http://xoomer.virgilio.it/lusebra/NuoviFile/PrevenzioneTVP.pdf

Prevention of venous thromboembolism

Mitogen-activated protein (MAP) kinases comprise a family of ubiquitous proline-directed, protein-serine/threonine kinases, which participate in signal transduction pathways that control intracellular events including acute responses to hormones and major developmental changes in organisms. MAP kinases lie in protein kinase cascades. This review discusses the regulation and functions of mammalian MAP kinases. Nonenzymatic mechanisms that impact MAP kinase functions and findings from gene disruption studies are highlighted. Particular emphasis is on ERK1/2.

/pdf/mitogen-activated-protein-map-kinase-pathways-regulation-and-3nsauvepr2.pdf

Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions.

https://agrilinks.org/sites/default/files/resource/files/Williams_Aflatoxicosis_AJCN_2004.pdf

Human aflatoxicosis in developing countries: a review of toxicology, exposure, potential health consequences, and interventions

http://www.mmh.org.tw/taitam/car_int/Documents/amipdf99edits.pdf

ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction

DURING prolonged general anesthesia and any period of limited mobility following surgery, thrombus formation may be initiated in the deep veins of the legs. Studies employing Radio-labeled fibrinogen or venography have revealed deep-vein thrombosis in 20 to 30 percent of patients who have undergone general surgery and in an even larger proportion of patients who have had orthopedic surgery.1 2 3 Most such thromboses are subclinical and resolve completely when mobility is restored, although some do produce permanent valvular damage and chronic venous insufficiency. A few, however, may travel to the lungs and, depending on how much of the pulmonary circulation is . . .

Reduction in fatal pulmonary embolism and venous thrombosis by perioperative administration of subcutaneous heparin. Overview of results of randomized trials in general, orthopedic, and urologic surgery.

DO CD4-POSITIVE CYTOTOXIC T CELLS DAMAGE ISLET β CELLS IN TYPE 1 DIABETES?

Glucose stimulates translocation of the homeodomain transcription factor PDX1 from the cytoplasm to the nucleus in pancreatic beta-cells

Loss of functional KATP channels in pancreatic β–cells causes persistent hyperinsulinemic hypoglycemia of infancy

Loss of Functional KATP Channels in Pancreatic Beta-Cells Causes Persistent Hyperinsulinemic Hypoglycemia of Infancy

The p38/reactivating kinase mitogen-activated protein kinase cascade mediates the activation of the transcription factor insulin upstream factor 1 and insulin gene transcription by high glucose in pancreatic beta-cells.

R. F. L. James

Papers

DO CD4-POSITIVE CYTOTOXIC T CELLS DAMAGE ISLET β CELLS IN TYPE 1 DIABETES?

Glucose stimulates translocation of the homeodomain transcription factor PDX1 from the cytoplasm to the nucleus in pancreatic beta-cells

Loss of Functional KATP Channels in Pancreatic Beta-Cells Causes Persistent Hyperinsulinemic Hypoglycemia of Infancy

The p38/reactivating kinase mitogen-activated protein kinase cascade mediates the activation of the transcription factor insulin upstream factor 1 and insulin gene transcription by high glucose in pancreatic beta-cells.

CD4+ T-cell damage to islet beta cells.