The effects of different syringe volume, needle size and sample volume on blood gas analysis in syringes washed with heparin

Introductıon: We evaluated the effect of different syringe volume, needle size and sample volume on blood gas analysis in syringes washed with heparin. Materials and methods: In this multi-step experimental study, percent dilution ratios (PDRs) and final heparin concentrations (FHCs) were calculated by gravimetric method for determining the effect of syringe volume (1, 2, 5 and 10 mL), needle size (20, 21, 22, 25 and 26 G) and sample volume (0.5, 1, 2, 5 and 10 mL). The effect of different PDRs and FHCs on blood gas and electrolyte parameters were determined. The erroneous results from nonstandardized sampling were evaluated according to RiliBAK’s TEa. Results: The increase of PDRs and FHCs was associated with the decrease of syringe volume, the increase of needle size and the decrease of sample volume: from 2.0% and 100 IU/mL in 10 mL-syringe to 7.0% and 351 IU/mL in 1 mL-syringe; from 4.9% and 245 IU/mL in 26G to 7.6% and 380 IU/mL in 20 G with combined 1 mL syringe; from 2.0% and 100 IU/mL in full-filled sample to 34% and 1675 IU/mL in 0.5 mL suctioned sample into 10 mL-syringe. There was no statistical difference in pH; but the percent decreasing in pCO2, K+, iCa2+, iMg2+; the percent increasing in pO2 and Na+ were sta-tistical significance compared to samples full-filled in syringes. The all changes in pH and pO2 were acceptable; but the changes in pCO2, Na+, K+ and iCa2+ were unacceptable according to TEa limits except fullfilled-syringes. Conclusions: The changes in PDRs and FHCs due nonstandardized sampling in syringe washed with liquid heparin give rise to erroneous test results for pCO2 and electrolytes

Pankreatikopyelostominin pankreas ve böbrek fizyolojilerine etkisi

Bu tezin, veri tabanı üzerinden yayınlanma izni bulunmamaktadır. Yayınlanma izni olmayan tezlerin basılı kopyalarına Üniversite kütüphaneniz aracılığıyla (TÜBESS üzerinden) erişebilirsiniz.[Abstarct Not Available

Interleukin-1B (-511) gene polymorphism is associated with acute coronary syndrome in the Turkish population

Objectives: acute coronary syndrome (ACS) is defined as an inflammatory disease associated with development of atherosclerosis and instability. IL-1 is a candidate inflammatory cytokine that is thought to trigger ACS. The purpose of this study was to determine the relationship between IL-1 gene family polymorphisms (IL-1RN, IL-1B in positions -511 and +3953) and ACS in the Turkish population. Methods: a total of 381 people participated in the study, with 117 control subjects and 264 ACS patients. Of the 264 ACS patients, 112 were diagnosed with stable angina pectoris (SAP) and 152 were diagnosed with unstable angina pectoris (USAP). The polymerase chain reaction (PCR) was used to determine the genotype of IL-1RN. The genotypes of IL-1B (-511 and +3953) were determined by PCR, followed by restriction enzyme digestion of the PCR products. Results: there were no significant differences in both IL-1RN, IL-1B (-511 and +3953) genotype distributions and IL-1RN allele frequencies between ACS patients and the control subjects. In addition, no association was observed in the allele frequency of IL-1B (-511 and +3953) between ACS patients and controls (p = 0.113 and p = 0.859, respectively), or between SAP patients and controls (p = 0.575 and p = 0.359, respectively). However, IL-1B allele 1 (C) (-511) polymorphism in USAP patients was found to be significantly different from that of control subjects (p = 0.041, OR: 2.01; 95% CI: 1.985-3.933). A significant difference was also observed between USAP and SAP patients for IL-1B (+3953) allele 1 (C) polymorphism; (p = 0.043, OR: 1.522; 95% CI: 1.012-2.88). Conclusion: these results show that IL-1RN gene polymorphism has no association with ACS. However, the allele 1 (C) of IL-1B (-511) may be a risk factor for susceptibility to USAP in the Turkish population

Multiple sclerosis: association with the interleukin-1 gene family polymorphisms in the Turkish population

Background: Multiple Sclerosis (MS) is a neurodegenerative disease. It involves inflammation and demyelination. Since cytokines play an important role in the development of MS, genes encoding cytokines such as the Interleukin (IL)-1 family are candidate genes for MS susceptibility. Objective: To determine the relationship between IL-1 gene family and MS in the Turkish population. Methods: A total of 409 MS patients and 256 healthy controls were included in the study. IL-1A -889 (rs1800587), IL-1 RN variable number tandom repeat (VNTR), IL-1B -511 (rs 16944) and IL-1B +3953 (rs 1143634) polymorphisms were investigated from the genomic DNA, obtained via blood samples. Results: No association was found between IL-1A and IL-1RN polymorphisms and susceptibility to MS. However, we have found significantly decreased frequency of IL-1B -511 genotype (p = 0.004) in MS patients compared to controls. In addition, there was a significant association between IL-1B -511 (1/2) genotype and early onset MS (EOMS) (p = 0.0001). Conclusions: Individuals with the 2/2 genotype of IL-1B -511 have significantly decreased incidence of MS, suggesting a protective role for this genotype in the Turkish population. Additionally, IL-1B -511(1/2) genotype was determined as a possible risk factor for EOMS

Assessment of Interleukin-1 Gene Cluster Polymorphisms in Lone Atrial Fibrillation: New Insight into the Role of Inflammation in Atrial Fibrillation

BackgroundSystemic inflammation is accepted as one of the pathophysiological mechanisms of atrial fibrillation (AF). The role of inflammation has been shown previously. Interleukin (IL) system is the main modulator of the inflammatory responses and genetic polymorphisms of IL-1 cluster genes are associated with increased risk for inflammatory diseases. ObjectivesTo investigate the association between polymorphisms of IL-1 cluster genes and lone AF. Subjects and MethodsDNA samples were collected from 70 proven lone AF patients and 70 healthy subjects. Genomic DNA was typed for the variable number of the tandem repeat (VNTR) IL-1 receptor antagonist (RN) gene polymorphism, IL-1B -511 C > T(rs16944) promoter polymorphism, and +3953 C > T(rs1143634) polymorphism in exon 5 by polymerase chain reaction. ResultsIn lone AF group the frequency of IL-1RN2/2 and IL-1RN1/2 genotypes were higher than in the control group (7.2% vs 4.3% and 48.5% vs 22.8%, respectively; (2) = 14.1; P = 0.028). The frequency of allele 2 was significantly higher in the lone AF group (32.1% vs 15.7%; (2) = 10.7; P = 0.005). Allele and genotype distribution of IL-1B -511 C > T and +3953 C > T polymorphisms were not statistically different between the groups. C-reactive protein (CRP) levels were higher in lone AF patients compared to the control group (median = 1.25, interquartile range [IQR] = 0.85 vs median = 1.08, IQR 0.46 mg/L, respectively; P = 0.02). In multivariate regression analysis, presence of allele 2 of IL-1 VNTR polymorphism and elevated plasma high-sensitive-CRP levels were the independent predictors of lone AF. ConclusionPresence of allele 2 of VNTR polymorphism of IL-1RN gene may cause increased risk for lone AF probably due to the inadequate limitation of inflammatory reactions

Novel Growth Hormone Receptor Gene Mutation in a Patient with Laron Syndrome

Growth Hormone (GH) is a 22 kDa protein that has effects on growth and glucose and fat metabolisms. These effects are initiated by binding of growth hormone (GH) to growth hormone receptors (GHR) expressed in target cells. Mutations or deletions in the growth hormone receptor cause an autosomal disorder called Laron-type dwarfism (LS) characterized by high circulating levels of serum GH and low levels of insulin like growth factor-1 (IGF-1). We analyzed the GHR gene for genetic defect in seven patients identified as Laron type dwarfism. We identified two missense mutations (S40L and W104R), and four polymorphisms (S473S, L526I, G168G and exon 3 deletion). We are reporting a mutation (W104R) at exon 5 of GHR gene that is not previously reported, and it is a novel mutation

Effects of selected antibiotics on pancreatitis induced liver and pulmonary injury.

OBJECTIVE: To investigate the protective effect of antibiotherapy in the early phase of acute pancreatitis on cellular injury induced in lungs and liver. BACKGROUND: Cellular viability and plasma nitric oxide (NO) levels were assessed to determine the efficacy of highly bactericidal imipenem and quinolones on liver and lung injury. METHODS: Imipenem, levofloxacin or saline were administered to rats with caerulein induced pancreatitis. Twenty-four hours later serum amylase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and NO levels, pancreatic interstitial inflammation, acinar cell necrosis, acinar cell vacuolisation, peripancreatic fat necrosis; spotty necrosis, focal inflammation of liver and inflammatory processes in the lungs were assessed. RESULTS: Enzyme levels in the antibiotherapy groups were lower than in the control group. Serum NO levels were higher only in the imipenem group. Levofloxacin decreased acinar cell vacuolisation in the pancreas; interstitial edema, neutrophilic infiltration and interstitial enlargement in the lungs. Antibiotherapy decreased spotty necrosis, apoptosis and focal inflammation in the liver. CONCLUSIONS: Although treatment with imipenem is associated with higher NO levels than levofloxacin, levofloxacin prevents organ injury more effectively than imipenem in acute pancreatitis. Our results indicate that antibiotherapy in the early period of necrotizing pancreatitis prevents cellular damage induced in pancreas, liver and lungs