Low Carb Medical Newsline. Articles Directory.

“After the inoculation of a variety of genetically modified mice with this bacterium, the laboratory found that mice lacking fibrin showed a significantly reduced survival and repair significantly increased the number of bacteria in blood and tissues,” said Dr. . Smiley. “These results add to a growing body of evidence that fibrin helps protect the body during infection.”Unless effective antibiotics are administered early, these infections can lead to sepsis, a syndrome in which the immune system releases so that they fight the infection causes inflammation damage than good, leading to organ failure, shock and death . With the spread of resistant bacteria such as MRSA, most drugs, the incidence of sepsis is increasing, even in the state of the art hospitals. In general, doctors say only members of the family that these deaths are caused by an infection, but in many cases the actual cause of death was sepsis.

In addition, the study identified a number of key molecular players Trudeau in regulating levels of fibrin produced by the coagulation of the blood protection. The smiles laboratory suggested that the drugs for sepsis should keep these channels of protection, avoiding excess, oxygen-private blood clotting that leads to organ failure. Above all, have identified at least one target of drugs that can selectively enable them to prevent dangerous blood clots while maintaining the protective fibrin. In particular, showed that the mode of coagulation “extrinsic” coagulation of blood is essential for protection during sepsis, while the path “intrinsic” seems to be superfluous. Studies are underway to assess whether the anti-clotting drugs that selectively block the intrinsic pathway will help prevent deaths from infections that cause septicemia.

Trudeau Institute, a new study may help explain why anticoagulation therapies have largely failed to extend the life of patients with sepsis. The study was conducted by Deyan Luo, a postdoctoral fellow in the laboratory of Stephen Smiley. This shows that fibrin, a key product of the process of blood clotting is essential for host defense against Yersinia enterocolitica, a Gram-negative bacterium that causes septicemia in humans and in experimental mice. The new data will be published in the August 15 issue of the Journal of Immunology, and is now available online prior to printing.

Infectious diseases remain a leading cause of death worldwide. Many of these deaths followed, mostly from our own body excessive response to certain types of infections. That infectious agents before entering the body through a wound, a line or intravenous catheter, and if you first establish infection in our skin, lungs or intestines, all too often escape our natural mechanisms of defense Immune and then spread, causing a generalized infection in most parts of the body.

One of the reasons is difficult to treat sepsis is the excessive inflammatory response, which requires changes in the system of another powerful body, the blood coagulation system. The blood clot is expected in response to trauma, as a way to prevent bleeding. However, excessive inflammation accompanying sepsis causes blood clotting in our blood vessels, even in the absence of trauma, blocking the flow of blood and tissues starved of life giving oxygen. It seems logical to treat patients with drugs that block with sepsis (blood thinners, for example) the coagulation of blood. However, anticoagulant therapies have largely failed to extend the life of patients with sepsis. The study provides a spectacular demonstration of Trudeau in the process of blood coagulation during sepsis, thus helping to explain why anticoagulants usually fail to help patients with sepsis.