Sustitución de comunidades y concentración de nutrientes en plantas tras incendios forestales en una cuenca subárida del S.E. de España

Specific plant communities replacement in a subarid basin (Sierra de Almijara, S.E. Spain) is described related with internal concentration of C, N and compartimental P in several post-fire representative and dominant species. Plots were burnt 1, 6, 12 and 30 years before respectively, because fire is a recurrent phenomenon in that mediterranean shrublands. Juniperus oxycedrus is typical of the advanced stages of succession and presents low concentration of P and N, specially in old plants. Genista spartioides minimizes C:N ratio due to its symbiotic activity; and Cistus clusii shows an active cumulative metabolism specially in that concerning the phosphorus retention. In the frame of the general theory of sucession, C . clusii takes advantages of its ability to internalize high concentration of phosphate and Fabaceae of N accumulation. A dilution effect is detected in plants which are characteristic of the vegetation at the end of recolonization.Se describe la sustitución de comunidades tras incendios en una cuenca subárida (Sierra de Almijara, S.E. España), en relación con las concentraciones de carbono, nitrógeno y varios compartimentos de fósforo en tejidos de 5 especies de plantas representativas, en parcelas incendiadas hace 1, 6, 12 y 30 años respectivamente. El fuego se presenta de modo recurrente en estos matorrales mediterráneos. Juniperus oxycedrus, propia de formaciones de monte alto y de etapas avanzadas de la sucesión, presenta bajas concentraciones de P y N, especialmente en plantas viejas. Genista spartioides minimiza el indice C:N debido a su actividad simbiótica; y Cistus clusii muestra un activo metabolismo acumulador especialmente en lo que se refiere a la retención de fósforo. En el marco de la teoria general de la sucesión, C.clusii obtendria ventajas de su habilidad para internalizar altas concentraciones de fosfato y especies de la familia Fabaceae de su capacidad de acumulación de nitrógeno. En plantas caractensticas de las fases finales de la recolonización, se ha detectado un efecto de dilución de 10s nutrientes internos a medida que transcurre el tiempo tras el incendio

Relaciones Suelo-Planta en Bosques de Abies pinsapo Boiss. Disponibilidad de Nutrientes y Estatus Nutricional

Relaciones Suelo-Planta en Bosques de Abies pinsapo Boiss. Disponibilidad de Nutrientes y Estatus Nutricional. Se han evaluado las relaciones entre las propiedades del suelo y el estado nutricional de los árboles en pinsapares del Paraje Natural Los Reales de Sierra Bermeja y del Parque Natural Sierra de las Nieves (Málaga-España). Se seleccionaron pinsapares que difieren en cuanto a su estado sucesional (masas agradativas versus maduras) y sustrato litológico (serpentinas versus calizas), en los que se evaluaron variables morfoedáficas de perfiles de suelo, y se analizaron las concentraciones de nutrientes en muestras de suelo, hojarasca y acículas. Los suelos de pinsapares calcáreos en fase agradativa (Yunquera) mostraron las menores concentraciones de macro y micronutrientes totales. Esto se correspondía con contenidos también mínimos de N y P en tejidos foliares, indicando la existencia de un estrés nutricional general, como es habitual en masas forestales en fase de exclusión de tallos (máxima competencia intraespecífica). No obstante, la presencia de relaciones N/P foliares normales implica que dicho estrés nutricional no ha desencadenado desbalances internos entre dichos nutrientes en los árboles. En pinsapares calcícolas maduros (Ronda), la mayor acumulación de materia orgánica en la hojarasca y el suelo superficial se relaciona con un aumento de la disponibilidad de nutrientes en el suelo, y una reducción en el estrés nutricional de los árboles. El pinsapar serpentinícola de Los Reales de Sierra Bermeja mostró niveles anormalmente elevados de N, y de las relaciones N/P, tanto en el suelo como en los tejidos foliares. Estos síntomas son característicos de ecosistemas forestales en una fase temprana del denominado síndrome de saturación de nitrógeno, asociado a disfunciones en el ciclo del N

Contribution of non-genetic factors to the reproductive performance of mirandesa cows

Characterization of reproductive traits in Mirandesa beef cattle is important for breed improvement and conservation, mainly due to its little genetic diversity. Reduced individual and maternal performance is often associated with inbreeding depression, which could be further aggravate the environmental effects. In this study, 7386 herd records for Mirandesa were used to characterize the main reproductive traits, like age at first calving (AFC), pregnancy length (PL), calving interval (CI), yearly calving distribution (CD) and productive lifespan (PLf). The non-genetic effects were tested using non-parametric methods, as the target variables were not normally distributed. The median for AFC in Mirandesa was close to 32 months; AFC was affected by the production system, farm and by the year and season of birth. The mean for PL was 287±8.9 days, being affected by parity and calf gender. The median CI, of 378 days, was only affected by the breeding program, parity, season and year. Calving season was unevenly distributed over the year, showing different patterns after the production system. The mean productive lifespan of Mirandesa was 6.45 years, though 20% of the cows presented a PLf longer than ten years. The main non-genetic effects suggested that farmer´s decision and nutrition may constrain the expression of the reproductive traits in Mirandesa breed. This aspect needs to be addressed when designing any breeding programs which should prioritise for the increase in the number of calves per year along with a careful selection of reproducers to decrease reported inbreeding.The authors wish to thank ACBRM (Associação de Criadores de Bovinos de Raça Mirandesa) for providing access to the Mirandesa cattle Herdbook.info:eu-repo/semantics/publishedVersio

DNA methylation map in circulating leukocytes mirrors subcutaneous adipose tissue methylation pattern: a genome-wide analysis from non-obese and obese patients

The characterization of the epigenetic changes within the obesity-related adipose tissue will provide new insights to understand this metabolic disorder, but adipose tissue is not easy to sample in population-based studies. We aimed to evaluate the capacity of circulating leukocytes to reflect the adipose tissue-specific DNA methylation status of obesity susceptibility. DNA samples isolated from subcutaneous adipose tissue and circulating leukocytes were hybridized in the Infinium HumanMethylation 450 BeadChip. Data were compared between samples from obese (n = 45) and non-obese (n = 8-10) patients by Wilcoxon-rank test, unadjusted for cell type distributions. A global hypomethylation of the differentially methylated CpG sites (DMCpGs) was observed in the obese subcutaneous adipose tissue and leukocytes. The overlap analysis yielded a number of genes mapped by the common DMCpGs that were identified to reflect the obesity state in the leukocytes. Specifically, the methylation levels of FGFRL1, NCAPH2, PNKD and SMAD3 exhibited excellent and statistically significant efficiencies in the discrimination of obesity from non-obesity status (AUC > 0.80; p < 0.05) and a great correlation between both tissues. Therefore, the current study provided new and valuable DNA methylation biomarkers of obesity-related adipose tissue pathogenesis through peripheral blood analysis, an easily accessible and minimally invasive biological material instead of adipose tissue

Cardiovascular disease in immune-mediated inflammatory diseases: a cross-sectional analysis of 6 cohorts

Observational study[Abstract] To analyze in several immune-mediated inflammatory diseases (IMIDs) the influence of demographic and clinical-related variables on the prevalence of cardiovascular disease (CVD), and compare their standardized prevalences.Cross-sectional study, including consecutive patients diagnosed with rheumatoid arthritis, psoriatic arthritis, psoriasis, systemic lupus erythematosus, Crohn disease, or ulcerative colitis, from rheumatology, gastroenterology, and dermatology tertiary care outpatient clinics located throughout Spain, between 2007 and 2010. Our main outcome was defined as previous diagnosis of angina, myocardial infarction, peripheral vascular disease, and/or stroke. Bivariate and multivariate logistic and mixed-effects logistic regression models were performed for each condition and the overall cohort, respectively. Standardized prevalences (in subjects per 100 patients, with 95% confidence intervals) were calculated using marginal analysis.We included 9951 patients. For each IMID, traditional cardiovascular risk factors had a different contribution to CVD. Overall, older age, longer disease duration, presence of traditional cardiovascular risk factors, and male sex were independently associated with a higher CVD prevalence. After adjusting for demographic and traditional cardiovascular risk factors, systemic lupus erythematosus exhibited the highest CVD standardized prevalence, followed by rheumatoid arthritis, psoriasis, Crohn disease, psoriatic arthritis, and ulcerative colitis (4.5 [95% confidence interval (CI): 2.2, 6.8], 1.3 [95% CI: 0.8, 1.8], 0.9 [95% CI: 0.5, 1.2], 0.8 [95% CI: 0.2, 1.3], 0.6 [95% CI: 0.2, 1.0], and 0.5 [95% CI: 0.1, 0.8], respectively).Systemic lupus erythematosus, rheumatoid arthritis, and psoriasis are associated with higher prevalence of CVD compared with other IMIDs. Specific prevention programs should be established in subjects affected with these conditions to prevent CVD

Cardiovascular disease in immune-mediated inflammatory diseases: A cross-sectional analysis of 6 cohorts

To analyze in several immune-mediated inflammatory diseases (IMIDs) the influence of demographic and clinical-related variables on the prevalence of cardiovascular disease (CVD), and compare their standardized prevalences.Cross-sectional study, including consecutive patients diagnosed with rheumatoid arthritis, psoriatic arthritis, psoriasis, systemic lupus erythematosus, Crohn disease, or ulcerative colitis, from rheumatology, gastroenterology, and dermatology tertiary care outpatient clinics located throughout Spain, between 2007 and 2010. Our main outcome was defined as previous diagnosis of angina, myocardial infarction, peripheral vascular disease, and/or stroke. Bivariate and multivariate logistic and mixed-effects logistic regression models were performed for each condition and the overall cohort, respectively. Standardized prevalences (in subjects per 100 patients, with 95% confidence intervals) were calculated using marginal analysis.We included 9951 patients. For each IMID, traditional cardiovascular risk factors had a different contribution to CVD. Overall, older age, longer disease duration, presence of traditional cardiovascular risk factors, and male sex were independently associated with a higher CVD prevalence. After adjusting for demographic and traditional cardiovascular risk factors, systemic lupus erythematosus exhibited the highest CVD standardized prevalence, followed by rheumatoid arthritis, psoriasis, Crohn disease, psoriatic arthritis, and ulcerative colitis (4.5 [95% confidence interval (CI): 2.2, 6.8], 1.3 [95% CI: 0.8, 1.8], 0.9 [95% CI: 0.5, 1.2], 0.8 [95% CI: 0.2, 1.3], 0.6 [95% CI: 0.2, 1.0], and 0.5 [95% CI: 0.1, 0.8], respectively).Systemic lupus erythematosus, rheumatoid arthritis, and psoriasis are associated with higher prevalence of CVD compared with other IMIDs. Specific prevention programs should be established in subjects affected with these conditions to prevent CVD

A genome-wide association study follow-up suggests a possible role for PPARG in systemic sclerosis susceptibility

Introduction: A recent genome-wide association study (GWAS) comprising a French cohort of systemic sclerosis (SSc) reported several non-HLA single-nucleotide polymorphisms (SNPs) showing a nominal association in the discovery phase. We aimed to identify previously overlooked susceptibility variants by using a follow-up strategy.&lt;p&gt;&lt;/p&gt; Methods: Sixty-six non-HLA SNPs showing a P value &#60;10-4 in the discovery phase of the French SSc GWAS were analyzed in the first step of this study, performing a meta-analysis that combined data from the two published SSc GWASs. A total of 2,921 SSc patients and 6,963 healthy controls were included in this first phase. Two SNPs, PPARG rs310746 and CHRNA9 rs6832151, were selected for genotyping in the replication cohort (1,068 SSc patients and 6,762 healthy controls) based on the results of the first step. Genotyping was performed by using TaqMan SNP genotyping assays. Results: We observed nominal associations for both PPARG rs310746 (PMH = 1.90 × 10-6, OR, 1.28) and CHRNA9 rs6832151 (PMH = 4.30 × 10-6, OR, 1.17) genetic variants with SSc in the first step of our study. In the replication phase, we observed a trend of association for PPARG rs310746 (P value = 0.066; OR, 1.17). The combined overall Mantel-Haenszel meta-analysis of all the cohorts included in the present study revealed that PPARG rs310746 remained associated with SSc with a nominal non-genome-wide significant P value (PMH = 5.00 × 10-7; OR, 1.25). No evidence of association was observed for CHRNA9 rs6832151 either in the replication phase or in the overall pooled analysis.&lt;p&gt;&lt;/p&gt; Conclusion: Our results suggest a role of PPARG gene in the development of SSc

Evaluation of 12 GWAS-drawn SNPs as biomarkers of rheumatoid arthritis response to TNF inhibitors. A potential SNP association with response to etanercept

Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all nonredundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the metaanalysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNPsThis work was supported by the Instituto de Salud Carlos III (ISCIII, Spain) through grants PI14/01651, PI17/01606 and RD16/0012/0014 to AG and PI12/01909 to JJG-R. These grants are partially financed by the European Regional Development Fund of the EU (FEDER

Lack of validation of genetic variants associated with anti-tumor necrosis factor therapy response in rheumatoid arthritis: a genome-wide association study replication and meta-analysis

Introduction: In this study, our aim was to elucidate the role of four polymorphisms identified in a prior large genome-wide association study (GWAS) in which the investigators analyzed the responses of patients with rheumatoid arthritis (RA) to treatment with tumor necrosis factor inhibitors (TNFi). The authors of that study reported that the four genetic variants were significantly associated. However, none of the associations reached GWAS significance, and two subsequent studies failed to replicate these associations. Methods: The four polymorphisms (rs12081765, rs1532269, rs17301249 and rs7305646) were genotyped in a total of 634 TNFi-treated RA patients of Spanish Caucasian origin. Four outcomes were evaluated: changes in the Disease Activity Score in 28 joints (DAS28) after 6 and 12 months of treatment and classification according to the European League Against Rheumatism (EULAR) response criteria at the same time points. Association with DAS28 changes was assessed by linear regression using an additive genetic model. Contingency tables of genotype and allele frequencies between EULAR responder and nonresponder patients were compared. In addition, we combined our data with those of previously reported studies in a meta-analysis including 2,998 RA patients. Results: None of the four genetic variants showed an association with response to TNFi in any of the four outcomes analyzed in our Spanish patients. In addition, only rs1532269 yielded a suggestive association (P = 0.0033) with the response to TNFi when available data from previous studies were combined in the meta-analysis. Conclusion: Our data suggest that the rs12081765, rs1532269, rs17301249 and rs7305646 genetic variants do not have a role as genetic predictors of TNFi treatment outcomes

Evaluation of 12 GWAS-drawn SNPs as biomarkers of rheumatoid arthritis response to TNF inhibitors. A potential SNP association with response to etanercept

Research in rheumatoid arthritis (RA) is increasingly focused on the discovery of biomarkers that could enable personalized treatments. The genetic biomarkers associated with the response to TNF inhibitors (TNFi) are among the most studied. They include 12 SNPs exhibiting promising results in the three largest genome-wide association studies (GWAS). However, they still require further validation. With this aim, we assessed their association with response to TNFi in a replication study, and a meta-analysis summarizing all non-redundant data. The replication involved 755 patients with RA that were treated for the first time with a biologic drug, which was either infliximab (n = 397), etanercept (n = 155) or adalimumab (n = 203). Their DNA samples were successfully genotyped with a single-base extension multiplex method. Lamentably, none of the 12 SNPs was associated with response to the TNFi in the replication study (p > 0.05). However, a drug-stratified exploratory analysis revealed a significant association of the NUBPL rs2378945 SNP with a poor response to etanercept (B = -0.50, 95% CI = -0.82, -0.17, p = 0.003). In addition, the meta-analysis reinforced the previous association of three SNPs: rs2378945, rs12142623, and rs4651370. In contrast, five of the remaining SNPs were less associated than before, and the other four SNPs were no longer associated with the response to treatment. In summary, our results highlight the complexity of the pharmacogenetics of TNFi in RA showing that it could involve a drug-specific component and clarifying the status of the 12 GWAS-drawn SNP