Robbins Pathologic Basis of DiseasePresenting the latest edition of this popular, comprehensive and practical text of pathology. Written with great clarity for easy readability, this reference offers detailed discussions of genetic disorders, cellular injury and death, neoplasia, the skeletal system and soft tissue tumors, and much more. Completely revised and updated, this edition is even more user-friendly with the use of text boxes for key topics in each chapter and a new full-color design. Features 1200 excellent 4-color illustrations! |
From inside the book
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Page 54
... mechanisms have been proposed ( Fig . 3-4 ) : Formation of endothelial gaps in venules : This is the most common mechanism of vascular leakage and is elicited by histamine , bradykinin , leukotrienes , substance P , and many other ...
... mechanisms have been proposed ( Fig . 3-4 ) : Formation of endothelial gaps in venules : This is the most common mechanism of vascular leakage and is elicited by histamine , bradykinin , leukotrienes , substance P , and many other ...
Page 214
... mechanisms of self - tolerance , it is believed that additional fail - safe mechanisms must also exist . Much interest is focused on suppressor T cells with the ability to down - regu- late the function of other autoreactive T cells ...
... mechanisms of self - tolerance , it is believed that additional fail - safe mechanisms must also exist . Much interest is focused on suppressor T cells with the ability to down - regu- late the function of other autoreactive T cells ...
Page 318
... mechanisms may also participate in tumor cell destruction by two mechanisms : activation of comple- ment and induction of ADCC by natural killer cells . IMMUNOSURVEILLANCE Given the host of possible and potential antitumor mech- anisms ...
... mechanisms may also participate in tumor cell destruction by two mechanisms : activation of comple- ment and induction of ADCC by natural killer cells . IMMUNOSURVEILLANCE Given the host of possible and potential antitumor mech- anisms ...
Contents
GENERAL PATHOLOGY | 1 |
6 | 26 |
Acute and Chronic Inflammation | 50 |
Copyright | |
18 other sections not shown
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Common terms and phrases
abnormal acid activation acute adhesion amyloidosis angiogenesis antibodies antigens apoptosis associated bacteria bind blood cancer carcinogens carcinoma cause CD4+ cell cycle cell death cellular Chapter chemical chromosome chronic clinical collagen colon common cyclin cytokines damage deficiency develop disease disorders drugs edema effects endothelial cells endothelium enzymes epithelial cells extracellular matrix fever fibrosis Figure function gene genetic granulomas growth factor hepatitis host cells human immune increased induce infection infiltrate inflammation inflammatory integrins intracellular involved kinase lesions leukocytes liver lung lymph nodes lymphocytes lymphoma lysosomal macrophages malignant matrix mechanisms mediators membrane metabolism molecular molecules MORPHOLOGY muscle mutations necrosis neoplasms nervous system neutrophils normal occur oncogenes organisms oxidative parasites pathogenesis pathogens pathway patients peptide phagocytosis plasma platelet produce proliferation protein reactions receptor release renal respiratory response result signals skin surface syndrome synthesis T-cell tion tissue toxic toxin tumor tumor cells vascular viral virus viruses vitamin