Rheumatoid arthritis (RA) is an autoimmune, chronic, inflammatory and symmetric disease. In order to avoid joint destruction and reduce requires knowledge of the vital components causing the disease; so it is essential to start early in diagnosis and suitable treatment. Although clinical symptoms and results of radiographic help to identify and measure the activity of RA disease, biochemical markers also act as indicators of early diagnosis of the disease activity. So it is therefore the diagnosis of the disease in an early stage must choose a strong relationship with the disease. One of the vital signs related to rheumatoid arthritis is adenosine deaminase (ADA). The destruction of adenosine by the adenosine pathway facilitates a series of infections such as rheumatoid arthritis. So there are many questions that come to our mind namely. Can the level of adenosine activity (ADA) be a biomarker of the distinction between RA patients and controls? Can adenosine deaminase be a biomarker indicator for diagnosing of rheumatoid arthritis at the stage early pre-radiographically? And, does adenosine deaminase activity give an indication of the disease activity? In this review article, we're going to show the studies that pointed to those questions.

The genus Staphylococcus is an important microorganism because of its direct and dangerous impact on the lives of other organisms, and Alexander Ogaston was the first to release this designation in 1880 to denote spherical bacteria usually associated with pus in wound infections. The members of this species are found in various environments such as dust, water, air, feces, on the skin, and the mucous membranes of warm-blooded vertebrates, on clothing, and other places. Most species of this species live as natural flora on human skin and mucous membranes, but some are opportunistic pathologies. The species of staphylococcus is characterized by having several virulence factors that increase the efficacy and pathogenicity of its species on the occurrence of infection due to its possession of tequic acid and the adhesion factor and other factors that enable it to get rid of the host defenses as an enzyme (Staphylokinase) or enable it to invade and spread as an enzyme (Hyaluronidase). Its possession of cellular wall proteins, its formation of the capsule and the exogenous polysaccharides and its production of various types of extracellular enzymes and various toxins such as intestinal toxins fixed in the heat, secretion of immune system inhibitors and their containment of antibiotic resistance genes. It shows the total resistance to the degradation of lysozyme. Staphylococcus aureus is resistant to many antimicrobial agents and thus produces treatment problems. The sex of staphylococcus includes 36 species and 80 subtypes, where more is clarified From 20 types of staphylococcus aureus.

Adropin is a biomarker for cardiac disease and atherosclerosis. Discovered in 2008, this peptide is involved in controlling the metabolism of carbohydrates and fatty acids. Detailed knowledge of these peptides' mechanisms and the factors that affect their release can provide new diagnostic and treatment of metabolic disorders, including cardiac disease and atherosclerosis. This study aimed to estimate the level of adropin for Iraqi patients with cardiac disease and atherosclerosis and the factors affecting its level and its relationship with the studied variables. This study was conducted on 130 adults, including 90 patients suffering from cardiac disease and atherosclerosis, and 40 uninfected adults were considered a control group. Serum levels of adropin and lipid profile (HDL, LDL, and TC) were estimated . The results of the study showed a significant decrease in the level of adropin (p 0.0001) in the following cases: generally in all patients who affected with cardiac disease and atherosclerosis (4.3 ± 1.5 ng ml) compared with healthy subjects (10.2 ± 2.3 ng mL); in obese patients (3.4 ± 0.7 ng mL) compared to non-obese patients (5.2 ± 1.2 ng mL); in patients who also affected with diabetes mellitus type 2 (3.2 ± 0.8 ng mL) and patients who also affected with hypertension (4.1 ± 1.2 ng mL) when compared with patients who do not have other diseases (5.7 ± 1.5 ng mL). A negative significant correlation between serum adropin level and BMI (r=0.493; p=0.0001), LDL (r=-0.628; p=0.0001) level and TC (r=-0.249, p=0.018) level. A positive significant (r=0.395, P=0.0001) appeared correlation of adropin level with HDL level. It was observed that a lower adropin level could play a vital role in cardiac pathophysiology and atherosclerosis. Also, a decrease in the adropin level can be considered a risk factor for these patients. Therefore, measurement and surveillance of changes in serum adropin can consider as a new diagnosis and assessment of disease progression.

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Alpha-L-fucosidase (FUCA) degrades many fucosylated glycans and has long been recognized as a tumor marker associated with the early detection of some cancers. this study aimed to purify and characterize alpha-L-fucosidase from the serum of patients with hepatocellular cancer and estimate its toxic effect against hepatocellular carcinoma HepG2, prostate cancer PC3 cell lines and the standard hepatocyte WRL-68 cell line. SDS-Page Electrophoresis technique was used to determine the purity of the purified alpha-L fucosidase and estimate its molecular weight. Three purification steps were used for FUCA purification: precipitation with 65% ammonium sulfate saturation, DEAE-cellulose ion exchange, Sephadex G-75 gel filtration. The procedure resulted in 54% recovery of the enzyme with 27.5-fold purification and 14 U/mg specific activity. It was demonstrated that FUCA purified from the serum of HCC patients showed a more toxic effect on HepG2 cells (IC 50 of 65.74 µg/ml) than on PC3 prostate cancer cells (IC 50 of 111.5 g/ml) and less toxic effect against standard hepatocyte WRL-68cells (IC 50 of 214.5 µg/ml). We can conclude that the inhibitory effect of the purified FUCA on hepatocellular carcinoma is more than its effect on prostate cancer cells. Also, the purified FUCA may be used in studies on anticancer drug development in liver cancer. K e y w o r d s: alpha-L-fucosidase, hepatocellular cancer, HepG2 and PC3 cell lines, ion exchange chromatography, gel filtration .