Books on the topic 'Genome damage'
To see the other types of publications on this topic, follow the link: Genome damage.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 34 books for your research on the topic 'Genome damage.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Aging of the genome: The dual role of the DNA in life and death. Oxford ; New York: Oxford University Press, 2007.
Find full text
2
Yosef, Shiloh, and SpringerLink (Online service), eds. The DNA Damage Response: Implications on Cancer Formation and Treatment. Dordrecht: Springer Netherlands, 2009.
Find full text
3
Genes and the environment. London: Taylor & Francis, 1999.
Find full text
4
Achary, V. Mohan Murali, Anca Macovei, Kaoru Okamoto Yoshiyama, and Ayako N. Sakamoto, eds. Maintenance of Genome Integrity: DNA Damage Sensing, Signaling, Repair and Replication in Plants. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-820-7.
Full text
5
Vijg, Jan. Aging of the Genome: The Dual Role of DNA in Life and Death. Oxford University Press, USA, 2007.
Find full text
6
Vijg, Jan. Aging of the Genome: The Dual Role of DNA in Life and Death. Oxford University Press, USA, 2007.
Find full text
7
Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Pathophysiological changes of ageing and their relevance to anaesthesia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0002.
Full textAbstract:
The molecular basis of ageing is reviewed. This includes the concept of a summation of DNA damage over a lifetime causing genome instability. Epigenetic alterations, telomeric shortening, and the possibility of their modification are discussed. Oxidative and mitochondrial DNA damage and the resulting dysfunction leading to senescence are briefly described. Systemic problems and resultant behavioural adaptation may mask the decline in functional reserve and cause some of the difficulties in identifying its presence in ill elderly patients. Specific organ system changes are then described in some detail. These include the major concerns with the cardiovascular, respiratory, renal, hepatic, neurologic, endocrine, and musculoskeletal systems. The effect of ageing on the special senses of vision and hearing are covered, with emphasis on issues of informed consent.
8
Clement, Jan, and Piet Maes. Hantaviral infections. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0188_update_001.
Full textAbstract:
Hantavirus disease is a viral zoonosis, caused by inhalation of infectious aerosolized excreta from chronically infected rodents, which are both the reservoir and the vector of different hantavirus species. Hantavirus infections manifest mainly as haemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome, which traditionally but incorrectly were thought to be caused by exclusively Old World hantaviruses and New World hantaviruses, respectively.Hantavirus diseases are characterized by non-specific flu-like symptoms, followed by a sometimes lethal capillary leak syndrome, haemorrhage, and rarely by shock. Infection is accompanied by augmented release of pro-inflammatory cytokines which indirectly causes organ damage. Diagnosis can be made by serology or plaque reduction neutralization tests, detection of viral proteins by Western blot assay, or detection of hantavirus genome by reverse transcription-polymerase chain reaction. Treatment is mainly supportive.Together with leptospirosis, haemorrhagic fever with renal syndrome is the only form of acute kidney injury against which vaccines are in use, but a World Health Organization-licensed vaccine is still lacking.
9
Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.
Full textAbstract:
It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
10
Catherine, Rice-Evans, and Burdon R. H, eds. Free radical damage and its control. Amsterdam: Elsevier, 1994.
Find full text
11
Emery, Roger. Disorders of the scapula. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.004012.
Full textAbstract:
♦ Sprengel’s deformity causes a high riding, fixed, hypoplastic scapula♦ Sprengel’s deformity may be associated with Klippel Fiel syndrome♦ Winging of the scapula can be caused by trapezius palsy or serratus anterior palsy♦ Trapezius palsy is usually due to damage to the spinal accessory nerve♦ Serratus palsy is usually caused by damage to the long thoracic nerve♦ Fascio-scapulo-humeral dystrophy presents with loss of scapula control from the late teens to the late twenties♦ FSHD is autosomal dominant and linked to alteration of the 4q35 gene.
12
Fox, Susan H. Seizures and Shakes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0017.
Full textAbstract:
Wilson’s disease is an autosomal recessive, treatable heredodegenerative disorder characterized by excessive deposition of copper in the liver, brain, and other tissues including the kidneys, pancreas, and joints. Early recognition of the disorder, which can present with a variety of movement disorders and neuropsychiatric phenomena, is critical to avoid irreversible end organ damage through the initiation of copper chelating agents. Diagnosis relies first on demonstrating evidence of brain iron deposition on magnetic resonance imaging of brain and elevated urinary copper excretion in the appropriate clinical context. Genetic testing for mutations in the ATP7B gene will identify a mutation in up to 90% of cases.
13
New Research on Genomic Instability. Nova Biomedical Books, 2007.
Find full text
14
Seyfried, Thomas N., and Laura M. Shelton. Metabolism-Based Treatments to Counter Cancer. Edited by Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0012.
Full textAbstract:
Accumulating evidence indicates that cancer is a type of mitochondrial metabolic disease. Chronic damage to mitochondria causes a gradual shift in cellular energy metabolism from respiration to fermentation. Consequently, fermentable metabolites become the drivers of cancer. Mitochondrial injury can explain the long-standing “oncogenic paradox,” and all major hallmarks of cancer including genomic instability. Restriction of fermentable fuels therefore becomes a viable therapeutic strategy for cancer management. The ketogenic diet (KD) is a metabolic therapy that lowers blood glucose and elevates blood ketone bodies. Ketone bodies are a “super fuel” for functional mitochondria, but cannot be metabolized efficiently by tumor mitochondria. The efficacy of KDs for cancer management can be enhanced when used together with drugs and procedures (such as hyperbaric oxygen therapy) (that further target fermentation. Therapeutic ketosis can represent an alternative, nontoxic strategy for managing and preventing a broad range of cancers while reducing healthcare costs.
15
Klein, Thomas, Ivo Ritzer, and Peter W. Schulze, eds. Crossing Frontiers. Schüren Verlag, 2012. http://dx.doi.org/10.5771/9783741000195.
Full textAbstract:
Der Band untersucht das Western-Genre erstmals eingehend in seinen komplexen und vielschichtigen interkulturellen Auffächerungen, die sich in nationalspezifischen Western-Variationen finden. Er eröffnet interessante Perspektiven auf diesen film- und kulturgeschichtlich kaum erschlossenen Bereich. Ein Schwerpunkt gilt den verschiedenen nationalen Western-Varianten in Osteuropa. Beiträge von Spezialisten aus Polen und Russland arbeiten bislang unbekannte Übereinstimmungen und Differenzen im Gebrauch des Genres in den damals kommunistischen Ländern zu Tage.
16
Rees, David. Haemoglobinopathies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0172.
Full textAbstract:
Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
17
Rees, David. Haemoglobinopathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0172_update_001.
Full textAbstract:
Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
18
Storey, Elsdon. Ataxias. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0007.
Full textAbstract:
This chapter explores the historical development of understanding about the structure, function, and disorders of the cerebellum. The chosen papers represent the following development: the discovery that the cerebellum is concerned with movement control rather than movement generation; the first recognition of a distinct spinocerebellar disorder; recognition of the existence of dominantly-inherited ataxias; the delineation of the classic motor features of ataxia; the formal recognition of paraneoplastic cerebellar degenerations; the description of truncal ataxia due to anterior vermal damage in chronic alcoholics; the demonstration of long-term depression at the parallel fibre; the discovery of the first gene (ATXN 1) for a dominantly-inherited spinocerebellar ataxia; the revelation that episodic ataxia type 2 is an ion channel disorder; and the recognition of a cerebellar role in cognition and emotional regulation.
19
Giacca, Mauro, and Borja Ibáñez. Advanced therapies to treat cardiovascular diseases: controversies and perspectives. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0028.
Full textAbstract:
There is a pressing need to develop novel therapies for myocardial infarction and heart failure, two conditions that affect over 20% of the world population. Despite important advances in achieving revascularization of the ischaemic myocardium and the usefulness of devices in assisting failing hearts, therapy for these conditions remains poor. The final extent of myocardial tissue loss after infarction is a major determinant of post-infarction mortality due to heart failure. In this chapter we review the current strategies aimed at counteracting injury due to acute myocardial ischaemia–reperfusion and the experimental approaches to achieve cardiac and vascular regeneration once damage has occurred. We critically discuss the possibility of inducing tissue restoration by gene transfer or exogenous cell implantation, and report on the exciting possibility of stimulating the endogenous capacity of cardiac regeneration using growth factors and small regulatory RNAs.
20
Canli, Turhan. Molecular Psychology. Edited by Turhan Canli. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.18.
Full textAbstract:
Molecular psychology is the study of behavior and its underlying brain systems using the tools of molecular biology. Although a variety of biological tools have been used to discover the relation of brain and behavior since the beginning of psychology, these have largely been confined to nonhuman animal models or brain-damaged patients. Technical advances in the past two decades in molecular genetics and in noninvasive brain imaging have transformed the field. These advances made it possible to conduct detailed examinations—across all species and subjects including healthy human volunteers—of the relation among genes, brains, and behavior; gene-by-environment (G×E) interactions; and the underlying regulatory mechanisms of gene expression through life experience and other environmental variables. This chapter provides a brief history of the major milestones of this field, along with updates from the contemporary literature, and introduces the reader to the contents of this volume.
21
Gonzalez-Albarrán, Olga, and Luis M. Ruilope. The kidney and control of blood pressure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0210.
Full textAbstract:
The kidneys can be at the root of the development of arterial hypertension or they can participate in the maintenance of hypertension and its sequels. Renal alterations interfering with the regulation of sodium homeostasis or facilitating the generation of vasoconstrictors, particularly angiotensin II, are involved in the dysregulation of arterial blood pressure that underlies the development of arterial hypertension. The biology of angiotensin is described in detail.The kidneys are also the mediator of hypertension in such examples as renal ischaemia and hyperaldosteronism. The role of renal nerves, and renal depressor substances, are also described.Transplantation experiments in animals and observations in human transplantation, as well as some primary gene defects, show the importance of renal mechanisms in hypertension. Once kidneys have been damaged, they often contribute to an increase in arterial pressure. Salt sensitivity is probably a major part of the mechanism, but it is mediated by multiple pathways.
22
Levtchenko, Elena N., and Mirian C. Janssen. Cystinosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0339_update_001.
Full textAbstract:
Cystinosis is a rare autosomal recessive disease caused by mutations in the lysosomal cystine transporter cystinosin encoded by the CTNS gene (17p.13.2). Cystinosis is characterized by lysosomal cystine accumulation throughout the body with renal Fanconi syndrome being the most common presenting symptom of a multisystem disorder. It must be distinguished from cystinuria in which formation of cystine stones is the core problem. When left untreated, kidney dysfunction gradually progresses towards end-stage renal failure during the first 10 years of life. The advent of renal replacement therapy allowed cystinosis patients to survive into adulthood, but revealed numerous extrarenal manifestations of the disease, affecting eyes, endocrine organs, gastrointestinal tract, muscles, and central and peripheral nervous systems. The disease mechanism of cystinosis is not fully understood. The administration of the cystine-depleting agent cysteamine slows down renal and extrarenal organ damage, pointing to the pivotal role of cystine accumulation in the disease pathogenesis. Treatment with cysteamine should be initiated as early as possible and continued lifelong, and also after kidney transplantation for protecting extrarenal organs. Cysteamine eye drops are an indispensable part of the treatment of corneal cystine accumulation. Life expectancy of cystinosis patients has substantially improved and is now above 50 years.
23
Deegan, Patrick. Porphyria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0179.
Full textAbstract:
This chapter discusses six diseases caused by inborn errors of metabolism affecting the biosynthesis of haem. Haem is a tetracyclic metal-binding compound involved in oxygen transport (in haemoglobin and myoglobin) and redox reactions (e.g. in the cytochrome P450 system). Each of these conditions is caused by a single gene defect in one of the enzymes involved in the biosynthesis of haem. Inheritance is usually autosomal dominant with incomplete penetrance. The enzyme defect results in disease, not as a result of deficiency of the reaction product, but as a result of accumulation of precursors. Early, soluble precursors, 5-aminolaevulinic acid, and porphobilinogen (not porphyrins as such) are neurotoxic and, when present in great excess, as occurs when flux through the haem synthetic pathway is increased in response to particular medications or hormones, lead to acute neurovisceral crises. Later cyclical precursors (porphyrins) in the pathway are also water soluble and excreted in urine, but are susceptible to activation by electromagnetic radiation in the visible spectrum and are converted to free-radical metabolites that cause pain, inflammation, and tissue damage in the skin. The final haem precursors (also porphyrins) are hydrophobic and excreted in the bile and faeces and are also activated by light to toxic metabolites.
24
Tandon, Teena, and Rajiv Agarwal. Hypertension as a cause of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0100.
Full textAbstract:
There is a strong association between hypertension and progressive renal disease, and it has long been assumed that a variable but often large proportion of end-stage renal disease is caused by essential hypertension damaging the kidney. While it is clear that malignant hypertension can cause renal damage, several lines of evidence cast doubt on the idea that more moderate blood pressures are commonly a primary cause of renal disease. These include (a) observational studies showing that microalbuminuria precedes hypertension; (b) morphological studies in animals and man suggest that changes traditionally described as due to hypertension correlate poorly with blood pressure; and (c) mutations in or near the APOL1 gene appear to underlie the development of renal disease in many black Americans previously labeled as suffering from hypertensive renal disease. The same mutations strongly predispose to focal segmental glomerulosclerosis. The mechanism of the association with ‘hypertensive’ renal disease is not established but it may act as a risk factor for progression of renal disease. Hypertension is associated with reduced renal mass. It is described as a consequence of renal cysts, simple as well as multiple. Obesity may be associated with accumulation of fat in the renal sinus and with hypertension.
25
Gagliano, Marco da. Madrigals, Part 6. Edited by Edmond Strainchamps. A-R Editions, 2021. http://dx.doi.org/10.31022/b223.
Full textAbstract:
Il sesto libro de madrigali a cinque voci, Marco da Gagliano's final book in the genre, was published in 1617, nine years after its predecessor. In the book's dedication Gagliano indicated that its music was composed the year before, and not earlier in the gap between the two books. Book 6 was popular enough that it was reprinted in 1620, and although he lived another twenty-six years, Gagliano published no more madrigals. There are sixteen compositions in the book, fourteen of them by Gagliano, one by Lodovico Arrighetti, and one by an unnamed composer who was most certainly Ferdinando Gonzaga, duke of Mantua. The poets now recognized as authors of the texts are Giovanni Battista Guarini, Torquato Tasso, Francesco Petrarca, Ottavio Rinuccini, Gabriello Chiabrera, Gasparo Murtola, and Antonio Ongaro. In the diversity of their style, the madrigals of the Sesto libro provide a conspectus of the compositional craft evinced in Gagliano's earlier books: now the rush and brevity of canzonetta-influenced madrigals like those in the fourth and fifth books stand next to madrigals with the more traditional manner of text setting so often found in his first three books. There is also a drinking song that alternates duets with a refrain and a seven-voiced concertato piece, both taken from Medici court entertainments. One of the most telling madrigals in the book, “Filli, mentre ti bacio,” is an abbreviation and a recasting of the madrigal as it appears in his Primo libro, thereby disclosing the remarkable change in Gagliano's aesthetic thinking about the genre during the fifteen years that lie between his first and last books. Shortly after the appearance of the Sesto libro, a vicious attack on its madrigals and on Gagliano himself was made by Mutio Effrem. Although its condemnation of the book on theoretical grounds is misguided and without merit, Effrem's Censure seems to have damaged Gagliano's standing in Florence and to some degree may have influenced his decision to abandon the genre.
26
Richards, Rashna Wadia. Cinematic TV. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190071257.001.0001.
Full textAbstract:
In the last two decades, media scholars have often suggested that television has become cinematic. Once considered “a mere instrument of transmission,” as Rudolf Arnheim put it, or derided as a vast wasteland, TV is now praised for its visual density and complexity. Serial dramas, in particular, are acclaimed for their imitations of cinema’s stylistically innovative and narratively challenging conventions. But what exactly does “cinematic TV” mean? Cinematic TV takes up this question comprehensively, arguing that TV dramas quote, copy, and appropriate (primarily) American cinema in multiple ways and toward multiple ends. Putting together an innovative framework by combining intertextuality and memory studies, Cinematic TV focuses on four modalities of intermedial borrowings: homage, evocation, genre, and parody. Through close readings of such exemplary shows as Stranger Things, Mad Men, Damages, and Dear White People, the book demonstrates how serial dramas reproduce and rework, undermine and idolize, and, in some cases, compete with and outdo cinema. Ultimately, Cinematic TV argues that serial dramas function archivally in relation to cinema, for cinematic moments, motifs, and contours hover around the televisual frame, constantly breaking through. How serial dramas handle such cinematic hauntings is the story that this book tells.
27
Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
Full textAbstract:
Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
28
Naicker, Saraladevi, and Graham Paget. HIV and renal disease. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0187_update_001.
Full textAbstract:
The human immunodeficiency virus (HIV) infection epidemic has particularly affected the poorest regions of the world. HIV can directly or indirectly affect different aspects of renal function, and results in a variable expression of kidney disease.Acute kidney injury (AKI) occurs in approximately 20% of hospitalized patients. The prevalence of chronic kidney disease (CKD) amongst HIV-infected patients is reported at 3.5–38% in different regions of the world. The complex interplay between the pheno- and/or genotypic variants of the virus, the genetic make-up of the host, and environmental factors determine the clinical manifestations of renal disease. The association of APOL1 gene variants G1 and G2 with the risk of focal segmental glomerulosclerosis explains the high frequency of HIV-associated nephropathy (HIVAN) in populations of black ethnicity.Anti-retroviral therapy (ART) is effective in preventing progression of HIVAN. Some of the drugs used in ART regimens are potentially nephrotoxic and require dose adjustment or even avoidance in CKD. Progression to end-stage renal disease (ESRD) in HIVAN has been reported to correlate with the extent of chronic damage quantified by renal biopsy.HIV-infected patients requiring dialysis, who are stable on ART, are achieving survival rates comparable to those of non-HIV dialysis populations. Similarly, HIV infection does not seem to adversely affect patient and graft survival rates after kidney transplantation, and there has been no increase in the prevalence of opportunistic infections in transplant recipients on effective ART.
29
Achenbach, Bernd, ed. »Euer Konzipient war ein sinnreicher Kopf«. Wallstein Verlag, 2021. http://dx.doi.org/10.5771/9783835346062.
Full textAbstract:
Der beste Kenner der Druckgeschichte von Lichtenbergs Werken und findige Interpret rätselhafter Wendungen legt hier die Quintessenz eines Forscherlebens vor. Dass Juristen mit ihrer strengen deduktiven Methode oft die besseren Literaturhistoriker sind, besonders, wenn ihre Findigkeit als Sammler noch ihre genaue Recherche bestimmt, hatte schon der Dr.jur. Otto Deneke in der ersten Hälfte des 20. Jahrhunderts mit seinen zahlreichen Lichtenberg-Aufsätzen bewiesen. Als der Richter am Landessozialgericht Bernd Achenbach 1976 zum ersten Mal seine damals noch kleine Lichtenberg-Sammlung in der Stadtbibliothek Duisburg öffentlich vorzeigte, wird er schwerlich geahnt haben, dass er alsbald der beste Kenner der Druckgeschichte von Lichtenbergs Werken werden - und wie viele Funde und Entdeckungen er in den folgenden 45 Jahren aus seiner Sammlung noch ziehen würde. Sie alle haben unsere Kenntnis von Lichtenbergs Leben, Werk, Edition und Wirkung beachtlich erweitert, zahlreiche uralte Irrtümer sind seither damit ausgeräumt, offene Probleme gelöst - und zahlreiche neue Fragen, an denen frühere Leser achtlos vorbeigegangen waren, nun endlich gestellt und dann auch zumeist beantwortet. Hier sind die wichtigsten aus den ca. 100 Aufsätzen, Miszellen und Rezensionen, die an ihren ersten Publikationsorten schier unauffindbar geworden sind, als Summe einer mehr als fünfzigjährigen Beschäftigung mit dem Göttinger Gelehrten und Schriftsteller versammelt.
30
Roddy, Edward, and Michael Doherty. Calcium pyrophosphate crystal deposition (CPPD). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0142.
Full textAbstract:
Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β (IL-1β)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β blockade is much needed.
31
Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.
Full textAbstract:
Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
32
Die Flucht nach Ägypten: Königlich böhmischer Teil. Das ist, wahrhaftige und genaue Beschreibung sämtlicher Vorfälle, Zufälle und Ereignisse wie auch mehrerer Wunder, welche sich damals bei Durchzug der bethlehemitischen Wandersleute im Königreich Böhmen begeben haben, teils Amts-, teils Zivilpersonen betreffend sowie auch Tiere. Geschätztem Leser zu erbaulicher Unterhaltung. Thienemann Verlag, 1998.
Find full text
33
Haymann, Jean-Philippe, and Francois Lionnet. The patient with sickle cell anaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.
Full textAbstract:
In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an increased effective plasma renal flow and glomerular filtration rate, glomerular hypertrophy, and damaged vasa recta system leading to albuminuria and impaired urinary concentration.Early onset of hyperfiltration occurs in 60% of SCA patients often associated with microalbuminuria. SCAN risk factors are still under investigation, but may be related to chronic haemolysis at an early time point. Other lesions in patients with sickle cell anaemia include papillary necrosis, and recurrent acute kidney injury in association with crises or infections.ACEI are recommended if there is proteinuria. There is no current agreement on whether angiotensin-converting enzyme inhibitors (ACEI) should be introduced earlier, but systematic screening for microalbuminuria and hypertension, and avoidance of nephrotoxic agents are strongly advised.Patients with sickle cell trait (carriers for sickle cell anaemia) are prone to microscopic haematuria and abnormalities of the vasa recta have been described. A very rare tumour, renal medullary carcinoma, is largely restricted to this group (in whom it is still extremely rare). Increased risk of other renal problems is still largely hypothetical rather than proven.The prevalence of nephropathies in other sickle cell diseases (in particular haemoglobin SC disease) is much lower.
34
Biodefence Mechanisms Against Environmental Stress. SPRINGER-VERLAG, 1998.
Find full text