Osteoarthritis (OA) is a group of overlapping disorders, which may have different aetiology but similar biological, morphologic and clinical outcome. In osteoarthritis, process will not encompass the joint cartilage only, but the entire joint, including sub-hondral bone, ligaments, capsule, and sinovial membrane and surrounding muscles. Osteoarthritis is a multi-factor disorder of sinovial joints, which occurs as result of mechanical and biological factors, which destabilise normal hondrocyte function, partitioning of cartilage, extra-cellular matrix and sub-hondral bone. The earliest changes, which are restricted to the joint cartilage surface only, do not cause any subjective feeling. The pain in arthrosis occurs (or re-occurs) a bit later, Diagnosis will be determined based on clinical exam as well as signs and symptoms present. Symptomatic and functional treatment of osteoarthritis as one of rheumatic disorders must be taken throughout years, sometimes throughout a lifetime. It encompasses application of many medications and physical therapy procedures.

Combination of insulin and metformin has been shown to improve glycaemic control in clinical trials, particularly in obese patients with diabetes type 2. Insulin therapy can improve function of pancreatic beta cells and periphery insulin activity in target cells in order to enhance glycaemic homeostasis (1, 2, 3). In our study we included obese patients with diabetes type 2 in the early stage of the disease. The study is partially retrospective and partially prospective. The study encompassed 40 patients split in two groups. The first group of 20 patientsreceived insulin therapy combined with metformin, while the patients of the second group were treated with oral antidiabetic drugs, sulfonylureas and metformin. Three months later, the group treated with insulin and metformin showed improvement in the monitored parameters, namely significant reduction in HbA1c (p = 0.003), MFBG (p = 0.0009), PPG (p = 0.028). Insulin therapy administered together with metformin, in obese patients with diabetes type 2, in the early stage of the disease, resulted in well regulated fasting blood glycaemia, as well as post challenge glycaemia and HbA1c.

Morphological aspect of tracheal preparations and pulmonary tissue was studied in vitro. The material was obtained from autopsy of newborns that died from different causes. Examinations were made in different gestational periods (immature 23-29 weeks; premature 30-37 weeks; mature >38 weeks). Material for examination was obtained up to 6 hours after death. Pulmonary and tracheal tissue was incubated for fixation in buffered formalin (10%). Special histochemical and histoenzymatic methods were used for coloring of pulmonary and tracheal tissue and the activity of ATP-ase and dopaoxidase was monitored. Cut out models were made in series of 7μ, 10 μ and 20 μ. In peripheral axons of tracheobronchial pathways, degenerative alterations of adrenergic nerve endings in lung inflammatory processes were documented. These morphologic neuronal changes were described: Walerians degeneration, neuro-axonal degeneration and segment demyelinisation. These changes are well seen with argentafine coloring (Sevier-Munger modification for nerve endings) and with dopaoxidase reaction. In mature newborns that died from respiratory distress syndrome, we found different forms of metabolic and toxic degenerative damage in peripheral axons, such as: segment demyelinisation, neurotubular fragmentation, Schwan cell proliferation, fragmentation and bulging out of axonal neurotubules and neurofilaments. In tracheo-bronchial tissue, chromafine granules are homogenously distributed on Lamina propria layer and through glandular structures. This gives as a contradiction, according to some authors, that adrenergic nerve fibers for muscle tissue are absent and that adrenaline and noradrenalin diffuse in muscle tissue from interstice.

The objective of the study was to analyze the doppler sonography findings of vertebrobasilar circulation (VB) in patients with Parkinson's disease. 40 patients were analyzed (25 men's and 15 women) with Parkinson's disease, average age was 61.9 years (SD=11.43), treated at the Clinic for Neurology in Tuzla. Device for doppler sonography was Multidop x 4. Doppler sonography findings of VB circulation were analyzed in order to computerized tomography (CT) findings of the brain (with or without ischemic lacunar lesions) and in order to presence of postural disturbances as one of dominant Parkinson's disease symptoms during actual hospitalization. Our results suggest that vertebrobasilar insufficiency is more frequent in patients with Parkinson's disease (no matter of type) and postural disturbances as a dominant symptom comparing to group of Parkinson's disease patients without postural disturbances. These results implicate the importance of doppler sonography findings of vertebrobasilar circulation in patients with Parkinson's disease and possibility of considering role of vertebrobasilar insufficiency in development of postural disturbances.

Numerous studies conducted on acetylsalicylic acid (ASA, aspirin) confirmed that ASA inhibits proliferation and induces apoptosis in various types of human cells. Therefore, it was of interest to examine possible effects of different concentrations of ASA on viability and proliferation of lymphocytes in the cell culture. After separation from blood, lymphocytes were suspended in RPMI 1640 medium and cultured at 37 degrees C. Solution of ASA was added to cultures after 24 h, in final concentrations of 1, 3 and 5 mmol/l. After 48 h, proliferative response was evaluated by WST-1 assay. Significant difference in viability between controls and cell cultures treated with ASA in three different concentrations was observed (p<0.01). Percents of viable cells in cultures after application of 1, 3 and 5 mmol/l ASA were 9.9%, 2.5% and 16.9% (compared to controls), respectively. To determine whether this cytotoxic effect was result of induction of apoptosis, DNA from cell cultures was isolated and subjected to agarose gel electrophoresis. Fragmentation of DNA was not detected, excluding apoptosis as possible cause of cytotoxic effects. Addition of ASA caused change of initial extracellular pH value for each treated culture. After addition of 1 mmol/l ASA, pH of culture was 7.19, after 3 mmol/L, 6.99 and after addition of 5 mmol/l solution, pH was 6.75. Decreased lymphocyte viability could be attributed to either the effects of the added substance or possible further acidification of cell cultures during three days of incubation.

The aim of this retrospective study was to evaluate the results of the immunosuppressive regiment in managing of IgA nephropathy associated with primary nephrotic syndrome at the Nephrology Clinic, University of Sarajevo Clinics Centre in period of 1997-2007. We studied 19 patients (4 women and 15 men) with idiopathic nephrotic syndrome, where pathomorphologic changes of IgA nephropathy were proved by kidney biopsy. The levels of diuresis, proteinuria, albuminemia, lipidemia and kidney function, as measure of efficiency of used therapy, were monitored. The IgA nephropathy present with the nephrotic syndrome was shown in 15.8% (19) patients underwent renal biopsy due to primary nephrotic syndrome in the period of observation. The average age of patients with IgA nephropathy was 34.9+/-14.1 years. Eight patients from this group were treated with corticosteroid therapy (1-1.5 mg/kg of body weight for 4 weeks, followed by 0.5 mg/ kg of body weight until therapeutic response was achieved, and finally gradual exclusion of therapy after eight weeks in responsive patients), 6 patients with corticosteroids and bolus cyclophosphamide (10-15 mg/kg BW), and in 5/19 patients cyclosporine therapy was used (3 mg/kg BW). Complete remission of nephrotic syndrome was achieved in 42.1% of the patients. In conclusion, in adults patients with primary nephrotic syndrome associated with IgA nephropathy, used immunosuppressive therapy resulted in a high percentage of achieved remissions.

Anticoagulant therapy is most commonly assessed by measuring the effect of the drug on global clotting assay, such as APTT. It is known that response of the APTT to heparin may be decreased in patients with high levels of factor VIII. In this work, we have attempted to determine in vitro conditions of experiment for obtaining relationship between different concentrations of heparin and values of APTT, and to investigate influence of factor VIII on correlation between concentrations of heparin and APTT. Measurement of the effect of heparin, added in vitro in normal coagulation control plasma (NCCP) showed that heparin in concentrations from 0.1 to 1.0 IU/mL prolonged APTT from 0.73 s to 99.26 s. Linearity of the relation of natural logarithm of APTT and concentration of added heparin in plasma for concentrations from 0.5 to 1.0 IU/mL (r = 0.995), and other characteristics of the validated method (RSD = 1.17%), made possible investigation of the influence of factor VIII addition in the solution. The addition of the Factor VIII concentrate, markedly influenced these APTT results. Increased factor VIII activity shortened the APTT, having more pronounced effect in the presence of the large amounts of heparin. Increased factor VIII was associated with downward shift in the concentration -- logAPTT response curve (y = 24644 x + 30.17 vs. y = 10.864 x + 27.256). This finding suggests the possibility for modeling of ex vivo establishment of correlation between plasma activity of FVIII and needed doses of heparin for appropriate management of heparin therapy.

This study investigated outcomes in patients undergoing coronary artery bypass grafting (CABG) without cardiopulmonary bypass (CPB), who needed conversion to CPB. Between September, 1998 and September, 2003, 1000 CABG procedures were performed in a Cardiovascular Clinic, University Clinical Centre Tuzla. Multivessel CABG were selected arbitrarily for CABG without CPB (OPCAB) or CABG with CPB (ONCAB). Patients who required conversion due to technical difficulty with grafting were performed with ONCAB including cardioplegic arrest. Patients with severe hemodynamic instability and cardiac arrest were performed as ONCAB without crossclamping, while patients converted for mild to moderate hemodynamic instability were given cardioplegic arrest or not, depending on surgeon preference. 493 operations were scheduled and performed as ONCAB (49.3%), 468 as OPCAB (46.8%) and 39 originally scheduled OPCAB operations were converted to ONCAB (7.7% of originally scheduled OPCAB patients or 3.9% of total number of CABG). Reasons for conversions were: mild to severe hemodynamic instability--28 (71.8%); poor vessels or difficult graft revision--11 (28.2%). Patients converted because of technical difficulty or mild hemodynamic instability behaved as regular ONCAB patients. In the 9 patients who were emergently converted due to cardiac arrest or ventricular fibrillation, 3 patients had stroke and 3 severe myocardial ischemia requiring intraaortic balloon pump. It is of great importance to keep conversions to CPB due to cardiac arrest at a low level. The serious complications seen in such patients can significantly impede the overall benefits of a successful OPCAB program.