Its dysfunction is a progressive and multifactorial phenomenon in the elderly polamine resulted in elevated

According to the results, the concentration of the MBL-AJ-binding CEA of the healthy patients and the patients with the benign Sorafenib neoplasm were determined to be 48.5611.8 U/ml versus the concentration of 11.467.5 U/ml of the patients with the cervical cancer diagnosis. The total CEA, which can be synthesized by both malignant and normal cells, were excluded from analysis because the cervical specimens were collected from the local source of the cancer CEA biosynthesis. A high sensitivity and specificity of the MBL-AJ-CEA interaction allowed detecting the lectin-binding structures in the vaginal secretion in the concentration of CEA 3–50 ng/mL. The method specificity and sensitivity were 93.6 and 87.8%, respectively, for patients with cervical cancer with the cut-off level of 12.74 ng/mL. Whereas the method prognostic valuation was calculated to be 87% and 95.2% for the positive and negative diagnosis, respectively. Thus, this method has advantages compared to those associated with determining of concentration of CEA and squamous cell carcinoma antigen in blood serum,,. However, the wild-type lectin MBL-AJ derivation from the holothurian A. japonicus coelomic liquid has many restrictions, namely: low concentration of MBL-AJ in the native source, preservation of the wild life of the Far Eastern holothurian A. japonicus, the narrow habitat of the endemic species of the holothurian. A recombinant analogue of MBL-AJ was attempted to be produced in the E. coli Top10/pQE_80L expression system. However, the protein was expressed in the body inclusion, and its refolding resulted in 20%-yield of the soluble recombinant lectin of 69% of homology with the wild-type MBL-AJ by the level of interaction with the antibodies against MBL-AJ. Cardiovascular diseases are the leading cause of death and disability in the world, especially among an aged population. Because CVD mortality rates increase with age in the later years of life, the aging process is recognized as the main risk factor for the development of CVD. Aging involves a natural decline in the chances of survival that all species experience with increasing age. Biological aging is termed senescence. The process involves numerous changes to the molecular and cellular structures disrupting metabolism, eventually leading to deterioration or death. Senescence is classified as organismal senescence and cellular senescence. Because organismal senescence is composed of cellular senescence, increased consideration has been given to cellular senescence. Cellular senescence was first described by Hayflick and his colleagues in 1961, when they made the observation that normal human fibroblasts would enter into an irreversible state of growth cessation after several continuous passages. This phenomenon was called replicative senescence. Thereafter, researchers found many stressors that are able to induce senescence that is known as stress-induced premature senescence. Among many of the stressors, hydrogen peroxide is a better candidate for inducing senescence, because an H2O2-induced process could mimic the oxidative environment that occurs in the aging population with high efficiency. The vascular endothelium is a thin layer of cells lining the innermost surface of blood vessels that acts as a semi-selective barrier, preventing lipid infiltration.