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(the medical term for gapping is diathesis) ..

Other methods Examples of other methods that have received recent attention and may find some more use in the future include: energy dispersive X-ray fluorescence (Holynska & Markowicz, 1977); differential pulse polarography (Bound & Forbes, 1978); anodic (Andrews & Johnson, 1976) or cathodic (Blades et al., 1976) stripping voltammetry; atomic fluorescence spectrometry (Thompson, 1975); gas-liquid chromatography (Ermakov, 1975; Poole et al., 1977); and spark source mass spectrometric isotope dilution (Paulsen, 1977).

Chest x-ray (CXR)-There are no pathognomonic radiographic finding for PH.

Define, correctly use, and recall (given the definition) the following ubiquitous pathology words: anatomic pathology clinical pathology diagnosis diathesis doctor etiology finding forensic pathology forme fruste functional disease general pathology incidence lesion organic disease pathogen pathogenesis pathognomonicpathophysiology prevalence prognosis risksign symptom syndrome systemic pathology Distinguish the different kinds of tissue samples that you will obtainfor examinationby pathologists.

Tumor diathesis - Medical information and advice

Similiar Diathesis Stress Model Examples Keywords

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Risk factors for both COPD and asthma can be categorized as host and environmental factors. The genetic risk factor that has been most closely linked to COPD is a rare deficiency of α1-antitrypsin.(1) Because only 15% of smokers go on to develop COPD, genetics and other susceptibility factors are thought to play an important role. Polymorphisms in genes related to proteases, antioxidants and inflammation have been found to relate to some of the features characteristic of COPD. Polymorphisms in any of three classes of proteases, the serine proteases, cysteine proteases, and matrix metalloproteinases may lead to development of COPD.15 Antioxidant enzymes known to be present in the airways include glutathione-S-transferase, superoxide dismutase and catalase. Cigarettes smoke causes a large number of free radicals, and alterations in these enzymes may also raise susceptibility to COPD.(15) Many pro- and anti-inflammatory mediators, including TNF-a, IL-1, IL6 and TGF-ß are also felt to be important in the development of COPD.(15) A candidate gene—the promoter polymorphism-1111 in the interleukin-13 gene(5)—was identified in populations with either COPD or asthma. This finding provides additional evidence in support of a genetic susceptibility to COPD and asthma.

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