Introduction:Acute leukemia, accounting for 20% of all cancers diagnosed in individuals younger than 19 years old, is the most prevalent childhood malignancy. Among environmental risk factors, parental occupational exposures have attracted scientific interest as potential predisposing factors for childhood leukemia. The role of parental occupational exposure to social contacts, harmful chemicals, electromagnetic fields and ionizing radiation has been investigated with conflicting and inconsistent results.Aim:A case-control study aiming to assess the association between parental occupational exposures to social contacts, chemicals and electromagnetic fields and the risk of offspring acute leukemia.Material and Methods:108 children with acute leukemia and equal number of matched controls were included. Data on parental occupations before conception, during pregnancy, during breastfeeding and after birth, and on potential risk factors was recorded. Associations between parental exposure and risk of childhood leukemia were estimated.Results:Parental occupational exposure during the four periods of exposure was not associated with childhood leukemia. High birth weight and family history of cancer were associated with the development of childhood acute leukemia. A weak association of maternal medication use during pregnancy and leukemia risk emerged.Conclusions:Since the causative factors of childhood leukemia remain unknown, further investigation is mandatory for the reduction of disease burden.
BackgroundB-cell non-Hodgkin’s lymphoma (B-NHL) is one of the major complications of primary Sjögren’s syndrome (SS). Chronic inflammation and macrophages in SS minor salivary glands have been previously suggested as significant predictors for lymphoma development among SS patients. Lipoprotein-associated phospholipase A2 (Lp-PLA2)—a product mainly of tissue macrophages—is found in the circulation associated with lipoproteins and has been previously involved in cardiovascular, autoimmune, and malignant diseases, including lymphoma.ObjectiveThe purpose of the current study was to investigate the contributory role of Lp-PLA2 in B-NHL development in the setting of primary SS.MethodsLp-PLA2 activity in serum samples collected from 50 primary SS patients with no lymphoma (SS-nL), 9 primary SS patients with lymphoma (SS-L), and 42 healthy controls (HC) was determined by detection of [3H]PAF degradation products by liquid scintillation counter. Moreover, additional sera from 50 SS-nL, 28 SS-L, and 32 HC were tested for Lp-PLA2 activity using a commercially available ELISA kit. Lp-PLA2 mRNA, and protein expression in minor salivary gland (MSG) tissue samples derived from SS-nL, SS-L patients, and sicca controls (SC) were analyzed by real-time PCR, Western blot, and immunohistochemistry.ResultsSerum Lp-PLA2 activity was significantly increased in SS-L compared to both SS-nL and HC by two independent methods implemented [mean ± SD (nmol/min/ml): 62.0 ± 13.4 vs 47.6 ± 14.4 vs 50.7 ± 16.6, p-values: 0.003 and 0.04, respectively, and 19.4 ± 4.5 vs 15.2 ± 3.3 vs 14.5 ± 3.0, p-values: <0.0001, in both comparisons]. ROC analysis revealed that the serum Lp-PLA2 activity measured either by radioimmunoassay or ELISA has the potential to distinguish between SS-L and SS-nL patients (area under the curve [AUC]: 0.8022, CI [95%]: 0.64–0.96, p-value: 0.004 for radioimmunoassay, and AUC: 0.7696, CI [95%]: 0.66–0.88, p-value: <0.0001, for ELISA). Lp-PLA2 expression in MSG tissues was also increased in SS-L compared to SS-nL and SC at both mRNA and protein level. ROC analysis revealed that both MSG mRNA and protein Lp-PLA2 have the potential to distinguish between SS-nL and SS-L patients (area under the curve [AUC] values of 0.8490, CI [95%]: 0.71–0.99, p-value: 0.0019 and 0.9444, CI [95%]: 0.79–1.00, p- value: 0.0389 respectively). No significant difference in either serum Lp-PLA2 activity or MSG tissue expression was observed between SS-nL and HC.ConclusionsLp-PLA2 serum activity and MSG tissue mRNA/protein expression could be a new biomarker and possibly a novel therapeutic target for B-cell lymphoproliferation in the setting of SS.
This study presents the results of the response of Sparus aurata to three different musical stimuli, derived from the transmission (4 h per day, 5 days per week) of particular music pieces by Mozart, Romanza and Bach (140 dB(rms) re 1 μPa), compared to the same transmission level of white noise, while the underwater ambient noise in all the experimental tanks was 121 dB(rms) re 1 μPa. Using recirculating sea water facilities, 10 groups, 2 for each treatment, of 20 specimens of 11.2 ± 0.02 g (S.E.), were reared for 94 days, under 150 ± 10 l× 12L-12D, and were fed an artificial diet three times per day. Fish body weight showed significant differences after 55 days, while its maximum level was observed after the 69th day until the end of the experiment, the highest value demonstrated in Mozart (M) groups, followed by those of Romanza (R), Bach (B), control (C) and white noise (WN). SGR (M = B), %WG (M = B) and FCR (all groups fed same % b.w.) were also improved for M group. Brain neurotransmitters results exhibited significant differences in DA-dopamine, (M > B), 5HIAA (C > B), 5HIAA:5HT (WN > R), DOPAC (M > B), DOPAC:DA and (DOPAC + HVA):DA, (C > M), while no significant differences were observed in 5HT, NA, HVA and HVA:DA. No differences were observed in biometric measurements, protease activity, % fatty acids of fillet, visceral fat and liver, while differences were observed regarding carbohydrase activity and the amount (mg/g w.w.) of some fatty acids in liver, fillet and visceral fat. In conclusion, present results confirm those reported for S. aurata, concerning the observed relaxing influence--due to its brain neurotransmitters action--of the transmission of Mozart music (compared to R and B), which resulted in the achievement of maximum growth rate, body weight and improved FCR. This conclusion definitely supports the musical "understanding" and sensitivity of S. aurata to music stimuli as well as suggesting a specific effect of white noise.
Background:One of the major complications of primary Sjogren’s syndrome (SS) is the development of B-cell non-Hodgkin’s lymphoma (B-NHL). The contribution of tissue macrophages in the pathogenesis of B-NHL, based on previous histopathological studies, appears to be significant. Extracellular lipoprotein-associated phospholipase A2 (Lp-PLA2) is a product of tissue macrophages which is found in the circulation associated with lipoproteins and has been involved in both cardiovascular and malignant diseases, including B-NHL lymphoma.Objectives:The purpose of the current study was to investigate the role of serum Lp-PLA2 activity as a potential biomarker for the development of B-NHL in the setting of primary SS.Methods:Extracellular Lp-PLA2 activity was determined by measuring [3H]PAF degradation products in liquid scintillation counter in serum samples obtained from 48 primary SS patients, 9 primary SS patients complicated by lymphoma (SS-lymphoma) and 40 healthy controls. Similar results were obtained in an independent cohort of 25 primary SS patients, 17 primary SS-lymphoma and 10 healthy controls, when a commercially available ELISA kit was implemented. Statistical analysis was performed with the Graph Pad software.Results:The activity of Lp-PLA2 was statistically significant increased in patients with primary SS-lymphoma compared to primary SS patients without lymphoma [mean±SD (nmol/min/ml): 62.0±13.4 vs 47.7±14.7, p=0.003 and 19.7±4.7 vs 15.2±3.2, p=0.005, respectively], as well as healthy controls [mean±SD (nmol/min/ml): 62.0±13.4 vs 52.0±16.3, p=0.03 and 19.7±4.7 vs 15.7±3.1, p=0.06, respectively]. No statistical significant differences in Lp-PLA2 activity were detected between primary SS patients without lymphoma development and healthy controls.Conclusion:Evaluation of extracellular Lp-PLA2 activity in primary SS patients could be a useful serological biomarker for B-NHL development in the context of primary SS.References[1] Fragkioudaki S, Mavragani CP, Moutsopoulos HM. Predicting the risk for lymphoma development in Sjogren syndrome: An easy tool for clinical use. Medicine (Baltimore). 2016Jun;95(25):e3766.[2] Li D, Wei W, Ran X, Yu J, Li H, Zhao L, Zeng H, Cao Y, Zeng Z, Wan Z. Lipoprotein-associated phospholipase A2 and risks of coronary heart disease and ischemic stroke in the general population: A systematic review and meta-analysis. Clin Chim Acta. 2017Aug;471:38-45.[3] Markakis KP, Koropouli MK, Grammenou-Savvoglou S, van Winden EC, Dimitriou AA, Demopoulos CA, Tselepis AD, Kotsifaki EE. Implication of lipoprotein associated phospholipase A2 activity in oxLDL uptake by macrophages. J Lipid Res. 2010Aug;51(8):2191-201.[4] Lecointe N, Meerabux J, Ebihara M, Hill A, Young BD. Molecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase(Pafah1a2) in human lymphoma. Oncogene. 1999May6;18(18):2852-9.Disclosure of Interests:None declared
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