three factors of epitheliumbasal lamina
cell adhesion
differentiation potency pathology HirotoShishido
what is the target of
①Vimentin ②S-100 ③desmin ④cytokeratin
(immunohistochemical stain)①viMEntin→MEsenchymal tissue(sarcoma, endometrial carcinoma, RCC, meningioma)
Even with adequate treatment of a malignancy, the areas affected by field cancerization remain at higher risk of developing multiple primary malignancies, as seen in this patient. Therefore, patients diagnosed with any of these cancers require comprehensive evaluation and continued surveillance of the at-risk area. pathologyoncologyUWorld HirotoShishido
wound dehiscenceWound dehiscence is the rupturing of a previously closed wound, and can result from insufficient granulation and scar tissue formation, inadequate wound contraction, or excessive mechanical stress.
Such wound rupture most commonly occurs in abdominal wounds that are subject to ☆increased intraabdominal pressure. pathologyUWorld HirotoShishido
cachexia
pathophysiologyWeight loss, muscle atrophy, and fatigue that occur in chronic disease (eg, cancer, AIDS, heart failure, COPD).
Mediated by TNF-α, IFN-γ, IL-1, and IL-6, which stimulate the ☆ubiquitin-proteasome pathyway to degrade muscle proteins pathologyUWorld HirotoShishido
sensitive indicator of colorectal cancer recurrencecarcinoembryonic antigen(CEA)
mechanism of cancer cells evading apoptosisdevelopment of the ability to ☆splice out a particucar exon that codes for the transmembrane domain of the Fas receptor(FasR) converting it to a soluble form that is not expressed on the cell surface, which allows the cells to evade apoptosis
hypertrophy and hyperplasiastructural proteins and organellesin size of cells (☆high rate of mRNA synthesis)
Example: cardiac hypertrophy.
controlled proliferation of stem cells and differentiated cells in number of cells (high rate of mitotic activity)
Excessive stimulation pathologic hyperplasia (eg, endometrial hyperplasia), which may progress to dysplasia and cancer.
Example: benign prostatic hyperplasia. pathologyUWorld SIM1 HirotoShishido
histologic features of AMI, ischemic brain strokedifference
AMI
・(4-8)-24hrs coagulative necrosis caused by ☆massive calcium influx
・>2weeks contracted scar
common
・1-3days necrosis+neutrophil
・3-5days macrophages (+☆microglia infiltration→ stroke) pathologyUWorld HirotoShishido
what cell junction does calcium dependent adhesion molecules form?Adherens junction (belt desmosome, zonula adherens),
desmosome (spot desmosome, macula adherens)
→removing calcium from extracellular fluid will cause dissociation of these cadherin-mediated junctions, leading to loss of cell-cell adhesion biologypathologyUWorld SIM1 HirotoShishido
how does CpGs workThe methylation of cytosine residues in CpGs(cytosine-guanine dinucleotide repeats) prevents ☆transcription factors from binding to the promoter, effectively silencing transcription of genes not required by terminally differentiated somatic cells. pathologybiologyUWorld SIM1 HirotoShishido