Pathology, LEcture 7, Tissue Repair #1
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Transcript of Pathology, LEcture 7, Tissue Repair #1
8/8/2019 Pathology, LEcture 7, Tissue Repair #1
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Vasodilatation
Increased vascular permeability
Leukocyte recruitment and activation
Fever
Pain
Tissue damage
Prostaglandins Nitric Oxide Histamine
Histamine and serotonin C3a and C5a (by liberating vasoactive amines
from mast cells, other cells) Bradykinin
Leuktrienees C4, D4, E4 PAF Substance P
TNF, IL-1 Chemokines C3a, C5a Lukotriene B4 (Bacterial products, e.g., N-formyl methyl
peptides)
IL-1, TNF Prostaglandins
Prostaglandins Bradykinin Neuropathies
Lysosonal enzymes of leukocytes Reactive oxygen species
Nitric oxide
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NM Almasri JUST
INFLAMMATORY EVENT CHEMICAL MEDIATOR
Vasodilation PGs; NO
o vascular permeability Vasoactive amines; C3a & C5a; Bradykinin;
LTC 4 , D4, & E 4; PAF
Chemotaxis,leukocyte adhesion
C5a; LTB4; bacterial products ;cytokines (IL-8)
Fever IL-1; IL-6; TNF; PGs
Pain PGs; Bradykinin
Tissue damage Lysosomal enzymes;Oxygen metabolites; NO
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Vision:
The vision of Faculty of Medicine at Jordan
University of Science & Technology is to leadmedical education using creativity and
innovation, to advance health with quality and
compassion, to search and discover with
imagination and innovation; and to achieve and
maintain human health and well-being to the
maximum attainable levels.
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Mission:
Faculty of Medicine at Jordan University
of Science & Technology is a communityof scholars who stimulate & inspiremedical students to be leaders inadvancing medicine at different levels of health care and who participate inadvancing medical science and research.
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Restoration of tissue architectur e and functionafter an injury.
Regeneration Replacement of damaged cells by similar par enchymal cells, e.g. liver r egeneration
Requir es intact connective tissue scaffold Returns to normal state
Healing & Fibrosis (scar formation ) ECM framework is sever ely damaged Replacement by connective tissue Or ganization : in tissue spaces occupied by an
inflammatory exudates (or ganizing pneumonia)
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Remnants of the injured tissue
(attempting to restore normal structure )
Vascular endothelial cells( create new blood vessels )
Fibroblasts ( source of fibrous tissue )
Proliferations of these cells is driven by
proteins that are called GROWTHFACTORS
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Labile cells (continuously dividing & continuously dying) Stem cells divide: self r enewal and diff er entiation
Examples:
x Skin epidermis,oral cavity,vagina,cervix,ducts draining exocrine or gans.x GIT epithelium, uterus, fallopian tubes, bladder urothelium.
x Bone marrow cells
Stable cells (quiescent) Examples:
x Liver and pancr eas
x Kidney
x Smooth muscle, endothelial cells, fibroblasts
Permanent (nondividing), Examples:
x Cardiac muscle
x Neurons12
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G2
(Labile cells)G0
(Stable
cells)
(Permanent
cells)
G0
G1
S
M
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Self r enewal capacity Asymmetric r eplication (after each cell division,
some progeny enter a diff er entiation pathway, while others
r emains undiff er entiated )
Capacity to develop into multiple lineagesExtensive prolif erative potential
Embryonic stem cells: Pluripotent cells that
can give rise to all tissues of the body
Adult stem cells: Restricted differentiation capacity
(lineage specific), except BM and some other adult
tissues« 16
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Study of specific cell signaling and
diff er entiation steps
Production of knockout micePotentially, generation of specific cell types to
r egenerate damaged tissue (therapeutic
cloning)
Diff er entiation plasticity and transdiff er entiationhas led to the Regenerative Medicine
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Bone marrow
Liver
Skeletal muscle
Intestine
Skin
Hemetopoietic stem cells
Hering canal
Satellite cells
Base of crypts
Hair follicle bulge
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Family of proteins that control entry of the cells atspecific stages of cell cycle
Level of a specific cyclin incr eases at a specific stage,
then decr eases rapidly after the cell departs that stage In order to accomplish their function, they have to bind
to cyclin-dependent kinases (CDKs) Diff er ent combinations ar e associated with each phase
of the cell cycle They exert their function by phosphorylating certainproteins (kinase phosphorylate proteins)
Examples: Cyclin B-CDK1 activate G2 to M transition Cyclin D-CDK4,6 activate G1 to S phase
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Hypophosphorylated RB, forms a complex with E2Ftranscription factor and DP1, blocking the eff ect of E2F.
Blocking is mediated by histone deacetylase causing chromatin compaction.
CyclinD/CDK4, and cyclinE/CDK2 phosphorylate RB. Phosphorylated RB dissociated from the complex,
leading to activation of E2
F. Tar get genes for E2F include: cyclin E, DNApolymerase, thymidine kinase, dihydrofolate r eductase, and others.
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