BACKGROUND/OBJECTIVE: Aetiology and significance of exercise-induced troponin release remains a contentious issue. We investigated the effect of a 28 km mountain run on cardiac troponin I (cTnI), in relation to training, performance, nutritional, biochemical and echocardiography variables, in a group of 25 recreational male master athletes. MATERIAL AND METHODS: A comprehensive list of variables related with nutrition, training, performance and echocardiography, was collected pre- and post-race. Twenty-four months later, outcomes regarding cardiovascular events were obtained. RESULTS: Serum cTnI values were increased after the race, with mean values rising from 7.2 +/- 2.2 (before) to 80.0 +/- 33.2 ng/L (post race), (p < 0.001) and 23/25(92%) exceeding Upper Reference limit (50 ng/L). Echocardiography did not reveal significant alterations, or correlations with cTnI values. The percentage difference in hs-cTnI concentrations pre- and post-race correlated positively with age, race-induced changes of selected muscle damage indices, resistance training volume and negatively with endurance capacity and training volume (r: -0.727 to 0.725, p < 0.05). All athletes reported no cardiovascular event during the 24-month period post-race. CONCLUSION: cTnI elevation induced by a 28 km mountain running race was not correlated with echocardiographic, nutritional parameters and was less pronounced in athletes with larger endurance training history, in contrast with resistance training and age

Clinicians trust medical laboratories to provide reliable results on which they rely for clinical decisions. Laboratories fulfil their responsibility for accurate and consistent results by utilizing an arsenal of approaches, ranging from validation and verification experiments to daily quality control procedures. All these procedures verify, on different moments, that the results of a certain examination procedure have analytical performance characteristics (APC) that meet analytical performance specifications (APS) set for a particular intended use. The APC can in part be determined by estimating the measurement uncertainty component under conditions of within-laboratory precision (u(Rw)), which comprises all components influencing the measurement uncertainty of random sources. To maintain the adequacy of their measurement procedures, laboratories need to distinguish aspects that are manageable vs. those that are not. One of the aspects that may influence u(Rw) is the momentary significant bias caused by shifts in reagent and/or calibrator lots, which, when accepted or unnoticed, become a factor of the APC. In this paper, we postulate a model for allocating a part of allowable u(Rw) to between-reagent lot variation, based on the need for long-term consistency of the measurement variability for that specific measurand. The allocation manages the ratio between short-term and long-term variation and indicates laboratories when to reject or correct certain variations due to reagent lots

BACKGROUND: Burn injury (BI) is one of the most serious causes of morbidity and mortality in the pediatric population. BI triggers an initial stage of hyperinflammation, followed by hypersecretion of both pro- and anti-inflammatory cytokines. IL- 18 is a vital pro-inflammatory cytokine, the effect of which has been investigated not only in animal models but also in adult patients. No study has yet examined the association of serum IL- 18 levels and the clinical significance in the course of pediatric BI. METHODS: We conducted a prospective study including all children with burn injuries who were hospitalized from December 2015 to December 2018 in a tertiary Children's Hospital. RESULTS: A total of 55 children with BI were included. In the present study, we found a strong positive correlation between total body surface area (TBSA) and the levels of IL-18 at admission and on the third day postburn, respectively. The WBC count, the number of lymphocytes and the CRP levels at admission revealed a strong, positive correlation with IL-18 levels. The correlation between IL-18 levels at admission and the length of stay (LOS) was moderate. CONCLUSIONS: This study has shown that the levels of IL-18 collected at admission correlate positively with the extent of TBSA and inflammatory indices in pediatric patients. Moreover, IL-18 levels at admission may not be the most accurate prognostic factor regarding the LOS. However, further research is needed in order to establish more accurate predictive factors for the outcome of BIs in pediatric patients

INTRODUCTION: This study evaluated complete blood count-derived inflammation indices in patients with retinal vein occlusion (RVO). METHODS: Participants in this case-control study were 54 patients with RVO and 54 age- and sex-matched control subjects. All participants underwent a thorough ophthalmic examination, as well as blood sample testing for complete blood count. Comparison of all parameters derived from complete blood count as well as calculation of specific indices was performed between patients with RVO and controls. RESULTS: Patients with RVO presented significantly higher white blood cell count (p = 0.033), neutrophil count (p = 0.003), neutrophil-to-lymphocyte ratio (NLR, p = 0.002), red cell distribution width (RDW, p = 0.009), mean platelet volume (MPV, p = 0.023), and systemic immune-inflammatory index (SII, p = 0.007) compared to controls. Receiver operator characteristic curve (ROC) analysis showed that NLR was superior to other inflammatory indices, having the greatest area under the curve. The optimal cutoff value for NLR to predict RVO was 2.29 with 46.2% sensitivity and 77.8% specificity. CONCLUSION: Patients with RVO presented increased NLR, RDW, MPV, and SII, providing evidence that inflammation plays an important role in the pathogenesis of RVO. Complete blood cell count-derived indices can be easily calculated and may serve as an easy, simple, and cost-effective tool to evaluate the degree of systemic inflammation in patients with RVO, so as to potentially guide treatment

PURPOSE: To evaluate the association between serum vitamin B12/folate and retinal vein occlusion (RVO). METHODS: A comprehensive search of the PubMed database was performed, which identified 271 abstracts to be screened. Ten studies met our inclusion criteria and a meta-analysis of these comparative case-control studies was performed on the mean +/- standard deviation serum vitamin B12 and folate levels, without language restrictions. Nine studies with 720 patients with RVO and 613 controls were included in the meta-analysis for vitamin B12, and 10 studies with 784 patients with RVO and 677 controls in the meta-analysis for folate. RESULTS: There was no statistically significant difference between patients with RVO and controls in serum vitamin B12 levels (mean difference: - 40.25 pg/mL, p = 0.28), either central RVO (mean difference: - 18.24 pg/mL, p = 0.71) or branch RVO (mean difference: - 23.56 pg/mL, p = 0.48). On the contrary, the plasma folate level was significantly lower in RVO patients than in controls (mean difference: - 1.34 ng/mL, p = 0.001), as well as in patients with CRVO compared to controls (mean difference: - 1.48 ng/mL, p = 0.006), but not in BRVO patients (mean difference: - 0.72 ng/mL, p = 0.11). CONCLUSIONS: RVO is associated with low serum folate levels, but not with serum vitamin B12 levels

Accumulating data has shown a contribution of the renin-angiotensin system in COVID-19 pathogenesis. The role of angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism as a risk factor in developing COVID-19 disease comes from epidemiological data and is controversially discussed. We conducted a retrospective case-control study and assessed the impact of ACE I/D genotype in COVID-19 disease prevalence and severity. In 81 COVID-19 patients explicitly characterized and 316 controls, recruited during the first wave of COVID-19 pandemic, ACE I/D genotype, and ACE activity were determined. A generalized linear model was used and Poisson regression analysis estimated the risk ratios (RRs) of alleles and genotypes for disease severity. DD patients had almost 2.0-fold increased risk (RR: 1.886, confidence limit [CL] 95%: 1.266-2.810, p = 0.0018) of developing a more severe disease when contrasted to ID and II individuals, as did D allele carriers compared to I carriers (RR: 1.372; CL 95%: 1.051-1.791; p = 0.0201). ACE activity (expressed as arbitrary units, AU/L) was lower in patients (3.62 +/- 0.26) than in controls (4.65 +/- 0.13) (p < 0.0001), and this reduction was observed mainly among DD patients compared to DD controls (3.97 +/- 0.29 vs. 5.38 +/- 0.21; p = 0.0014). Our results demonstrate that ACE DD genotype may predispose to COVID-19 increased disease severity via a mechanism associated, at least in part, with the significant fall in their ACE activity. Our findings suggest a more complex pattern of synergy between this polymorphism and ACE activity in COVID-19 patients compared to healthy individuals and set the grounds for large-scale studies assessing ACE genotype-based optimized therapies with ACE inhibitors and angiotensin receptor blockers

BACKGROUND: the apolipoprotein e4 allele (APOE4) constitutes an established genetic risk factor for Alzheimer's Disease Dementia (ADD). We aimed to explore the frequency of the APOE isoforms in the Greek population of Southern Greece. METHODS: peripheral blood from 175 Greek AD patients, 113 with mild cognitive impairment (MCI), and 75 healthy individuals. DNA isolation was performed with a High Pure PCR Template Kit (Roche), followed by amplification with a real-time qPCR kit (TIB MolBiol) in Roche's Light Cycler PCR platform. RESULTS: APOE4 allele frequency was 20.57% in the ADD group, 17.69% in the MCI group, and 6.67% in the control group. APOE3/3 homozygosity was the most common genotype, while the frequency of APOE4/4 homozygosity was higher in the AD group (8.60%). APOE4 carrier status was associated with higher odds for ADD and MCI (OR: 4.49, 95% CI: [1.90-10.61] and OR: 3.82, 95% CI: [1.59-9.17], respectively). CONCLUSION: this study examines the APOE isoforms and is the first to report a higher APOE frequency in MCI compared with healthy controls in southern Greece. Importantly, we report the occurrence of the APOE4 allele, related to ADD, as amongst the lowest globally reported, even within the nation, thus enhancing the theory of ethnicity and latitude contribution

Multiple lines of evidence support an immunologic response along with inflammation to be implicated in the pathophysiology of primary rhegmatogenous retinal detachment (RRD) and the development of proliferative vitreoretinopathy (PVR). The purpose of this review is to provide an update on the signaling molecules in the vitreous and subretinal fluid (SRF) involved in these processes. A detailed literature search was performed in PubMed database until November 2021. We identified all papers referring to inflammatory and immunological mediators in the context of primary RRD and in cases complicated by PVR. We analyzed prospective and retrospective cohort studies and reference lists of the retrieved articles. A comprehensive investigation of immunological and inflammatory responses provides significant evidence for the implication of varying signaling molecules in the pathophysiology of RRD and the development of PVR. The reviewed series has revealed that disruption of the normal equilibrium during these processes may be present in the vitreous and SRF of these eyes. The precise role of cytokines, chemokines, and growth factors in the pathophysiology of these disorders remains to be clearly elucidated. Overall, immunological and inflammatory signaling molecules are widely implicated in both primary RRD and PVR. The reviewed literature indicates that precise knowledge concerning the pathological milieu sheds light on the underlying pathophysiology and potential therapeutic targets and highlights unmet needs to be addressed by future research

AIMS: To investigate potential laboratory and imaging biomarkers as treatment response predictors to intravitreal anti-vascular endothelial growth factor (anti-VEGF) agents in patients with retinal vein occlusion (RVO). METHODS: Participants in this prospective study were 53 patients with treatment naive macular edema secondary to RVO, treated with intravitreal anti-VEGF agents and followed-up for 12 months. At baseline, all participants underwent best-corrected visual acuity measurement, dilated fundoscopy, optical coherence tomography and fluorescein angiography (FFA), while full blood count and biochemical analysis of various parameters was also performed. At month 12, treatment response was examined and classified as "favorable" or "non-response". Potential associations between laboratory/imaging biomarkers and treatment response were assessed. RESULTS: Univariate analysis showed that "favorable" response at month 12 after initiation of anti-VEGF treatment was correlated with baseline central subfield thickness (CST) < 464 mum (p < 0.001), absence of subretinal fluid (p = 0.004), absence of hyperreflective foci (HF) (p = 0.004), intact ellipsoid zone (EZ) and external limiting membrane (ELM) (p < 0.001 and p = 0.001, respectively), absence of epiretinal membrane (ERM) (p = 0.020) and absence of macular ischemia on FFA (p < 0.001), while increased monocytes-to-lymphocytes ratio was also associated with "favorable" treatment response (p = 0.010). All other laboratory parameters did not reach statistical significance. However, at the multivariate analysis, EZ and ELM status, HF, macular ischemia and monocytes-to-lymphocytes ratio were found to be independent predictors of treatment response. CONCLUSIONS: Intact EZ and ELM, absence of HF, absence of macular ischemia and increased monocytes-to-lymphocytes ratio at baseline can predict "favorable" treatment response in patients with treatment naive macular edema secondary to RVO

Vitamin D receptor (VDR) gene single nucleotide polymorphisms (SNPs) have been investigated over the past years with the aim of identifying any association with the development of Alzheimer's disease (AD). However, information regarding the potential association of VDR SNP haplotypes with AD is limited. The aim of the present study was to provide additional knowledge on the effects of VDR haplotypes on the development of late-onset AD in a cohort of Southeastern European Caucasians (SECs). The study sample included 78 patients with late-onset AD and 103 healthy subjects as the control group. VDR SNPs that were analyzed were TaqI (rs731236), BsmI (rs1544410) and FokI (rs2228570). The CAC (TaqI, BsmI and FokI) haplotype was found to be associated with a 53% lower risk of developing the disease (OR, 0.47; 95% CI, 0.23-0.96; P=0.04) and the TAC (TaqI, BsmI and FokI) haplotype was associated with an ~6-fold greater risk of developing AD (OR, 6.19; 95% CI, 1.91-20.13; P=0.0028). Female subjects carrying the TAC haplotype had a ~9-fold greater risk of developing AD in comparison to female control subjects (OR, 9.27; 95% CI, 1.86-46.28; P<0.05). The TaqI and BsmI polymorphisms were in high linkage disequilibrium (D'=0.9717, r=0.8467) and produced a haplotype with a statistically significant different frequency between the control and AD group. The TA (TaqI and BsmI) haplotype was associated with an ~8-fold greater risk of developing AD (OR, 8.27; 95% CI, 2.70-25.28; P<0.05). Female TA carriers had an ~14-fold greater risk of developing the disease in comparison to female control subjects (OR, 13.93; 95% CI, 2.95-65.87; P<0.05). On the whole, the present study demonstrates that in the SEC population, TAC and TA are risk haplotypes for AD, while the CAC haplotype may act protectively. SEC women carrying the TAC or TA haplotype are at a greater risk of developing AD, thus suggesting that women are markedly affected by the poor utilization of vitamin D induced by the VDR haplotype

The role of vitamin D in Alzheimer's Disease (AD) has been studied over the past years. The results from numerous studies have indicated that the molecular pathways involved in the development of AD are closely related to the molecular pathways of the mechanisms of action of vitamin D. However, only a limited number of studies have described the key role of vitamin D receptor (VDR) in the regulation of the functions of vitamin D and the potential effect of single nucleotide polymorphisms (SNPs) of the VDR gene. Thus, the aim of the present study was to investigate the VDR TaqI polymorphism in relation to AD in a Southeastern European Caucasian (SEC) cohort. Further, the present study aimed to compare the results obtained with those of other AD populations. For this purpose, blood samples from 90 confirmed patients with AD [median age, 74 years; median mini-mental state examination (MMSE) score of 21; median frontal assessment battery (FAB) score of 10] and 103 healthy controls (median age, 57 years) were analyzed to determine the genotypes of TaqI (rs731236) using quantitative PCR. The frequencies (%) of the TaqI TT, TC and CC genotypes in the controls/patients were 34/48.9, 47.6/41.1 and 18.4/10.0, respectively. Statistically significant differences were observed for the TaqI C allele [odds ratio (OR). 0.54; 95% confidence interval (CI), 0.30-0.96; P=0.035], the TaqI TT genotype (OR, 1.86; 95% CI, 1.04-3.32; P=0.035) and the TaqI CC genotype (OR, 0.119; 95% CI, 0.014-0.995; P=0.032,) in relation to the MMSE score <21 in the patient's group. The TaqI TT allele was found to increase the risk of developing AD by 1.86-fold in the SEC population, while the TaqI C allele may act protectively, with a 46% lower risk of developing the disease. Patients with the TaqI CC genotype were found to have an 88% less likelihood of developing severe cognitive impairment based on the MMSE score. On the whole, the present study did not confirm the results of previous studies on the VDR TaqI C allele in patients with AD