Books on the topic 'RPE in-Cell'

Like any realignment in politics, the Democratic takeover of Congress in the 2006 midterm elections inspired a raft of instant analyses. One take on the results that is surely wrong is that the change in control of Congress and the spike in Democratic hopes for the 2008 presidential race mark an end to the culture wars that conventional wisdom blamed (or credited) for George W. Bush's re-election in 2004. This book sets the stage for a new consideration of the contemporary culture wars by examining their antecedents—from the Scopes trial to Prohibition to the controversy over the Supreme Court's desegregation and school-prayer rulings to loyalty-oath battles of the 1950s to the pre- Roe v. Wade campaign to liberalize abortion laws. Even during times of supposed conformism, Americans have been presented with competing claims about what sort of culture this is and how and to what extent government should reflect, and police, values. The author covers such topics as same-sex marriage, stem cell research, intelligent design, and other hot button issues that are debated not just between the religious and secular, but more and more among the ranks of the religious themselves, where a religious left has emerged to counter arguments from the religious right. Anyone interested in the intersection of religion and politics, in the rise of the so-called moral majority, and in the current state of affairs with regard to values and public life in America will gain a better understanding from reading this book.

This introductory chapter offers a brief definition of entanglement and contrasts it with four other versions of the relationship between religion and secularity. Unlike these other four models, in which religion and secularity sit apart from each other as separate domains, entanglement presents a contentious but oddly intimate relationship. Neither side simply wins by displacing the other. Two examples flesh out this definition of entangled religious and secular interests. The first example comes from the so-called War on Christmas; the second comes from controversies surrounding stem cell research. In both of these cases, religious and secular elements entangle and complicate each other, even as they engage in adversarial conversation. The introduction then examines recent scholarly re-evaluations of the term “secularity” and connects it with the concept of entanglement.

The regulatory evolution of medical technologies in the EU offers a unique perspective with regard to highlighting significant elements of both European science policy and the development of European institutions, especially with regard to the passage from their (primarily) economic to their political phases. Since the early 1990s, while establishing a market for biotechnology, the European Communities have been developing some policy-related visions of technoscience and its potential risks, while at the same time framing the concept of European citizenship through European values and rights. The emerging and re-emerging medical technology of xenotransplantation, namely the clinical use of cells, tissues, and organs between species, while having evolved from its primary focus on organs to so-called advanced therapies (cell therapy, gene therapy, and tissue-engineered products), also provided an opportunity to test and implement different science policy models in dealing with risks and uncertainties in the European knowledge-based and innovation-oriented society.

Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.

One often hears stories of people in terrible and seemingly intractable situations who are preyed upon by individuals offering empty promises of help. Frequently these cases are condemned as “exploiting the hope” of another. These accusations are made in a range of contexts, including human smuggling, the beauty industry, and unproven medical interventions. This concept is meant to do heavy lifting in public discourse, identifying a specific form of unethical conduct. However, it is poorly understood what is meant to be wrong by the accusation of exploiting hope, the range of activities that can accurately be captured under this concept, and what should be done about it. Thus, it is an ethical concept that is ripe for extended analysis and discussion. This book offers a close study of the concept of exploiting hope. First, it examines this concept in the abstract, including a close look at how this term is used in the popular press and individual examinations of the concepts of exploitation and hope. This theory-based section culminates in the author’s own account of what it is to exploit hope and when and why doing so is morally problematic. The second section of the book examines how hope for improved health from unproven medical interventions can be exploited. This includes exploitation of hope in the context of participants in clinical trials, purchasing unproven stem cell interventions, right to try legislation, and crowdfunding for unproven interventions.

Genitourinary tract diseases in the palliative care setting most commonly involve urinary tract obstruction, intractable bleeding, fistulae, and bladder-associated pain. Sources of obstruction in the lower urinary tract include benign prostatic hyperplasia, invasive prostate or bladder cancer, urethral stricture, or bladder neck contracture. Upper tract obstruction includes intraluminal or extraluminal blockage of the renal collecting system and ureters, such as transitional cell carcinoma, fibroepithelial polyps, stricture, stones, pelvic or retroperitoneal malignancy, fibrosis, or prior radiation. Untreated, obstructive uropathy leads to elevated bladder, ureter, and kidney pressures, bladder dysfunction, urolithiasis, renal failure, pyelonephritis, or urosepsis. Intractable haematuria can cause problematic anaemia, frequent transfusions, clot retention, haemorrhagic shock, and death. In addition, urinary tract fistulae such as vesicovaginal and vesicoenteric fistulae are common in patients who have had prior pelvic surgery or radiation especially in the setting of immunocompromise, poor nutrition, and infection. Untreated, these symptoms lead to rash, skin breakdown, ulcers, chronic infection, and sepsis. Lastly, pelvic and bladder pain, depending on aetiology can be treated with oral medications, intravesical therapies, or surgical therapies such as palliative resection or urinary diversion. Selection of tests and treatment modalities in the palliative care setting should be based on using the least invasive means to achieve the most relief in suffering. Some genitourinary conditions are potentially fatal, and in the acute or subacute setting, require re-evaluation of the end-of-life goals and wishes of the patient and family.

The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.

The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.

The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drug usage (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), such thrombotic microangiopathies as thrombotic thrombocytopenic purpura and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.

Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.