Rubin's Pathology: Clinicopathologic Foundations of Medicine by Emanuel Rubin, David S. Strayer

By Emanuel Rubin, David S. Strayer

Rubin's Pathology units the root for scientific education and perform with specialist assurance of ailment tactics and their results on cells, organs, and members. Now in its 7th variation, the textual content is praised for being "exactly correct for scientific students" —a ideal stability of simple pathology and bedside viewpoint, with no extraneous element that's past the forums.

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Extra info for Rubin's Pathology: Clinicopathologic Foundations of Medicine (7th Edition)

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Cancer: The involvement of autophagy in the development and progression of cancer is complex and represents a double-edged sword. , Beclin-1 and some Atg genes) act as tumor suppressors (see Chapter 5) and are deleted or mutated in many human tumors. Autophagy can also protect cancer cells if they are deprived of nutrients or oxygen because of therapy or insufficient blood supply. Miscellaneous: Mutations in genes that encode proteins involved in autophagosome–lysosome fusion are linked to a disease of skeletal muscle (inclusion body myopathy), Paget disease of bone and frontotemporal dementia.

Mutation in parkin, a ubiquitin ligase, is implicated in the pathogenesis of some hereditary forms of Parkinson disease, in which undegraded parkin accumulates as Lewy bodies (see Chapter 32). Regulation of ubiquitination may be important in tumor development. Thus, human papillomavirus strains that are associated with human cervical cancer (see Chapters 5 and 24) CELL ADAPTATION, INJURY AND DEATH CHAPTER 1: CELL ADAPTATION, INJURY AND DEATH 24 SECTION I: MECHANISMS OF DISEASE TABLE 1-3 INVOLVEMENT OF THE UBIQUITIN–PROTEASOME SYSTEM IN DISEASE Disease Ubiquitin–Proteasome System Activity Anatomic Effect Neurologic Diseases (Diseases Associated with Neuron Loss) Parkinson disease Decreased Lewy bodies Alzheimer disease Decreased Amyloid plaques, neurofibrillary tangles Amyotrophic lateral sclerosis Decreased Superoxide dismutase aggregates in motor neurons Huntington disease Decreased Polyglutamine inclusions Decreased Chronic inflammation Type 2 diabetes mellitus Increased Insulin insensitivity Cataract formation Decreased Aggregated oxidized proteins Aging Increased Atrophy Cancer and other chronic disease Increased Atrophy Ischemia/reperfusion Decreased Myocyte apoptosis Pressure overload Decreased Myocyte apoptosis Autoimmune Diseases Sjögren syndrome Metabolic Diseases Muscle Wasting Cardiovascular produce E6 protein, which inactivates the p53 tumor suppressor.

Macroautophagy also handles damaged cytoplasmic organelles and aggregated proteins, for both of which specific recognition is needed. In such circumstances, target identification depends on the nature of the dysfunction. For example, a damaged mitochondrion that produces excess reactive oxygen species from dysfunctional electron transport suffers altered membrane potential, thereby causing a cytosolic protein, Nix, to bind to the outer mitochondrial membrane. This complex recruits a protein called parkin (for its likely involvement in Parkinson disease).

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