Diabetes mellitus is one of the most common non-communicable chronic diseases, which is the combined action of genetic factors, environmental factors and lifestyle. Specific conditions occur in the oral cavity in the course of diabetes that cause changes in all oral tissues with different symptoms and signs. Increased salivary glucose level is followed by increased accumulation of dental plaque and decreased resistance to noxious agents. The most common oral manifestations in diabetic patients include higher prevalence of periodontal desease, burning mouth syndrome, disruption in salivary flow, opportunistic infections, higher prevalence of denture stomatitis, oral lichen planus, fissured tongue, angular cheilitis etc. Dental interventions in patients with well-controlled diabetes are not different from those applied to nondiabetic patients. Regular monitoring of these patients is required because of the complications that can occur.

The most important characteristic of calcium channels is selective regulation of slow incoming stream of calcium into the cell tissue providing the slow increasement of action potential. Such tissues include smooth muscles of blood vessels, cardiocytes and heart noduses (AV and SA node). Different calcuim antagonists have different effects on previous tissues due to their different chemical formula. Verapamile, Nifedipin and Diltiazem are the most frequently used of all. Their commonest characteristic is blocking the calcium channels causing vasodilatation of blood vessels as well as negative inotropic and chronotropic influence. By blocking the incoming calcium through slow channels of myofibrils of smooth muscles, the antagonists of calcium decrease the quantity of available calcium for contraction which causes vasodilatation. The most famous and most frequently used calcium antagonist is Verapamile. In terms of electrophysiology, Verapamile inhibits action potentials of heart noduses, especially the AV node, where the slow incoming of calcium is the most important for depolarization. Prolongation of the efective refractory period of SA node causes the heart frequency decreasement while prolongation of the effective refractory period of AV node slows down the work of chambers in case of flater and fibrillation of atriums. The molecules of calcium-bonding protein called kalmodulin are located in synaptic endings. Each kalmodulin can bond four calcium ions providing transfer into active calcium-kalmodulin complex which activates the kinase protein. Activated kinase protein starts the exocytosis of neurotransmitters into synaptic gap. Apart from activating kinase protein, calciumkalmodulin complex also starts the activity of calcium pump presynaptic membrane which pumps calcium out of presynaptic ending stopping the further exocytosis of neurotransmitters into synaptic gap. Taking into consideration the fact that opening the calcium channels on membrane of presynaptic ending is necessary to free the neurotransmitter out of the vesicle, the aim of our work is to study whether Verapamile has effects on the membrane of presynaptic endings of sympathetic nervous system checking the level of catecholamine in serum. The experiment was conducted in 6 healthy dogs which were, after 10-minute- infusion (0.9% NaCl), treated with intravenous bolus veramapile injections in three occasions, in every 5 minutes, until the first signs of intoxication had appeared. This caused bradycardia, heart rhythm disorder and blood pressure drop. In order to determine the level of catecholamine, blood was taken sequentially, in every 5 minutes, before the new dose of verapamile was given. Verapamile (given intravenous) significantly decreases the concentration of adrenaline and noradrenaline in the serum of dogs.

Uz tradicionalne faktore rizika smatra se da i inflamacija doprinosi nastanku ishemičnog moždanog udara (IMU). U toku inflamacije neutrofilni leukociti se degranulišu, kada može doći do oslobađanja njihovog enzima mijeloperoksidze (MPO) u ekstracelularni prostor. Osim peroksidazme MPO poseduje i hlorinišuću aktivnost kojom stvara hipohlornu kiselinu i dugoživeće oksidanse hloramine. U ovoj studiji je određivana hlorinišuća aktivnost MPO i koncentracija ukupnih hloramina u serumu. U studiju je bilo uključeno 29 pacijenata sa akutnim IMU, starosti 69.0 godina (64.2–78.0), i 25 ispitanika kontrolne grupe bez IMU, starosti 69.0 godina (67.0–72.0). Nađeno je da je u grupi sa IMU broj neutrofilnih leukocita u perifernoj krvi značajno veći od kontrolnih vrednosti (4.56±1.76 vs. 7.74±3.35 × 109/L, u kontrolnoj grupi i kod pacijenata; p<0.05). Takođe je i hlorinišuća aktivnost MPO seruma bila veća u grupi sa IMU (67.2 U/L vs. 92.3 U/L, kod kontrole i kod pacijenata; p<0.05). Iako je koncentracija ukupnih hloramina bila nešto veća kod IMU nego u kontrolnoj grupi, razlika nije bila statistički značajna (p=0.178). Aktivnost MPO je značajno korelirala sa koncentracijom triglicerida (p<0.05). Korelacija između hlorinišuće aktivnosti MPO i ukupnih hloramina nije bila značajna (p=0.402), dok su korelacije MPO aktivnosti i broja neutrofila (p=0.071) odnosno MPO aktivnosti i prisustva aritmije (p=0.094) bile nešto veće. Rezultati ove studije ukazuju da MPO verovatno ima ulogu u patogenezi IMU, što se delimično može zasnivati na hlorinaciji biološki značajnih molekula vaskularnog kompartmana.

In the last ten years significant progress has been made in understanding of role of neutrophil granulocytes and their enzyme myeloperoxidase in the evolution and complications of atherosclerosis. Myeloperoxidase plays the role in the development of vulnerable plaque associated with the development of acute coronary syndrome. There is much evidence that suggests the role of myeloperoxidase in the development of vulnerable plaque. We investigate the value of myeloperoxidase as marker of the presence of vulnerable plaques in patients with acute coronary syndrome. Myeloperoxidase activity was significantly high in serum of the patients with the diagnosis of acute coronary syndrome as reflection of the presence of vulnerable plaques. Increase in myeloperoxidase activity in serum of patients with the diagnosis of acute coronary syndrome precedes to myocardial damage.

Oxidative stress and associated oxidative damage are mediators of vascular injury and inflammation in many cardiovascular diseases, including hypertension, atherosclerosis, ischemic heart disease, diabetes. Xanthine oxidoreductase is one of the enzymes producing free radicals in the cardiovascular system, and it can contribute to the increment of the oxidative stress and, consequently, blood pressure. The xanthine oxidase is a molybdoenzyme capable of catalyzing the oxidation of hypoxanthine and xanthine in the process of purine metabolism. Xanthine oxidase can exist in two interconvertible forms, either as xanthine dehydrogenase or xanthine oxidase. The aim of the paper was investigate the activity xanthine oxidoreductase in the plasma patients with age related cataract, with hypertensive, and with heart failure. Clinical and biochemical researches were carried out in 73 patients with age related cataract, mean age 72±7 years, divided into group with hypertensive (N=35), with heart failure (N=22) and group normotensive and without heart failure (N=16). Plasma xanthine oxidoreductase activity was determined spectrophotometrically by measuring the formation of uric acid from hypoxanthine at 293 nm. The concentration of triglycerides (TG), total cholesterol (TC), LDL-C, HDL-C in plasma were determined. Our findings show a significantly increased activity xanthine oxidoreductase in plasma hypertensive patients (XO 9.18±1.5 U/L) (p< 0.001) and patients with heart failure (XO 10.44±1.53U/L) (p< 0.001), compared with values plasma xanthine oxidoreductase activity in normotensive and patients without heart failure (XOD 6.02±1.4 U/L). Concentrations of plasma TG, TC and LDL-C were elevated in groups with hypertensive and with heart failure, and we to find significant differences with group normotensive and without heart failure values. Elevated activity of plasma xanthine oxidoreductase contribute to the increasåd oxidative stress and may play a role in accelerated atherosclerosis. 

The increased protein concentration in cerebrospinal fluid is among most prominent biochemical parameter of intensified passage of macromolecules through blood-brain barrier. It is often found in cases of meningeal inflammation, neurodegeneration, neoplastic and traumatic processes developed on brain or spinal cord structures. Protein concentration in cerebrospinal fluid is often determined, but determination of albumin concentrations as well as mathematical models utilizing albumin are more reflective to the pathologic processes on the brain and spinal cord. Our study was limited to the determination of referent values for our laboratory for cerebrospinal fluid albumin concentrations, albumin quotient, as well as albumin transudat and exudat in the function of the age of probands. The results of the study show great agreement with previously published data.

Myeloperoxidase (MPO), a heme enzyme present in the primary granules of polymorphonuclear leukocytes (PMNs) participate in oxygen-dependent microbicidal activity of these cells. During the course of bacterial meningitis plenty of PMNs leave blood vessels and migrate to cerebrospinal fluid (CSF) space, and some of their MPO may become, extracellular. MPO activity in control CSF is low (Me = 0.5 U/L), comparing with patients CSF samples of all three groups of proteinorrachia where elevated values were found already on admission (3.5 U/L, 5.0 U/L and 12.0 U/L, respectively), with highest values found during second lumbal punction (5.5 U/L, 7.5 U/L and 14.0 U/L, respectively). Poor correlation was found between albumin quotient and MPO activity CSF/serum, but significant correlation between MPO in CSF and CSF PMNs count.

Nitric oxide (NO) is a major messenger molecule that plays key roles in many physiological processes. NO is produced by nitric oxide synthase (NOS), which catalyzes the conversion of L-arginine to L-citruline and NO. At least three isoforms of NOS have been identified and characterized, namely, neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynytrite, produced from the diffusion controlled reaction betwen NO and another free radical, the suproxide anion. Peroxynitrite interacts with protein, DNAand lipids via direct oxidative reactions or via indirect radical mediated mechanisms

Reactive products of oxygen are among the most potent and omnipresent threats faced by the living organism. Intracellular accumulation of reactive oxygen species such as superoxide anion, hydrogen peroxide, hydroxyl radical, and peroxy radical, can arise from toxic insults or normal metabolic processes. These species may perturb the cell's natural antioxidant defence systems, resulting in damage to all of the major classes of biological macromolecules, including nuclear acids, proteins, carbohydrates and lipids. Oxidative stress has been defined as a disturbance in the prooxidant-antioxidant balance, resulting in potential cell damage. It has been implicated in several biological and pathological processes like ageing, inflammation, carcinogenesis, ischemia-reperfusion and in diseases including diabetes mellitus, atherosclerosis, and/or neurodegenerative diseases

Bone tissue infections caused by non-specific agents (non-specific osteomyelitis) occur most frequently among children and young individuals demanding surgical and antibiotic therapy, although with unpredictable clinical outcome. While mobilization of cellular response to infectious agents takes place, a bulk of oxygen-derived free radicals emerge with concomitant participation of various elements of endogenous antioxidative defense. Vitamin C is an endogenous antioxidant active in the aqueous phase. It is very likely that ostoemyelitic patients already have some kind of disorder in specific antioxidant system due to hematogenic origin of non-specific osteomyelitis. Our results show that serum total vitamin C concentrations among patients with non specific osteomyelitis are not significantly different from those obtained among control subjects. However, we found significantly different concentrations of ascorbate, dehyroascorbate and their concentration ratio in serum within osteomyelitic patients that points to enlarged consumption of ascorbate even before the bone localization of infection took place