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Growing body of evidence suggests that molecular markers are an important prognostic marker for non-small lung cancer (NSCLC). Using targeted therapy based on these markers leads to improved outcomes in lung adenocarcinoma. However, progress of targeted therapy in squamous lung cancer is still modest. p16(ink) protein acts as tumor suppressor and vascular endothelial growth factor (VEGF) promotes tumor angiogenesis. Purpose of this study was to evaluate the difference in p16(ink4) and VEGF expression between squamous and adenocarcinoma of the lung; to evaluate the relationship of p16(ink4) and VEGF expression to survival outcomes in NSCLC patients, and the difference of their prognostic values between squamous and adenocarcinoma subtypes. 100 NSCLC patients (50 squamous and 50 adenocarcinoma) and 80 healthy individuals were included. p16(ink4) and VEGF proteins were immunohistochemicaly detected on formalin-fixed tissues. One- and 2-year progression-free survival (PFS) and overall survival (OS) were observed. p16(ink4) expression was significantly lower in squamous type compared to adenocarcinoma. In both squamous and adenocarcinoma, high VEGF expression correlated with worse 1-year PFS and OS, but only with worse 2-year PFS. Low p16(ink4) expression correlated with worse 1- and 2-year PFS, as well as OS, in both NSCLC subtypes. In squamous lung cancer p16(ink4) expression was an independent negative prognostic marker. Our study confirms the difference of p16(ink4) protein expression in squamous and adenocarcinoma of the lung. Besides anti-VEGF therapy, the regulation of p16(ink4) expression could have a therapeutic potential in NSCLC, especially in squamous lung cancer.

B. Prnjavorac, Amina Deljkić, Albina Sinanović, R. Sejdinović, Amila Mehedović, J. Jukić, K. Krajina, L. Šaranović et al.

Background Recommended by Resolution of Immunotherapy, issued by EAACI, Specific immunotherapy (SIT) was established as a mainstream method of treating allergic diseases. SIT produces long term challenges. SIT team should be aware that at first injection of allergen, the immunotherapy may cause a long lasting reaction. Anaphylaxis during SIT is very rare, but it is possible. We’ve experienced anaphylaxis after four year of SIT, against ragweed allergen.

B. Prnjavorac, R. Sejdinović, J. Mehić, Albina Sinanović, Zlata Hajrić, D. Avdić, Omer Bedak, Jasmin A Fejzic et al.

BACKGROUND: Pulmonary embolism (PE) is many times life treating disease, and the diagnosis should be achieved as soon as possible. Presence of fever may be or not present at the start of PE. Haemoculture should be performed any time if PE is linked with fever. It is very important to check out any symptom and sign of PE. D-dimmer may only exclude the diagnosis, but for this purpose it is very important. AIM: To analyze the most important predictors for clinical course and outcome of septic or no septic PE: METHODS: Patients with PE treated in Department of Pulmology in General Hospital Tesanj. PE was considered if Geneve score was five points or more. For any patient CT scan of the chest, chest X-ray at admission, and 4th, 7th and 14th day of hospitalization. Lactat-dechidrogenase, Creatin-kinase, CRP, D-dimmer, ECG and blood gas analyzes were performed, so. RESULTS: During one year of follow up 36 patients were considered for PE, according to Geneve score, among them 11 with septic embolie. In patients with no septic PE no changes on control Chest X-ray were seen, but in any of septic ones X-ray appearance showed progression. Other parameters were nearly the same, with moderate higher level of CRP in PE. The gold standard for diagnosis of PE rest double scintigrafic imaging of the lung, with ventilation and perfusion phase. D-dimmer is very useful parameter to exclude if PE is not occurred. CONCLUSION: The most important parameter to distinguish septic or no septic PE was dynamic changes of chest X-ray appearance with substantial more progression in septic than in non septic ones.

Introduction: Several decades of basic science and animal research provided considerable support for significant role of plasma free fatty acids (FFAs) in etiology of Type 2 diabetes mellitus (T2DM). Contradicting data related to signifi cance of elevated FFAs in plasma of patients with Type 2 diabetes prompted us to study concentrations of palmitic acid, stearic acid, and linoleic acid, in patients and healthy controls in an attempt to possibly use them as potential biomarkers in progression of the disease. Since aging is associated withincreased plasma glucose and insulin levels that are consistent with an insulin resistant state, in this study,age differences in the concentration of the above mentioned acids were tested.Methods: Progressive changes in their concentrations were followed through a period 6 months. All subjects included in the study were free of evidence of hepatitis B or C viral infection or active liver and kidney damage. Analysis of glucose and glycated hemoglobin levels were performed on BT PLUS 2000 analyzer using standard IFCC protocols, while concentrations of FFAs were analyzed by gas chromatography.Results: Our data demonstrated signifi cantly higher FFA values in plasma of diabetic patients as compared to healthy controls. There was a trend of correlation of FFAs levels with the blood glucose levels in diabetic patients, which was more prominent in diabetic men than in women.Conclusion: With aging, levels of free fatty acids signifi cantly increased in plasma of diabetic patients, and this effect was also more profound in male than in female diabetics.

T. Dujic, T. Bego, B. Mlinar, S. Semiz, M. Malenica, B. Prnjavorac, Barbara Ostanek, J. Marc et al.

Introduction: The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) catalyzes the conversion of the hormonally inactive cortisone to active cortisol, thus facilitating glucocorticoid receptor activation in target tissues. Increased expression of 11β-HSD1 in adipose tissue has been associated with obesity and insulin resistance. In this study, we investigated the association of two 11β-HSD1 gene (HSD11B1) polymorphisms with the metabolic syndrome (MetS) and its characteristics in the Bosnian population. Materials and methods: The study included 86 participants: 43 patients diagnosed with MetS and 43 healthy controls. Subjects were genotyped for two HSD11B1 gene polymorphisms: rs846910: G>A and rs45487298: insA, by the high resolution melting curve analysis. Genotype distribution and an influence of genotypes on clinical and biochemical parameters were assessed. Results: There was no significant difference in the mutated allele frequencies for the two HSD11B1 gene polymorphisms between MetS patients and controls. In MetS patients, no significant associations between disease-associated traits and rs45487298: insA were found. Regarding rs846910: G>A variant, heterozygous patients (G/A) had significantly lower systolic (P = 0.017) and diastolic blood pressure (P = 0.015), lower HOMA-IR index (P = 0.011) and higher LDL-cholesterol levels (P = 0.049), compared to the wild-type homozygotes. In the control group, rs45487298: insA polymorphism was associated with lower fasting plasma insulin levels (P = 0.041), lower homeostasis model assessment insulin resistance (HOMA-IR) index (P = 0.041) and lower diastolic blood pressure (P = 0.048). Significant differences between rs846910: G>A genotypes in controls were not detected. Haplotype analysis confirmed the association of rs45487298: insA with markers of insulin resistance in the control subjects. Conclusions: Our results indicate that a common rs45487298: insA polymorphism in HSD11B1 gene may have a protective effect against insulin resistance.

Objective: The primary goal of this study was to determine the difference of abundance of CD4+, CD8+ and CD56+ bronchoalveolar fluid’s lymphocytes and their subpopulations between cancerous lung and healthy lung from the same patient. Methods: Mini-bronchoalveolar lavage was taken from 55 patients from lung with cancer and healthy lung. After laboratory processing and addition of CD4, CD8, CD27, CD28 and CD56 antibody, the material was analyzed by flow cytometer. Results from lung with cancer were compared to the ones from the healthy lung. The examined patients were the test and the control group at the same time. Results: CD27+28+ forms of CD4+ and CD8+ lymphocytes are more activated in the cancerous lung compared to healthy lung, while the CD27-28- forms are less activated in diseased lung. CD4+ forms of CD56+ lymphocytes are more activated in cancerous lung compared to the health lung, while the CD8+ forms are less activated in diseased lung. Conclusion: Immature helper and cytotoxic T lymphocyte response, as well as regulatory NK and NKT cell response are more activated in cancerous lung compared to the health lung of the same patient.

Aim: To study correlation of IgE level and C-reactive protein (CRP) for exacerbation of the disease in asthmatic patients. Methods: Asthmatic subject were examined for achieving of asthma control according to GINA recommendation. Numbers of exacerbation of asthma during one month were analyzed. The patients were followed in six month period (since first January to 30th of Jun. Average monthly days of exacerbations was calculated. IgE level in the blood was measured using Enzyme-linked Immunoassay (ELISA), and CRP was measured by immunotubidimetry. Assessment of asthma control was considered using Asthma Quality of Life Questionnaire (AQLQ). Results: The study includes 63 patients with asthma. Average level of IgE was 674 IU/mL (SD 167), range 56-3785 IU/mL, 1 IU=3,2 ng; average level of CRP was 16,4 mg/mL (SD 6,3), range 5-48; Average number of days in exacerbation during one month was 3,6 (SD 2,4), and varied from zero, patients with no exacerbation, to 21. Using test of multiple correlation it was shown statistical significant correlation (level p<0,05) between IgE and CRP from one side, and number of days with exacerbation from the other. Patients with higher level of CRP were most likely to have exacerbation, than those with higher level of IgE. AQLQ was worse in those with higher level of CRP, than in those with higher level of IgE. Conclusion: In this study CRP was shown as stronger predictor of asthma exacerbation and worse quality of life than total IgE level in asthmatic subjects.

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