Men's Health News - Part 3

28 Feb

The Total Artificial Heart: Clinical Application of the TAH

The Total Artificial Heart: Clinical Application of the TAHClinical Application of the TAH
Each year, 17,000 to 35,000 persons die of prese-nescent heart failure, 5,000 to 11,000 become eligible for kidney transplantation, and 5,000 to 10,000 become eligible for liver or pancreas transplants. Not all of these individuals will receive new organs—donor organs are scarce, the cost of transplantation is high, and it is incompletely reimbursed.
TAH and Heart Transplantation
Since the first government TAH study in 1967, heart transplants have become a successful treatment for presenescent heart failure. Three-fourths of transplant patients survive two years; more than half live five years. Many survivors return to premorbid levels of function with a quality of life that is comparable to those receiving kidney transplants and better than that of those on dialysis. Continue Reading »

27 Feb

The Total Artificial Heart: Deployment Costs

The TAH proponents hold that the modest outlay of $10 to $12 million dollars per year for pre-deployment research on all types of circulatory assistance is the only way to learn about the absolute and relative costs and benefits of a TAH. The argument that the TAH would draw funds from more pressing health or social needs improperly assumes that funds for TAH deployment would otherwise go to more beneficial uses. TAH proponents also note that the $2.5-5 billion annual TAH deployment costs derive in large part from the many persons who might benefit from the device rather than from unprecedented per-case costs estimated at $30,000 per year. Continue Reading »

26 Feb

The Total Artificial Heart

The Total Artificial HeartAn Ethics Perspective on Current Clinical Research and Deployment
Precent progress with the total artificial heart (TAH) has captured public interest, subjected preliminary human trials to unprecedented scrutiny, and fueled an intense debate among ethicists, policy. Investment in TAH research continues to yield insights into cardiovascular physiology and clinical problems such as anticoagulation which have wider clinical utility. TAH research is also a potent symbol of hope and social commitment to patients with heart disease and their families, much like chemotherapy research is for those dying of presently incurable malignancies. buy actos 30mg Continue Reading »

23 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Completing the Circle: Effects of Pulmonary Injury and Infection on the Liver

Completing the Circle: Effects of Pulmonary Injury and Infection on the Liver
Lungs injured by blood-borne mechanisms during extrapulmonary sepsis are not passive bystanders in multiple organ dysfunction during ARDS, but instead may play active, sustaining roles in its evolution. The thesis has been advanced that pulmonary capillary endothelial injury alters pulmonary metabolism of vasoactive amines and eicosanoids, inducing changes in regional organ blood flow and abnormal dependency of oxygen uptake on oxygen availability (Fig 1). Superimposed direct pulmonary injury owing to localized pulmonary acid aspiration can affect cardiac performance and, potentially, hepatic blood flow due to pulmonary release of thromboxane A2. Reading here Continue Reading »

21 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Intermediary Role of the Liver in Protein Synthesis and Metabolism

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Intermediary Role of the Liver in Protein Synthesis and MetabolismIntermediary Role of the Liver in Protein Synthesis and Metabolism
Synthesis of essential plasma proteins by hepatocytes in the acute-phase response plays a key role in modulating hepatic reticuloendothelial system phagocytic performance and controlling substrate fluxes during the hypermetabolism accompanying ARDS with multiple systems organ failure. The liver is a principal source of soluble fibronectin. Reduced plasma fibronectin levels secondary to consumption during reticuloendothelial system phagocytosis of particulate material and microorganisms can result in an “hypo-opsonemic” state, characterized by impaired reticuloendothelial system phagocytic efficiency and multiple organ dysfunction. Inflammation also “re-prioritizes” hepatocyte protein synthesis to increase the release of other specialized acute-phase proteins, including C-reactive protein (CRP), fibrinogen, ceru-loplasmin, and o^-antitrypsin, as albumin, transferrin, and ai-macroglobulin are reduced. Continue Reading »

20 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Metabolic Inactivation of Inflammatory Mediators by Hepatocytes

Metabolic Inactivation of Inflammatory Mediators by Hepatocytes
Changes in normal hepatic parenchymal cell performance and hepatobiliary excretory function can significantly compromise host defense (Fig 1). Beside Kupffer cells, hepatocytes also clear endotoxin from the circulation under certain circumstances. Furthermore, hepatocytic clearance of two major endotoxin-induced inflammatory mediators limits their intravascular half-life. Hagmann et al found that endotoxin directly potentiates its activation of the arachidonate oxidation cascade by interfering with normal hepatobiliary clearance of the vasoactive sulfi-dopeptide leukotrienes, LTC4 and LTD4. Leukotriene involvement in systemic inflammation and trauma, experimental pulmonary injury, and clinical ARDS underscores the importance of normal parenchymal hepatic function in these settings. In addition to leukotrienes, Reutler et al found significant hepatic uptake of radiolabelled tumor necrosis factor. Acute hepatocellular injury causes endotoxin and recombinant tumor necrosis factor to have identical effects in greatly enhancing lethality following their administration. Prolonged circulation of these mediators owing to hepatocyte impairment may amplify pulmonary injury and multiple organ damage associated with other elements of the inflammatory response. In support of this, we found augmented mortality and amplication of neutrophilic alveolitis after endotoxemia if there was preexisting hepatocytic dysfunction. read only Continue Reading »

15 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Activated Hepatic Macrophages

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Activated Hepatic MacrophagesActivated Hepatic Macrophages: Endogenous Mediator Release
The pivotal role of the liver as a regulator of systemic host defenses affecting sepsis-induced acute pulmonary injury with multiple systems organ failure is not limited to its “import” or passive filtering function. Macrophages are target cells for endotoxin, and the liver contains most fixed tissue macrophages in the body In addition, endotoxemia leads to further recruitment and activation of mononuclear phagocytes in the liver. Therefore, the liver is able to “export” an array of macrophage-derived endogenous mediators such as tumor necrosis factor/cachectin, interleukin-1, products of arachidonic acid metabolism, and platelet-activating factor (Fig 1). These monokines mediate most acute pathophysiologic reactions formerly attributed to endotoxin, including fever, hypotension, neutrophilia, neutropenia, thrombocytopenia, disseminated intravascular coagulation, inflammatory cell activation, and systemic immune and metabolic changes. there Continue Reading »

14 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Hepatic dysfunction

In addition to gut factors, severe hepatic dysfunction can independently influence both the gut-liver axis of intestinal endotoxin control and clearance of phlogistic substances of systemic origin. A clinical sepsis syndrome may result, with associated tissue hypoxia and multiple organ failure. Acute, fulminant, or end-stage hepatic failure thus represents a paradigm of impaired host defense. Support for this thesis includes observations that patients with end-stage hepatic failure awaiting hepatic transplantation are at increased risk for severe nonresolving ARDS, and that enhanced predisposition for pulmonary and extrapul-monary organ injury occurs in models of hepatic reticuloendothelial system blockade and obstructive jaundice. Endogenous endotoxemia can occur in cirrhotic patients with less severe hepatic dysfunction. Portasystemic collaterals result in defective hepatic reticuloendothelial system phagocytosis of colloids, increasing the risk of “spillover.” Compromise of the vascular “filtering” function of the liver due to impaired Kupffer cell phagocytic defense may therefore adversely affect hemodynamic regulation, endothelial integrity, and multiple extrahepatic organ function during sepsis. this Continue Reading »

06 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Impact of the liver

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Impact of the liverSeveral anatomic factors account for the impact of the liver on control of systemic endotoxemia and bacteremia: (1) its strategic location immediately downstream from the large gastrointestinal (GI) reservoir of these substances; (2) the characteristics of the splanchnic circulation—receiving 25 percent of the cardiac output and comprising 20 to 25 percent of the systemic blood volume—which constitutes portal blood flow (approximately 75 percent of total hepatic blood flow); and (3) the extensively anastomosing sinusoidal microvasculature through which this volume must pass. Consequently ample opportunity exists for blood-cell contact and hepatic clearance prior to reentry of blood into the systemic circulation. An intact GI mucosal barrier prevents significant entry of intestinal endotoxin into the portal vein, but small amounts of endotoxin and, occasionally, bacteria gain access to portal blood; however, the in-series intestinal barrier and efficient Kupffer cell uptake of these substances in portal blood normally constitutes an effective first line of defense in host control of systemic endotoxemia and bacteremia. there Continue Reading »

05 Feb

Organ Interactions in the Adult Respiratory Distress Syndrome during Sepsis: Control of Systemic Endotoxemia and Bacteremia

Control of Systemic Endotoxemia and Bacteremia: Role of Hepatic Mononuclear (Kupffer) Cells
Circulating Gram-negative bacterial endotoxin has been extensively implicated in the mediation of early pathogenetic events relevant to sepsis-induced ARDS with multiple systems organ failure. There are a variety of mechanisms, including direct cytotoxic effects of endotoxin on endothelial cells, induction of endothelial cell surface factors that promote neutrophil adherence, activation of phagocytes, “priming” of phagocytes by endotoxin to become hyperactivated in response to other stimuli, and triggering of the complement, kinin, and coagulation protein cascades which synergistically alter endothelial cell metabolic function and structural integrity. Continue Reading »

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