RESUMO
Background: The initial inflammatory reaction starts following occlusion in ischemic stroke (IS). Interleukin-1ß (IL-1ß) is a pro-inflammatory cytokine with a crucial role in the pathogenesis of neurodegenerative disorders. Objective: To investigate the levels of IL-1ß and vitamin D (VitD) in patients with IS compared with controls and their correlation. Methods: The serum level of 25-OH VitD and IL-1ß was assessed in 102 IS patients (0-24 h after stroke) and 102 controls with an enzyme-linked immunosorbent assay (ELISA) kit. Results: We found a significant increase in IL-1ß (80.14±6.8 vs. 60.32±4.1 pg/ml, p<0.05) and a decrease in VitD level (24.3±1.4 vs. 29.9±1.5 ng/ml, p<0.01) in the IS patients compared with the controls. There was a significantly positive correlation between the National Institutes of Health Stroke Scale (NIHSS) and IL-1ß according to both the Spearman correlation (r=0.35, p=0.0003) and the linear regression (beta=0.255, p=0.014). Also, a significant negative association between VitD and NIHSS was detected by the Spearman correlation (r=-0.41, p<0.0001) and the linear regression (beta=-0.381, p=0.000). Moreover, we found a significant negative correlation (r=-0.26, p=0.006) between the serum levels of VitD and IL-1ß in the patient group. Conclusion: Ischemic stroke correlates positively with IL-1ß and negatively with VitD levels. The speculated role of VitD deficiency in the evolution and severity of stroke may be justified by its role in the modification of inflammation.
Assuntos
AVC Isquêmico , Acidente Vascular Cerebral , Deficiência de Vitamina D , Humanos , Interleucina-1beta/sangue , Interleucina-1beta/química , AVC Isquêmico/complicações , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/complicações , Estados Unidos , Vitamina D , Deficiência de Vitamina D/diagnóstico , Deficiência de Vitamina D/complicaçõesRESUMO
BACKGROUND: Previous studies have demonstrated the strong association of inflammatory cytokines and vitamin D (VitD) deficiency and ischemic stroke (IS) pathogenesis. Due to the negative correlation between long non-coding RNA (lncRNA) Malat1 and pro-inflammatory factors we decided to investigate the associations between Malat1 expression with serum interleukin-1ß (IL-1ß), and VitD levels in IS patients. MATERIALS AND METHODS: In this cross-sectional study, 63 IS patients were included. We used enzyme-linked immunosorbent assays to evaluate the serum levels of VitD and IL-1ß. Malat1 expression was evaluated by the real-time polymerase chain reaction test. The associations between Malat1expression with VitD and IL-1ß were analysed with linear regression (Stepwise model) and Pearson's correlation analysis. RESULTS: The Malat1 expression was inversely correlated with stroke severity (r=-0.25, P=0.043). Stepwise regression analysis showed a significant positive relationship between VitD level and Malat1 expression (Beta=0.28, P=0.02), and also showed a non-significant negative relationship between IL-1ß and stroke severity. VitD level showed a positive Pearson correlation with Malat1 (r=0.28, P=0.023) and a negative correlation with IL-1ß (r=-0.29, P=0.018) while it could not detect a significantly negative correlation with stroke severity. CONCLUSION: For the first time the associations between Malat1 expression with IL-1ß and VitD in IS patients was analyzed. We found a significant positive relationship between VitD and Malat1. This correlation needs to be investigated with a larger sample size to achieve a strong and reliable association between VitD and Malat1.
RESUMO
Testicular tumors are the most common tumors in adolescent and young men and germ cell tumors (TGCTs) account for most of all testicular cancers. Increasing incidence of TGCTs among males provides strong motivation to understand its biological and genetic basis. Gains of chromosome arm 12p and aneuploidy are nearly universal in TGCTs, but TGCTs have low point mutation rate. It is thought that TGCTs develop from premalignant intratubular germ cell neoplasia that is believed to arise from the failure of normal maturation of gonocytes during fetal or postnatal development. Progression toward invasive TGCTs (seminoma and nonseminoma) then occurs after puberty. Both inherited genetic factors and environmental risk factors emerge as important contributors to TGCT susceptibility. Genome-wide association studies have so far identified more than 30 risk loci for TGCTs, suggesting that a polygenic model fits better with the genetic landscape of the disease. Despite high cure rates because of its particular sensitivity to platinum-based chemotherapy, exploration of mechanisms underlying the occurrence, progression, metastasis, recurrence, chemotherapeutic resistance, early diagnosis and optional clinical therapeutics without long-term side effects are urgently needed to reduce the cancer burden in this underserved age group. Herein, we present an up-to-date review on clinical challenges, origin and progression, risk factors, TGCT mouse models, serum diagnostic markers, resistance mechanisms, miRNA regulation, and database resources of TGCTs. We appeal that more attention should be paid to the basic research and clinical diagnosis and treatment of TGCTs.
Assuntos
Cromossomos Humanos Par 12/genética , Predisposição Genética para Doença/genética , Neoplasias Embrionárias de Células Germinativas , Neoplasias Testiculares , Animais , Antígeno B7-H1/metabolismo , Progressão da Doença , Células Germinativas/patologia , Humanos , Masculino , Camundongos , MicroRNAs/genética , Neoplasias Embrionárias de Células Germinativas/diagnóstico , Neoplasias Embrionárias de Células Germinativas/tratamento farmacológico , Neoplasias Embrionárias de Células Germinativas/genética , Neoplasias Embrionárias de Células Germinativas/patologia , Receptor de Morte Celular Programada 1/antagonistas & inibidores , Fatores de Risco , Testes Sorológicos , Neoplasias Testiculares/diagnóstico , Neoplasias Testiculares/tratamento farmacológico , Neoplasias Testiculares/genética , Neoplasias Testiculares/patologiaRESUMO
BACKGROUND: Injuries are responsible for much child and adolescent mortality in the world. OBJECTIVE: To study the effect of parental birth country on the risk of fatal unintentional injuries. METHODS: We established a cohort by linkages between Swedish national registers through personal identification number. The main variable was country of birth of parents. Children with both parents born in Sweden were the reference group. The cohort was followed up from the starting date of the study (1 January 1961) or date of birth, whichever occurred last, until the exit date, which was death due to unintentional injury, first emigration or end of the follow-up (31 December 2007), whichever came first. We calculated HRs with 95% CIs adjusted for age at exit, parental education and calendar period of birth by Cox proportional hazards models. RESULTS: We found a significantly higher risk of fatal unintentional injuries among children with a foreign background than among native children. We found a higher risk of fatal transportation-related injuries and drowning among boys with a foreign background and a higher risk of fatal burns/fire and falls among girls with a foreign background than among same sex native children. We also found a higher risk of fatal unintentional injuries among children with a foreign background at older ages than among native children at the same ages. CONCLUSIONS: Injury prevention work against unintentional injuries among children of foreign origin is more complex than that among native children. We recommend designing specific studies to find out the factors responsible and planning preventive interventions aiming at this particular group of children with a foreign background.
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Acidentes/mortalidade , Emigrantes e Imigrantes/estatística & dados numéricos , Ferimentos e Lesões/mortalidade , Adolescente , Criança , Pré-Escolar , Feminino , Seguimentos , Humanos , Lactente , Masculino , Modelos de Riscos Proporcionais , Fatores de Risco , Suécia/epidemiologiaRESUMO
BACKGROUND: Injury risk during childhood and adolescence vary depending on socio-economic factors. The aim of this study was to study if the risk of fatal and non-fatal unintentional injuries among foreign-born children was similar across parental educational level or not. METHODS: In this retrospective cohort study we followed 907,335 children between 1961 and 2007 in Sweden. We established the cohort by linkage between Swedish national registers including cause of death register and in-patient register, through unique Personal Identification Numbers. The main exposure variable was parental (maternal and paternal) educational level. The cohorts was followed from start date of follow-up period, or date of birth whichever occurred last, until exit date from the cohort, which was date of hospitalization or death due to unintentional injury, first emigration, death due to other causes than injury or end of follow-up, whichever came first. We calculated hazard ratios (HR) with 95% confidence intervals (95% CI) by Cox proportional hazards regression models. RESULTS: Overall, we found 705 and 78,182 cases of death and hospitalization due to unintentional injuries, respectively. Risk of death and hospitalization due to unintentional injuries was statistically significantly 1.48 (95% CI: 1.24-1.78) and 1.10 (95% CI: 1.08-1.12) times higher among children with lowest parental educational level (9 years and shorter years of study) compared to children with highest parental educational level (+13 years of study). We found similar results when stratified our study group by sex of children, by maternal and paternal educational level separately, and injury type (traffic-related, fall, poisoning, burn and drowning). CONCLUSIONS: It seems injury prevention work against unintentional injuries is less effective among children with low parental education compared with those with higher parental education. We recommend designing specific preventive interventions aiming at children with low parental education.