Treat up to 25 cell lines in T75

Herbicides in this group prevent cell division primarily in developing root tips and are only effective on some germinating broadleaves and selected grasses. Alkylazine, benzamides, and nitriles are Cellulose Inhibitor herbicides that affect cell wall biosynthesis (cellulose) in susceptible plants causing inhibition of cell division.

Mention other chemical reactions that injure cells.

 Synergy with Cell Wall Synthesis Inhibitors is Not Always Observed In the Clinical Setting

Tell how you know a cell is dead.

If the patient lives, the edges of the necrotic area become inflamed, and eventually the dead cells will be removed by white cells and their noxious proteases.

Coagulation necrosis retains the outlines of the cells.

Remember: True coagulation necrosis involves groups of cells, and is almost always accompanied, after a day or so, by acute inflammation (next unit!) Apoptosis does not cause inflammation.


HOW DO YOU TELL A CELL IS DEAD?

(1) As it is dying, the cell cytoplasm becomes hypereosinophilic (loss of ribosomes is probablyless important since the hue changes little; the denatured proteins probably expose more arginine and lysine units that bind eosin).

This is probably something that lets dying cells signal distress.

(RULE: If the nucleus is smaller and darker than a resting lymphocyte's, or is small and dark and shows no euchromatin-heterochromatin textures, that cell isvery dead.) Other sure signs of cell death include KARYORRHEXIS, or fragmentation of the shriveled nucleus (into "NUCLEAR DUST"), and KARYOLYSIS, which simply means that nothing of the nucleus is visible any longer, except perhaps a purple haze (endonucleases destroyedthe DNA).

Cells actually expend energyin order to die.

Cells that are programmed to die; for example, the cells of the outer layers of the epidermis, cells in the gut epithelium, and the circulating neutrophils; Cells that are told to die by the local T-cells (many "immune imjury" disesases -- hepatitis withapoptotic hepatocytes is only the best-known of these)In hormone-dependent structures (lactating breast, ovarian follicles that don't make it, adult prostate) that regress by loss of cells following withdrawal of hormones; Destruction of inflammatory cells that might otherwise do harmto the neighboring tissue cells; notably eosinophils (J.

Apoptotic cells may be phagocytized bytheir neighbors.

Every cell on a microscopic slide is dead, but that only the necrotic ones were assuredly dead when the fixative froze their appearances in time.) Nuclear changes are the light microscopist's hallmark for irreversible injury.

Different cells react differently to starvation conditions.

(When there's antemortem necrosis, there's generally some vital reaction among the surviving cells, i.e., inflammation, congestion, a recognizable pattern of infarction at the organ level, a thrombus, etc., etc.

INFECTIOUS AGENTS injure cells in a variety of ways.

Words: AUTOLYSIS is the dead cell being self-digested by its lysosomal enzymes, whileHETEROLYSIS isthe cell being digested by the body's living white cells.

Cellular ATP content drops rapidly and work stops.

Groups of cells undergo programmed apoptosis in the embryo as structures vanish; we believe autoreactive lymphocytes are removed by apoptosis before birth (J.