Please help me write this paperBelow is a summary of an article about vitamin D deficiency. Create your own experiment to follow up with the vitamin D article I know the article wasn’t very focused on cellular biology but I would like you to be focused on cell biology. Use jargon on cell biology. Also please create separate sections for these include these ( Include hypothesis justification approach results that support and results that would refute.) There is no word count required but the paper has to be specific detailed and CELL BIOLOGY focused. Let me know if you need more time.Hypothesis Vitamin D deficiency is a risk factor for cardiovascular lesions and a good predictor of cardiovascular mortality in patients with chronic kidney diseases. The vitamin D deficiency leads to an increase in the arterial adventitial vasa vasorum systematic inflammation inflammatory vascular infiltration foam cell formation and plaque development; these systematical changes lead to atheromatous disease. Vitamin D deficiency also induces abnormal ectopic calcification through elevated PTH (parathyroid hormone). Sufficient serum levels of vitamin D lead to suppression of angiogenesis and cell proliferation and suppression of TNF-α by inhibiting its activator TNF converting enzyme. Based on previously stated information a murine model organism deficient for apolipoprotein E is used to conduct the next hypothesis. The relationship between vitamin D levels and arterial wall thickening and plaque formation has assumed that low concentrations of vitamin D impact the thickening of arterial walls and plaque formation leading to progression and worsening the atheromatous disease. Approach For research where used murine model animal knockouts for Apolipoprotein E animals were divided into control and vitamin D deficient mice. The deficiency was achieved by injecting paricalcitol that enhances vitamin D catabolism. After the deficiency was achieved both animal groups were fed with a high-fat diet (western diet). Calcium was added to the diet to avoid secondary hyperparathyroidism. The Control group was never deficient in vitamin D. Mice from each group was sacrificed in four periods 4 8 15 and 20 weeks since starting the diet. Serum analysis evaluated calcium phosphorus vitamin D and PTH levels using colorimetric analysis and different kits. The levels of cholesterol (HDL and LDL) and triglycerides were evaluated using a specific quantification kit. For histology analysis tissue was fixed in formalin subsequently rinsed in ethanol and paraffin-embedded. Slices of tissue were stained with Azan trichrome. For immunohistochemistry analysis slices were stained with anti-a-Smooth Muscle Actin antibody and anti-mouse HRP-DAB tissue staining kit. Statistical analysis used ANOVA and unpaired t-test. Results The model animals weights were analyzed before sacrifice and by comparing both groups in all four-time points it was observed that there wasnt a significant statistical difference; they had the same trend of gaining weight. Serum levels of vitamin D in the experimental group were at a lower threshold point of detection. Analyzing the development of atheroma shown that lesions can be detected in both groups of mice. Plaques were formed in both groups of mice are 15 and 20 weeks after the start of the diet but in vitamin deficient mice as early as eight weeks since the start. Plaques in the control group were more stable with fibrotic cap. Plaques formed in vitamin deficient mice had larger lipid-rich cores more collagen and reduced cap thickness. Plaques in carotid arteries have the same trend: in vitamin-deficient mice plaques had a chondrocyte-like phenotype that can promote calcification of plaque. The marker of fibrogenesis the levels of α-SMA were detected by immunochemical staining. In vitamin-deficient mice smooth muscle cells content was reduced which increased the instability of plaques. In both groups there were no changes in calcium levels in phosphorus compared to their physiological levels. The levels of triglycerides and cholesterol were the same in both groups. The same trend was observed in PTH serum levels; there wasn’t a difference in serum levels between these two groups.