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Leukemia is a type of cancer that develops in the bone marrow and blood cells. When the DNA of a cell undergoes one mutation or a series of mutations results in the formation of leukemia cells. These leukemia cells, "blasts," cannot mature into fully functioning WBCs. Leukemia increases WBCs which compete for space with RBCs and platelets that the body requires to function normally; each may be classified as acute or chronic, myeloid or lymphoid, depending on the originating cell and the growth rate. Nearly 2.5% of all new cancer cases and 3.1% of cancer-related deaths were attributable to Leukemia. Leukemia can strike at any age geographical and ethnic differences in leukemia rates are also present. Folate's significance in cancer was exclusively tied to antifolate-based cancer treatment. After discovering Antifolate associated based chemotherapy, contrary to the inhibitory action of antifolate on tumors, epidemiologic, clinical, and experimental data show that folate deficiency in normal tissues may predispose them to neoplastic transformation and that folate supplementation may suppress the development of tumors in normal tissues. Epidemiologic research reveals a negative connection between folate levels and numerous cancers, including Leukemia. The exact association between folate status and certain cancers is unknown. Vitamin B control one-carbon metabolism and human health. Folate-mediated one carbon (1C) metabolism supports a of processes that are essential for the cell. Through a number of interlinked reactions happening in the cytosol and mitochondria of the cell, folate metabolism contributes to de novo purine and thymidylate synthesis, to the methionine cycle and redox defense. Targeting the folate metabolism gave rise to modern chemotherapy. The folate and methionine cycles complete the one-carbon route with vitamin B9 or folate. Vitamin B6 regulates carbon cycling. Vitamin B dysregulation alters biochemical signaling and causes several illnesses. [ABSTRACT FROM AUTHOR]

Abstract: Neutrophil apoptosis and clearance by macrophages are essential for wound healing. Evidence suggests that hyperbaric oxygen (HBO) exposure may enhance neutrophil apoptosis, but HBO effects leading to neutrophil clearance [...]

Objective Obstructive lung diseases (OLD) are chronic inflammatory disorders of the respiratory tract including asthma and chronic obstructive pulmonary disease (COPD). Apo lipoprotein E (Apo E), is a multifunctional protein as it intervenes the binding of lipoproteins or lipid complexes to specific cell-surface receptors. Experimental studies referred to the function of Apo E as an endogenous negative regulator of airway hyper responsiveness and goblet cell hyperplasia. The protective role of Apo E pathways primarily in respiratory disease was explained in human studies and research utilizing experimental murine model systems. Literature data reveal a strong association between redox status, including the enzyme superoxide dismutase (SOD) with both the development a severity of OLD. This study aims to investigate the relation between SOD antioxidant enzyme activity in addition to investigating the level of Apo E and the development of obstructive lung diseases (OLD). Methods Patients with OLD (n = 40) and 40 age-matched healthy controls were enrolled in this study. Serum samples were collected to test the role of Apo E and to test the effect of antioxidant enzyme SOD, and their influence on OLD, all measured by ELISA. Result The results showed a significant decrease in the level of serum SOD activity in patients with OLD when compared with control group (P < 0.05). However, the levels of Apo E did not show a significant difference between the two groups. Conclusion Decreased level of antioxidant SOD suggests the presence of an oxidative stress in asthmatic airways favoring a more oxidative state is present in the airway inflammation. The level of Apo E was non significantly increased in serum of patient, this suggests that protein level of Apo E does not change but may be Apo E gene expression is altered. [ABSTRACT FROM AUTHOR]