of the fracture with muscle accelerated fracture healing and increased union strength. Here, we show that cells from muscle harvested after 3 d of exposure to an adjacent fracture differentiate into osteoblasts and form bone nodules in vitro. The osteogenic potential of these cells exceeds that of adipose and skin-derived stromal cells and is equivalent to bone marrow stromal cells. Supernatants from human fractured tibial bone fragments promote osteogenesis and migration of muscle-derived stromal cells (MDSC) in vitro. The main factor responsible for this is TNF-α, which promotes first MDSC migration, then osteogenic differentiation at low concentrations. However, TNF-α is inhibitory at high concentrations. In our murine model, addition of TNF-α at 1 ng/mL at the fracture site accelerated healing. These data indicate that manipulating the local inflammatory environment to recruit, then differentiate adjacent MDSC, may be a simple yet effective way to enhance bone formation and accelerate fracture repair. Our findings are based on a combination of human specimens and an in vivo murine model and may, therefore, translate to clinical care.