Tear from eyes from         barriers of innate immunity :-A Physical B Cellular C Physiological D Cytokine

Tear from eyes from         barriers of innate immunity :-A Physical B Cellular C Physiological D Cytokine

Which barrier of innate immunity first come in contact with pathogen ?A Skin and mucous membrane B Fever     C Interferon D Phagocytes

However, onions are perhaps best known for their ability to induce tears when chopped. When cut, onions release an irritant called______ which stimulates our eyes’ lachrymal glands so they release tear

Passage 4 (Questions 19 - 23)Cataract generation triggered by lens injury is considered to be driven by the action of the proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) as a complication of injury and inflammation. The epithelium quickly expands, creating a hundredfold increase in the number of cells. In response to trauma, irritation, or surgery, cytokines and growth factors increase in the aqueous humor and stimulate LECs to proliferate and undergo EMT. This response is significantly diminished in organisms where EMT is inhibited by the inactivation of transforming growth factor β (TGFβ), especially TGFβ2, the major isoform in the aqueous humor.During the process of EMT, LECs undergo cytoskeletal rearrangement, with the addition of a large amount of extracellular matrix proteins, such as collagen and fibronectin. In anterior cataracts, the proliferation and EMT of LECs in situ leads to the formation of opaque plaques just beneath the lens anterior capsule.The production of TGFβ is regulated by histone deacetylase-1 (HDAC1). HDAC1 removes acetyl groups from N-acetyl lysine groups on histone. Once synthesized, TGFβ is secreted by activated monocytes in the aqueous humor. Since monocytes mediate almost 80 percent of local TGFβ concentrations, researchers tested the theory that TGFβ is responsible for monocyte impact on LEC production. The number of LECs expressing MIB1, a nuclear protein, was utilized as a measure of LEC proliferation and expected EMT.Experiment 1After simulated injury, monocyte/LEC cultures were treated with an antibody that lyses all but a negligible fraction of available monocytes; a division of these cultures was also treated with a TGFβ agonist. A second set of cell cultures was treated with antagonists of epithelial cell TGFβ receptors TGFBR1 and TGFBR2 (Table 1).Table 1 Results of the study on monocyte lysis, TGF agonist, and TGF receptor antagonistsExperiment 2In an effort to determine whether MIB1 is associated with LEC regulation, LEC density was assessed during the course of epithelial growth in wild-type and MIB1-null cell cultures (Figure 1). Figure 1 Growth of LECs after an injury in both wild-type and MIB1-null strains Question 21After injury-induced cataract formation has begun, which of the following are LEAST likely to be found in nearby monocytes? A.TGFβ transportersB.TGFβ receptorsC.Tight junctionsD.Cytokines

Passage 4 (Questions 19 - 23)Cataract generation triggered by lens injury is considered to be driven by the action of the proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) as a complication of injury and inflammation. The epithelium quickly expands, creating a hundredfold increase in the number of cells. In response to trauma, irritation, or surgery, cytokines and growth factors increase in the aqueous humor and stimulate LECs to proliferate and undergo EMT. This response is significantly diminished in organisms where EMT is inhibited by the inactivation of transforming growth factor β (TGFβ), especially TGFβ2, the major isoform in the aqueous humor.During the process of EMT, LECs undergo cytoskeletal rearrangement, with the addition of a large amount of extracellular matrix proteins, such as collagen and fibronectin. In anterior cataracts, the proliferation and EMT of LECs in situ leads to the formation of opaque plaques just beneath the lens anterior capsule.The production of TGFβ is regulated by histone deacetylase-1 (HDAC1). HDAC1 removes acetyl groups from N-acetyl lysine groups on histone. Once synthesized, TGFβ is secreted by activated monocytes in the aqueous humor. Since monocytes mediate almost 80 percent of local TGFβ concentrations, researchers tested the theory that TGFβ is responsible for monocyte impact on LEC production. The number of LECs expressing MIB1, a nuclear protein, was utilized as a measure of LEC proliferation and expected EMT.Experiment 1After simulated injury, monocyte/LEC cultures were treated with an antibody that lyses all but a negligible fraction of available monocytes; a division of these cultures was also treated with a TGFβ agonist. A second set of cell cultures was treated with antagonists of epithelial cell TGFβ receptors TGFBR1 and TGFBR2 (Table 1).Table 1 Results of the study on monocyte lysis, TGF agonist, and TGF receptor antagonistsExperiment 2In an effort to determine whether MIB1 is associated with LEC regulation, LEC density was assessed during the course of epithelial growth in wild-type and MIB1-null cell cultures (Figure 1). Figure 1 Growth of LECs after an injury in both wild-type and MIB1-null strains Question 19HDAC1 MOST likely plays a direct role in: A.gene silencing.B.ribosomal inactivation.C.transfer of an acetyl group from acetyl-CoA.D.gene activation.