Browsing by Author "Jozic, Tanja (6504760115)"

Background Rapid clinical decision-making on further management of patients with out-of-hospital cardiac arrest may be challenging. Recently, a “futility” score (NULL-PLEASE) incorporating multiple adverse resuscitation features (Nonshockable rhythm, Unwitnessed arrest, Long no-flow or Long low-flow period, blood PH <7.2, Lactate >7.0 mmol/L, End-stage chronic kidney disease on dialysis, Age ≥85 years, Still resuscitation, and Extracardiac cause) has been proposed to help identify patients with out-of-hospital cardiac arrest unlikely to survive; however, external independent score validation is lacking. Methods We retrospectively validated the NULL-PLEASE predictive ability for early in-hospital outcome of out-of-hospital cardiac arrest in a single-center cohort of 547 consecutive patients with out-of-hospital cardiac arrest who were admitted from April 2013 to October 2016 (mean age, 66.3 ± 13.2 years); 227 patients (41.5%) died. Because pH and lactate were inconsistently measured, a modified NULL-PLEASE score excluding both variables was calculated as the principal analysis. A sensitivity analysis included the subgroup with pH data available (n = 177). Results Long low-flow period and age ≥85 years were independently associated with fatal outcome (both P <.001). Patients with a modified NULL-PLEASE score of ≥5 had a 3.3-fold greater risk of fatal outcome compared with a score of 0 to 4 (odds ratio, 3.34; 95% confidence interval [CI], 2.29-4.89; P <.001); 77% of nonsurvivors had a score ≥5; NULL-PLEASE showed a modest predictive ability for fatal outcome (c-statistic 0.658; 95% CI, 0.613-0.704; P <.001). Sensitivity analysis yielded similar results, with 88% of nonsurvivors having a score ≥5. Conclusions The NULL-PLEASE score was predictive for early in-hospital outcome of out-of-hospital cardiac arrest, with a 3.3-fold greater odds for fatal outcome at the score values of ≥5. © 2017 Elsevier Inc.

Background: Polymorphisms in genes encoding tumor necrosis factor-α (TNF-α) and its receptor TNF-R1 have been shown to affect one person's susceptibility to develop certain neoplastic diseases. The aim of the present association study was to investigate whether single nucleotide polymorphisms (SNPs) in TNF-α (−308G>A) and TNF-R1 (36A>G) genes modulate the susceptibility for keratocystic odontogenic tumors (KCOTs) development in Serbian patients. Methods: Genotyping was performed in 60 KCOT patients and 125 healthy individuals, using polymerase chain reaction/restriction fragment length polymorphism analysis. Results: A significant difference in genotype and allele frequencies was found between patients and controls for both SNPs (P < 0.05). Carriers of the TNF-α A variant had an eightfold increase of KCOT risk (OR = 8.12, 95% CI = 3.98–16.56, P < 0.0001), while carriers of the TNF-R1 G variant had approximately a fourfold increase of KCOT risk (OR=3.65, CI: 1.60–8.40, P = 0.001). Conclusions: Our findings suggest that the two polymorphisms are strong risk factors for KCOT development in Serbian population. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd

Background: Polymorphisms in genes encoding tumor necrosis factor-α (TNF-α) and its receptor TNF-R1 have been shown to affect one person's susceptibility to develop certain neoplastic diseases. The aim of the present association study was to investigate whether single nucleotide polymorphisms (SNPs) in TNF-α (−308G>A) and TNF-R1 (36A>G) genes modulate the susceptibility for keratocystic odontogenic tumors (KCOTs) development in Serbian patients. Methods: Genotyping was performed in 60 KCOT patients and 125 healthy individuals, using polymerase chain reaction/restriction fragment length polymorphism analysis. Results: A significant difference in genotype and allele frequencies was found between patients and controls for both SNPs (P < 0.05). Carriers of the TNF-α A variant had an eightfold increase of KCOT risk (OR = 8.12, 95% CI = 3.98–16.56, P < 0.0001), while carriers of the TNF-R1 G variant had approximately a fourfold increase of KCOT risk (OR=3.65, CI: 1.60–8.40, P = 0.001). Conclusions: Our findings suggest that the two polymorphisms are strong risk factors for KCOT development in Serbian population. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd