University of Alabama at Birmingham

About: University of Alabama at Birmingham is a education organization based out in Birmingham, Alabama, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 38523 authors who have published 86775 publications receiving 3930642 citations. The organization is also known as: UAB & The University of Alabama at Birmingham.

Thrombospondin causes activation of latent transforming growth factor-beta secreted by endothelial cells by a novel mechanism.

Abstract: Thrombospondin (TSP) forms specific complexes with transforming growth factor-beta (TGF-beta) in the alpha granule releasate of platelets and these TSP-TGF-beta complexes inhibit the growth of bovine aortic endothelial cells (BAE). In these studies, we report that TSP stripped of associated TGF-beta (sTSP) retained growth inhibitory activity which was partially reversed by a neutralizing antibody specific for TGF-beta. Since BAE cells secrete latent TGF-beta, we determined whether sTSP activates the latent TGF-beta secreted by BAE cells. Cells were cultured with or without sTSP and then the conditioned medium was tested for the ability to support TGF-beta-dependent normal rat kidney (NRK) colony formation in soft agar. Medium conditioned with sTSP showed a dose- and time-dependent ability to stimulate BAE-secreted TGF-beta activity, reaching maximal activation by 1-2 h with 0.4 micrograms/ml (0.9 nM) sTSP. The sTSP-mediated stimulation of TGF-beta activity is not dependent on serum factors and is not a general property of extracellular matrix molecules. The sTSP-mediated stimulation of TGF-beta activity was blocked by a mAb specific for sTSP and by neutralizing antibodies to TGF-beta. Activation of BAE cell secreted latent TGF-beta by sTSP can occur in the absence of cells and apparently does not require interactions with cell surface molecules, since in conditioned medium removed from cells and then incubated with sTSP, activation occurs with kinetics and at levels similar to what is seen when sTSP is incubated in the presence of cells. Serine proteases such as plasmin are not involved in sTSP-mediated activation of TGF-beta. Factors that regulate the conversion of latent to active TGF-beta are keys to controlling TGF-beta activity. These data suggest that TSP is a potent physiologic regulator of TGF-beta activation.

The human complement system in health and disease

Abstract: Introduction and Historical Notes, Michael M Frank Molecular Architecture Overview of the Complement System, John E Volanakis Clq and Mannose-Binding Lectin, Kenneth B M Reid Complement Enzymes, John E Volanakis and Gerard J Arlaud The Chemistry and Biology of C3, C4, and C5, John D Lambris, Arvind Sahu, and Rick A Wetsel Proteins of the Membrane Attack Complex, Mnason E Plumb and James M Sodetz Regulatory Proteins of Complement, M Kathryn Liszewski and John P Atkinson Complement Receptors, Joseph M Ahearn and Ariella M Rosengard Phylogeny of the Complement System, Masaru Nonaka Regulation of Complement Protein Gene Expression, Harvey R Colten and Gerard Garnier Biology Characterization of Complement Anaphylatoxins and Their Biological Responses, Julia A Ember, Mark A Jagels, and Tony E Hugli Complement-Mediated Phagocytosis, Melvin Berger Cellular Responses to the Membrane Attack Complex, Carolyn Mold Regulation by Complement of Acquired Immunity, Michael C Carroll and Douglas T Fearon Endothelial Cell Responses to Complement Activation, Soheyla Saadi and Jeffrey L Platt The Complement System in Reproduction, Teresa J Oglesby Bacteria and Complement, Franz Petry and Michael Loos Complement and Viruses, Neil R Cooper Complement and Disease Complement Deficiencies and Infection, Peter Densen Processing and Clearance of Immune Complexes by Complement and the Role of Complement in Immune Complex Diseases, Kevin A Davies and Mark J Walport C1 Inhibitor Gene and Hereditary Angioedema, Alvin E Davis III Paroxysmal Nocturnal Hemoglobinuria and Complement, Wendell F Rosse Complement in Central Nervous System Disorders, Moon L Shin, Horea Rus, and Florin Niculescu Development of Clinically Useful Agents to Control Complement-Mediated Tissue Damage, Eric Wagner and Michael M Frank Autoimmune Hemolytic Anemia, Alan D Schreiber Complement and Glomerular Diseases, Clark West Role of Complement in Diseased and Normal Human Skin, Kim B Yancey and Thomas J Lawley Complement and Neuromuscular Diseases, Milan Basta and Marinos C Dalakas

Global, regional, and national burden of suicide mortality 1990 to 2016: systematic analysis for the Global Burden of Disease Study 2016

Abstract: Objectives To use the estimates from the Global Burden of Disease Study 2016 to describe patterns of suicide mortality globally, regionally, and for 195 countries and territories by age, sex, and Socio-demographic index, and to describe temporal trends between 1990 and 2016. Design Systematic analysis. Main outcome measures Crude and age standardised rates from suicide mortality and years of life lost were compared across regions and countries, and by age, sex, and Socio-demographic index (a composite measure of fertility, income, and education). Results The total number of deaths from suicide increased by 6.7% (95% uncertainty interval 0.4% to 15.6%) globally over the 27 year study period to 817 000 (762 000 to 884 000) deaths in 2016. However, the age standardised mortality rate for suicide decreased by 32.7% (27.2% to 36.6%) worldwide between 1990 and 2016, similar to the decline in the global age standardised mortality rate of 30.6%. Suicide was the leading cause of age standardised years of life lost in the Global Burden of Disease region of high income Asia Pacific and was among the top 10 leading causes in eastern Europe, central Europe, western Europe, central Asia, Australasia, southern Latin America, and high income North America. Rates for men were higher than for women across regions, countries, and age groups, except for the 15 to 19 age group. There was variation in the female to male ratio, with higher ratios at lower levels of Socio-demographic index. Women experienced greater decreases in mortality rates (49.0%, 95% uncertainty interval 42.6% to 54.6%) than men (23.8%, 15.6% to 32.7%). Conclusions Age standardised mortality rates for suicide have greatly reduced since 1990, but suicide remains an important contributor to mortality worldwide. Suicide mortality was variable across locations, between sexes, and between age groups. Suicide prevention strategies can be targeted towards vulnerable populations if they are informed by variations in mortality rates.