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1
Patel, Sunit Mohanlal. The effects of the inhibitory amino acid gamma-aminobutyric acid (GABA) on food intake in the rat. Portsmouth: University of Portsmouth, 2003.
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2
Hughes, Sarah Jane. Investigation into the mechanism by which relaxin inhibits tension development in the uterus of the non-pregnant rat. Manchester: University of Manchester, 1994.
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3
Cheung, Hermia. Effect of dopamine depletion on D1 receptor binding in rat brain; and metabolism studies of D1 agonist R-[11C]SKF 82957 and phosphodiesterase-4 inhibitor R-[11C}rolipram. Ottawa: National Library of Canada, 2003.
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4
Michaud, Dominique. Recombinant Protease Inhibitors in Plants (Biotechnology Intelligence Unit). R. G. Landes, 2000.
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5
Allaerts, W. Involvement of Folliculo-Stellate Cells in Inhibitory Interactions in Rat Anterior Pituitary. Leuven University Press, 1989.
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6
Smith, Kevin Robert. Characterization of a disulfonic stilbene inhibitor binding to human red cell membranes. 1986.
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7
Longman, Susan Dawn. Cardiovascular studies with angiotensin converting enzyme inhibitors in the rat: Effects of arterial blood pressure and plasma and tissue angiotensin converting enzyme (ACE) activity of acute and chronic administration of ACE inhibitors in sodium deficient normotensive (NT) rats. Bradford, 1986.
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8
The effect of bestatin, an aminopeptidase inhibitor, in reducing ethanol consumption in the rat: Mechanism of action and clinical significance. Ottawa: National Library of Canada, 1994.
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9
Gitz, Dennis Corbin. The effects of the PAL inhibitor AIP on phenolic expression, growth and development, and UV-B tolerance in red cabbage and in duckweed. 1996.
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10
Valgimigli, Marco, and Marco Angelillis. Treatment of non-ST elevation acute coronary syndromes. Edited by Stefan James. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0311.
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Treatment of patients presenting with a non-ST elevation acute coronary syndrome (NSTE-ACS) aims at immediate relief of ischaemia and the prevention of serious adverse events, including death, myocardial (re)infarction, and life-threatening arrhythmias. In NSTE-ACS, patient management is guided by risk stratification (troponin, electrocardiogram, risk scores, etc.). Treatment options include anti-ischaemic and antithrombotic drugs and coronary revascularization including percutaneous coronary interventions, or coronary artery bypass grafting. While long-term secondary prevention with aspirin monotherapy is currently the gold standard approach for all NSTE-ACS patients who tolerate the drug, additional medications on top of aspirin such as oral P2Y12 inhibitors or oral anticoagulation have been investigated across clinical trials and their long-term use should be guided by the ischaemic versus bleeding risk status of each single individual patient.
11
Studying the binding of phosphodiesterase-4 inhibitor R-[11C]rolipram in rat brain: Effects of glutamatergic modulation on various neurotransmitter systems and validation binding assays. Ottawa: National Library of Canada, 2003.
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12
Pirani, Tasneem, and Tony Rahman. Diagnosis and management of upper gastrointestinal haemorrhage in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0177.
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Upper gastrointestinal haemorrhage is a medical emergency that may present with haematemesis and/or melena. An exhaustive history and careful examination aids in identifying the cause of bleeding and directing appropriate management. Validated scoring systems exist to guide the urgency of endoscopic therapy, although these should not be used in isolation, but in conjunction with complete patient assessment. The initial priority should be to resuscitate and stabilize the patient using the airway, breathing, circulation, and disability framework. Resuscitation should be guided by clinical and physiological parameters. Patients should be managed in an environment where vital signs such as heart rate, blood pressure, respiratory rate, conscious level, and urine output are monitored at least hourly. Attempts should be made to correct coagulopathy. Specialist advice should be sought from haematologists for guidance on the most appropriate use of packed red cells and blood products. Over-transfusion should be avoided. Initiation of pre-endoscopy proton pump inhibitor therapy, in particular to avoid definitive endoscopic therapy, is not recommended. Diagnostic endoscopy and therapy should be conducted within 24 hours of presentation. Numerous endoscopic therapies exist—when epinephrine is used for local tamponade and vasoconstriction, application of dual modality treatment is recommended. In cases where endoscopic therapy fails or is not possible, radiological diagnosis, and embolization may become necessary. Occasionally, surgery is required for definitive treatment—close liaison with surgeons is therefore necessary, especially where initial endoscopy is considered suboptimal or re-bleeding occurs.
13
Sternbach, Marion. Apheresis in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0268.
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This chapter describes therapeutic plasma exchange, as well as cytapheresis for hyperleukocytosis and essential thrombocythemia, as well as harvesting haematological stem cells (HSC) for transplantation. Instrumentation and techniques are mostly density centrifugation, much less column adsorption for antibodies or membrane filtration for noxious molecules. Pathophysiology of apheresis is dealt with in great detail with emphasis on prevention and treatment of side effects, much more critical in the intensive care unit (ICU) setting. Main manifestations are: hypocalcaemia due to chelation by anticoagulants, hypo- and less hypervolaemia, allergic reactions to sedimenting and volume replacement starches or plasma, depletion of coagulation factors, vitamin K, immunoglobulins, lymphocytes with long lifespan and platelets. Wash-out of drugs for comorbid or underlying conditions occurs inadvertently. Main indications for plasma exchange are thrombotic thrombocytopenic purpura (TTP)/haemolytic uraemic syndrome (HUS) with plasma or cryo-poor supernatant (based on RCT), hyperviscosity syndromes, post-transfusion purpura (PTP) and auto-immune haemolytic anaemia (AIHA), where all other treatments have failed. In cold agglutinin disease, cryoglobulinaemia, coagulation factor inhibitors and ABO incompatible HSC transplants, plasmapheresis has proven useful. Myeloma with renal failure does not seem to benefit significantly from plasma exchange (randomized controlled trials proven).
14
F, Lüscher Thomas, ed. The endothelium in cardiovascular disease: Pathophysiology, clinical presentation, and pharmacotherapy. Berlin: Springer, 1995.
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15
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0070.
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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.
16
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_001.
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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.
17
Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_002.
Full textAbstract:
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.
18
Abhishek, Abhishek, and Michael Doherty. Treatment of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0052.
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The treatment of calcium pyrophosphate crystal deposition (CPPD) is mainly symptomatic. Acute calcium pyrophosphate (CPP) crystal synovitis should be treated with rest, local application of ice packs, joint aspiration, and/or intra-articular corticosteroid injection (once joint sepsis has been excluded). Oral colchicine or prednisolone may be used if joint aspiration and/or injection are not feasible. Anti-inflammatory agents (with proton pump inhibitors) may be used but in general these should be avoided as most patients with acute CPP crystal arthritis are elderly, and at a high risk of gastrointestinal and renal complication of non-steroidal anti-inflammatory drug (NSAIDs). Principles of management of CPPD with osteoarthritis (OA) are identical to those for isolated OA. However, patients may have more inflammatory signs and symptoms and periodic joint aspiration and corticosteroid injection may be required more often than in isolated OA. Oral NSAIDs (with gastro-protection), colchicine, low-dose corticosteroids, hydroxychloroquine, and radiosynovectomy have been suggested as options for the treatment of chronic CPP crystal arthritis. There is growing interest in use of anti-interleukin-1 agents for acute or chronic CPP crystal arthritis but the efficacy of these agents has not been formally studied, and their use should be considered on an individual basis.
19
McMahon, Chris G. Ejaculatory disorders. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0105.
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Ejaculatory/orgasmic disorders are common male sexual dysfunctions, and include premature ejaculation (PE), inhibited ejaculation, anejaculation, retrograde ejaculation, and anorgasmia.Premature ejaculation management is largely dependent upon aetiology. Life-long PE is best managed with PE pharmacotherapy (selective serotonin re-uptake inhibitor [SSRI] and/or topical anaesthetics). The management of acquired PE is aetiology-specific and may include erectile dysfunction (ED) pharmacotherapy in men with co-morbid ED. Behavioural therapy is indicated when psychogenic or relationship factors are present and is often best combined with PE pharmacotherapy in an integrated treatment programme. Delayed ejaculation, anejaculation, and/or anorgasmia may have a biogenic and/or psychogenic aetiology. Men with age-related penile hypoanesthesia should be educated, reassured, and instructed in revised sexual techniques which maximize arousal. No drugs have yet been approved by regulatory agencies for this purpose, and most drugs identified for potential use have limited efficacy, impart significant side effects, or are considered experimental in nature.
20
Luscher, Thomas F. The Endothelium in Cardiovascular Disease: Pathophysiology, Clinical Presentation and Pharmacotherapy. Springer-Verlag Telos, 1995.
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21
Lüscher, Thomas F. Endothelium in Cardiovascular Disease: Pathophysiology, Clinical Presentation and Pharmacotherapy. Springer London, Limited, 2011.
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22
Luscher, Thomas F. The Endothelium in Cardiovascular Disease: Pathophysiology, Clinical Presentation, and Pharmacology. Springer-Verlag, 1995.
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23
Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.
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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
24
AlJaroudi, Wael. Risk Assessment in Acute Coronary Syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0013.
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Acute coronary syndromes (ACS) include unstable angina pectoris (UAP), non-ST elevation (NSTEMI), and ST elevation acute myocardial infarction (STEMI). Each year, more than 2 million people are hospitalized with ACS in the United States. The initial treatment has evolved over the last few decades from conservative management to early reperfusion therapy. Medical therapy has also significantly changed with the use of newer more potent antiplatelet agents, beta-blockers, angiotensin converting enzyme inhibitors, statins, and anti-anginal drugs, which have resulted in improvement of patient care and survival. There is no role for stress myocardial perfusion imaging (MPI) in the acute presentation; however, rest MPI may be used to identify the culprit lesion and risk stratify patients if injected during chest pain. In stable patients for ACS, submaximal exercise or vasodilator MPI can be performed as early as 48 hours after the event. Several gated MPI-derived variables such as left ventricular (LV) ejection fraction (EF), LV volumes, infarct size, mechanical dyssynchrony, and residual ischemic burden can risk stratify patients and provide prognostic data incremental to validated clinical risk scores such as GRACE (Global Registry of Acute Coronary Syndrome) and TIMI (Thrombolysis in Myocardial Infarction). Patients with depressed LVEF, remodeled LV, and large perfusion defects are at particularly high- risk for subsequent cardiac death or recurrent myocardial infarction. In such setting, MPI plays a pivotal role in the management of patients and guiding therapeutic decisions. The current chapter will review the clinical and MPI predictors of outcomes in patients presenting with ACS according to updated guidelines and a proposed algorithm integrating the role of MPI in guiding therapeutic decisions and management.
25
Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
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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.
26
Macdougall, Iain C. Iron management in renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0126.
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Although erythropoiesis-stimulating agent therapy is the mainstay of renal anaemia management, maintenance of an adequate iron supply to the bone marrow is also pivotal in the process of erythropoiesis. Thus, it is important to be able to detect iron insufficiency, and to treat this appropriately. Iron deficiency may be absolute (when the total body iron stores are exhausted) or functional (when the total body iron stores are normal or increased, but there is an inability to release iron from the stores rapidly enough to provide a ready supply of iron to the bone marrow). Several markers of iron status have been tested, but those of the greatest utility are the serum ferritin, transferrin saturation, and percentage of hypochromic red cells. Measurement of serum hepcidin, which is the master regulator of iron homoeostasis, has to date proved disappointing as a means of detecting iron insufficiency, and none of the available iron markers reliably exclude the need for supplemental iron. Iron may be replaced by either the oral or the intravenous route. In the advanced stages of chronic kidney disease, however, hepcidin is upregulated, and this powerfully inhibits the absorption of iron from the gut. Thus, such patients often require intravenous iron, particularly those on dialysis. Several intravenous (IV) iron preparations are available, and they have in common a core containing an iron salt, surrounded by a carbohydrate shell. The IV iron preparations differ in their kinetics of iron release from the iron–carbohydrate complex. In recent times, several new IV iron preparations have become available, and these allow a greater amount of iron to be given more rapidly as a single administration, without the need for a test dose.
27
Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.
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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.