Books: 'Biological disturbance'

1

Menstrual disorders and menopause: Biological, psychological, and cultural research. New York: Praeger, 1985.

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2

Beever, Erik A., Suzanne Prange, and Dominick A. DellaSala, eds. Disturbance Ecology and Biological Diversity. CRC Press, 2019. http://dx.doi.org/10.1201/9780429095146.

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3

A, Mansfield T., Goulding K. W. T, Sheppard L. J, and New Phytologist Symposium (3rd : 1997 Sept. 3-5 : University of Lancaster), eds. Major biological issues resulting from anthropogenic disturbance of the nitrogen cycle. Cambridge, [England]: Cambridge University Press, 1998.

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4

Defense, Department of. 21st Century Essential NBC Reference Series: National Guard Civil Disturbance Handbook (Bioterrorism, Nuclear, Biological, Chemical, Radiation and Radiological ... Destruction WMD, First Responder Ringbound). Progressive Management, 2004.

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5

Subramaniam, Banu, ed. My Experiments with Truth. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252038655.003.0006.

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This chapter focuses on biological invasions and presents one example of how we can experiment with an interdisciplinary repertoire of research questions, methods, and epistemologies to produce knowledge about the biological world—in short, an experiment about experimenting. The experiment under discussion is a collaborative project based in Southern California, where human-made disturbance has a very long and destructive history. Here, arbuscular mycorrhizal (AM) fungi and their role in plant ecology are observed within the environmental contexts of growth, especially the soil communities of plants. Mycorrhizal fungi and their relationship with native and exotic plant species offer a great context for a science/science studies project, and this work on fungi that were in “mutualistic” relationships also challenged the role of competition as the critical driver of ecology and evolution of plants.

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6

Weiner, Stephen, and Susanne Petermann. Stephen Weiner, Patient in the Mental Health System. Edited by John Z. Sadler, K. W. M. Fulford, and Cornelius Werendly van Staden. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780198732365.013.4.

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Excerpts from an interview with Stephen Weiner, who recounts his experience in the mental health care system from being told he had an emotional disturbance as a child (1957–1958) to his work with a psychiatrist on strengthening his more rational self. As a child, he was not given a diagnosis, making it difficult to know how “objectively” to evaluate his condition. Probably little was known about the phenomenology of derealization and solipsism then. After college he decided to seek treatment for his growing depression and alcohol abuse under a method known as Rolfing. He describes his skepticism toward psychiatrists and allied professionals unwilling to explain the scientific basis of their treatment. He suggests that the switch to the biological model of mental illness, while mostly good, brought about new difficulties for patients. After seeing three different doctors, Weiner settled with a psychiatrist who offered relief and palliative care.

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7

Haunton, Victoria, Aung Sett, Amit Mistri, and Martin Fotherby. Stroke. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0227.

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The World Health Organization defines stroke as ‘a clinical syndrome consisting of rapidly developing clinical signs of focal (at times global) disturbance of cerebral function lasting greater than 24 hours (or leading to death) with no apparent cause other than that of vascular origin’. Transient ischaemic attack (TIA) is defined as a rapid presentation of neurological deficit with complete recovery within 24 hours of the onset of symptoms. However, the 24-hour cut-off is arbitrary, has no biological basis, and is of limited use clinically. A shorter duration is now regarded as more appropriate, although it has yet to be universally accepted. In clinical practice, stroke and TIA are best thought of as comprising a continuum, as they have similar pathological mechanisms, etiologies, and management strategies. While subarachnoid haemorrhage is a type of stroke based on the above definition, it is not covered in this chapter, as its pathophysiology, clinical manifestations, and management are distinct from those for ischaemic stroke and haemorrhagic stroke.

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8

Veste, Maik, Vincent John Martin Noah Linus Felde, Steven D. Warren, and Nicole Pietrasiak, eds. Ecological Development and Functioning of Biological Soil Crusts After Natural and Human Disturbances. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-255-7.

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9

Holliday, Kate L., Wendy Thomson, and John McBeth. Genetics of chronic musculoskeletal pain. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0045.

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Chronic pain disorders are prevalent and a large burden on health care resources. Around 10% of the general population report chronic widespread pain, which is the defining feature of fibromyalgia. Fibromyalgia is a poorly understood idiopathic disorder which is also characterized by widespread tenderness and commonly occurs with comorbid mood disorders, fatigue, sleep disturbance, and cognitive dysfunction. A role for genetics in chronic pain disorders has been identified by twin studies, with heritability estimates of around 50%. Susceptibility genes for chronic pain are likely to be involved in pain processing or the psychological component of these disorders. A number of genes have been implicated in influencing how pain is perceived due to mutations causing monogenic pain disorders or an insensitivity to pain from birth. The role of common variation, however, is less well known. The findings from human candidate gene studies of musculoskeletal pain to date are discussed. However, the scope of these studies has been relatively limited in comparison to other complex conditions. Identifying susceptibility loci will help to determine the biological mechanisms involved and potentially new therapeutic targets; however, this is a challenging research area due to the subjective nature of pain and heterogeneity in the phenotype. Using more quantitative phenotypes such as experimental pain measures may prove to be a more fruitful strategy to identify susceptibility loci. Findings from these studies and other potential approaches are discussed.

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10

Holliday, Kate L., Wendy Thomson, John McBeth, and Nisha Nair. Genetics of chronic musculoskeletal pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0045_update_001.

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Chronic pain disorders are prevalent and a large burden on health care resources. Around 10% of the general population report chronic widespread pain, which is the defining feature of fibromyalgia. Fibromyalgia is a poorly understood idiopathic disorder which is also characterized by widespread tenderness and commonly occurs with comorbid mood disorders, fatigue, sleep disturbance, and cognitive dysfunction. A role for genetics in chronic pain disorders has been identified by twin studies, with heritability estimates of around 50%. Susceptibility genes for chronic pain are likely to be involved in pain processing or the psychological component of these disorders. A number of genes have been implicated in influencing how pain is perceived due to mutations causing monogenic pain disorders or an insensitivity to pain from birth. The role of common variation, however, is less well known. The findings from human candidate gene studies of musculoskeletal pain to date are discussed. However, the scope of these studies has been relatively limited in comparison to other complex conditions. Identifying susceptibility loci will help to determine the biological mechanisms involved and potentially new therapeutic targets; however, this is a challenging research area due to the subjective nature of pain and heterogeneity in the phenotype. Using more quantitative phenotypes such as experimental pain measures may prove to be a more fruitful strategy to identify susceptibility loci. Findings from these studies and other potential approaches are discussed.

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11

Jacobsen, Dean, and Olivier Dangles. A growing human footprint in the highlands. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198736868.003.0009.

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Chapter 9 reviews the threats imposed by human activities to aquatic life at high altitude. High altitude regions of the inter-tropical belt are generally much more densely populated than their temperate counterparts. Therefore, they are directly affected by a number of human-related disturbances such as land use changes, water contamination, use and diversion, and the introduction of invasive species. The chapter details several unique environmental conditions of high altitude environments that make their aquatic biota particularly at risk in the face of anthropogenic disturbances. Among others, glaciers concentrate pollutants, low oxygen concentrations affect the response of aquatic fauna to stress, ultraviolet B modifies the bioavailability of contaminants, high primary productivity of grasslands encourages cattle ranching and fuels fires over large scales, and isolated watersheds favour species extinction following biological invasions.

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12

Schmahl, Christian, K. Luan Phan, and Robert O. Friedel, eds. Neurobiology of Personality Disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.001.0001.

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This book outlines the principles of neural science that mediate personality and describes what is currently known about how these biological processes are impaired in individuals with personality disorders. What sets this book apart from others is that it focuses particularly on the neurobiology of disturbed personality. Personality disorders have a high prevalence, and these disorders cause a substantial amount of human suffering and harm, not only to the individuals and families directly affected but also to the population at large. Second, these disorders are known to have a heritability rate that is generally in excess of 50%, strongly suggesting that the behavioral disturbances caused by personality disorders have a significant biomedical etiology. However, with the exception of borderline personality disorder, little is known about the biological nature of personality and personality disorders and the effective treatment of the latter. The principles of the basic biological nature medical disorders have served well as the foundation in other disciplines in medicine and psychiatry but have received relatively little attention in the areas of personality, temperament, and personality disorders.

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13

Friedel, Robert O., Christian Schmahl, and Marijn Distel. The Neurobiological Basis of Borderline Personality Disorder. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0013.

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This chapter provides an overview of the biological underpinnings of borderline personality disorder (BPD). The total body of evidence indicates that BPD has a strong neurobiological basis. The material in this chapter is presented in five sections: one describing the structure of genetic and environmental risk factors for BPD and four describing our current knowledge about the anatomy and pathophysiology of symptom in each of the four domains of the disorder, that is, affective dysregulation, impulsive aggression, disturbances of perception and cognition, and interpersonal impairments. The chapter concludes with a discussion of the clinical, research, and educational implications of this information.

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14

The aliens among us: How invasive species are transforming the planet--and ourselves. Yale University Press, 2017.

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15

Peñagarikano, Olga, and Daniel H. Geschwind. CNTNAP2 and Autism Spectrum Disorders. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0016.

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Although autism was described in the early 1940s as a disorder of affective contact (Kanner, 1943), it was not classified as a neurodevelopmental disorder with a biological basis until the early 1980s, when studies reported its high heritability (Folstein & Rutter, 1977; Ritvo et al., 1985) and co-occurrence with chromosomal abnormalities (Gillberg & Wahlstrom, 1985; Wahlström et al., 1986). Today, autism is considered a heterogeneous neurodevelopmental syndrome and therefore termed autism spectrum disorder (ASD), characterized by variable deficits in social behavior and language, restrictive interests, and repetitive behaviors. Autism spectrum disorder has an estimated prevalence of 1:150–1:200 (Centers for Disease Control and Prevention, 2007), being one of the most common childhood disorders. In addition to the core domains necessary for diagnosis, a number of other behavioral abnormalities are frequently associated with ASD, including epilepsy, sensory abnormalities, hyperactivity, motor abnormalities, sleep disturbances, and gastrointestinal symptoms (Geschwind, 2009).

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16

Rigney, Gabrielle, Jason Isaacs, Shelly Weiss, Sarah Shea, and Penny Corkum. Sleep–Wake Disorders. Edited by Thomas H. Ollendick, Susan W. White, and Bradley A. White. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780190634841.013.25.

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Sleep is important for children’s physical, cognitive, and social functioning. The most common sleep disorder contributing to inadequate sleep and daytime impairments in pediatric populations is insomnia. There are both biological and behavioral factors that can contribute to insomnia; therefore, understanding sleep processes, how sleep changes throughout development, and which common behaviors influence sleep is important. Measurement of sleep through both objective and subjective measures plays an important role in the identification, diagnosis, and intervention of insomnia. First-line treatment for insomnia includes psychoeducation, healthy sleep practices, and behavioral and cognitive strategies. Children with special needs are at especially high risk for sleep problems, and treatment of insomnia in these populations should aim to minimize sleep disturbances without increasing other comorbid symptoms. Moving forward, healthcare professionals require access to more comprehensive education on pediatric sleep, and greater public awareness of the importance of sleep and health is needed.

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17

Singh, Harminder, Smeer Salam, and Theodore H. Schwartz. Endocrine Silent Pituitary Tumors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0016.

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Pituitary adenomas are the most common intracranial neoplasms in adults, with a prevalence of 7% to 17%. Clinically, they can be divided into 2 categories based on whether they secrete pituitary hormones: functional (secretory) and nonfunctional (nonsecretory or endocrine silent) adenomas. The biologic latency of nonfunctional (endocrine silent) adenomas makes them usually diagnosed at the stage of macro (>1 cm) and giant (>4 cm) adenomas. Because these tumors are nonfunctioning, their primary symptoms are due to mass effect, particularly on the optic chiasm and normal pituitary gland and stalk superiorly, and the cavernous sinus laterally. Visual field disturbance is the most common presenting complaint, followed by pituitary dysfunction and headaches. Surgical outcomes, therefore, are aimed at determining visual outcome in addition to rates of gross total resection, recurrence, and postoperative pituitary dysfunction. Several recent case series have documented the increased success of the endonasal endoscopic transsphenoidal approach for resecting nonfunctioning pituitary adenomas, particularly in relation to the classic open cranial and microsurgical transsphenoidal techniques.

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18

Tombetti, Enrico, and Justin C. Mason. Pathophysiology of vasculitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0017.

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Vasculitis represents a spectrum of disorders that are often divided on the basis of the predominant vessel size affected into large-, medium- and small-vessel vasculitides. This chapter will focus on the pathogenesis of the anti-neutrophil cytoplasmic antibody (ANCA)-associated medium- and small-vessel vasculitides (AAV), and large-vessel vasculitis, Takayasu arteritis, and giant cell arteritis. Underlying pathogenic mechanisms in vasculitis remain to be fully understood. In particular, the initiating event(s) are not known. A combination of infectious or other environmental triggers on a susceptible genetic background is currently favoured. In addition to the vessel size affected, the mechanisms of vascular injury vary. Moreover, extravascular granulomatosis may play an important role in disease manifestations. The innate and adaptive immune systems contribute to its pathogenesis. Although pathogenic antibodies have not been identified in large-vessel vasculitis, ANCA are directly implicated in small- and medium-vessel AAV. Disease manifestations are varied and diverse and may include arterial stenosis or aneurysms, glomerulonephritis and renal failure, gastro-intestinal, pulmonary, cutaneous, and neurological complications, visual disturbance, deafness, and nasal bridge collapse. Life-threatening cardiovascular disease is also seen, with myocarditis, pericarditis, valvular heart disease, thrombosis, systemic and pulmonary arterial hypertension, and accelerated coronary heart disease all reported. Despite this, the prognosis for patients with vasculitis has improved significantly in recent decades. Further understanding of the pathogenesis of vasculitis will lead to the discovery of further therapeutic targets and novel, safer biologic therapies.

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Books on the topic 'Biological disturbance'

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