Fire and resprouting in Mediterranean ecosystems: Insights from an external biogeographical region, the mexical shrubland

7 páginas, 3 tablas.We investigated modes of regeneration of dominant species of the mexical vegetation after fire. The mexical shrubland shows a remarkable structural, morphological, and floristic similarity to Mediterranean-type vegetation and is considered a relict of the Madro-Tertiary Geoflora under a non- mediterranean climate. This vegetation provides an ideal scenario to test the role of fire in Mediterranean ecosystems because historical fire occurrence is absent and the species assembly is constituted mostly by Madro-Tertiary elements and Neotropical species (some of them, endemic species from Mexico). The existence of congeneric species of the California chaparral allows us to determine the regeneration ability of these communities after fire in relation to resprouting and seeding strategies, which are widespread modes reported in the Mediterranean-type vegetation. By the experimental application of fire in the two biogeographical groups of species, we tested the hypothesis that low resprouting ability of California congeneric species (Madro-Tertiary species) after fire would indicate that fire has played an important selective force in the resprouting habit. A low resprouting ability in the Neotropical group of species would suggest that fire has molded the set of species dominating fire-prone environments. Our results indicated that resprouting is a widespread trait in the mexical species characterized by the presence of lignotubers and burls. Resprouting can be considered an ancient trait, probably linked to losses of aboveground biomass, that became a pre-adaptation in Mediterranean fire-prone communities. The Neotropical group of species showed less ability to regenerate after fire, and small plants were more likely to die after disturbance in this group than in the Madro-Tertiary group. The resprouting feature and the seeder strategy of other species after a fire in the mexical shrubland are similar to Mediterranean-type ecosystems, emphasizing their common origin and the relevance of phylogenetic and biogeographical studies to explain current patterns of vegetation.Peer reviewe

CoQ deficiency causes disruption of mitochondrial sulfide oxidation, a new pathomechanism associated with this syndrome

Coenzyme Q (CoQ) is a key component of the mitochondrial respiratory chain, but it also has several other functions in the cellular metabolism. One of them is to function as an electron carrier in the reaction catalyzed by sulfide:quinone oxidoreductase (SQR), which catalyzes the first reaction in the hydrogen sulfide oxidation pathway. Therefore, SQR may be affected by CoQ deficiency. Using human skin fibroblasts and two mouse models with primary CoQ deficiency, we demonstrate that severe CoQ deficiency causes a reduction in SQR levels and activity, which leads to an alteration of mitochondrial sulfide metabolism. In cerebrum of Coq9R239X mice, the deficit in SQR induces an increase in thiosulfate sulfurtransferase and sulfite oxidase, as well as modifications in the levels of thiols. As a result, biosynthetic pathways of glutamate, serotonin, and catecholamines were altered in the cerebrum, and the blood pressure was reduced. Therefore, this study reveals the reduction in SQR activity as one of the pathomechanisms associated with CoQ deficiency syndrome.Ministerio de Economía y CompetitividadERDF/SAF2013-47761-RERDF/SAF2014-55523-RERDF/RD12/0042/0011ERDF/SAF2015-65786-RJunta de AndalucíaNIH/P01HD08064

Bilateral Simultaneous Retinal Detachment in Pseudophakia

Cataract surgery is the most frequent surgical intervention, with approximately 700,000 operations per year in Germany alone. One of the most serious complications is retinal detachment, with a reported incidence rate of pseudophakic retinal detachment of 0.75-1.65%. We report the case of a patient who suffered from a simultaneous bilateral pseudophakic retinal detachment. Interestingly, the bilateral detachments in the left and the right eye started with only some hours' delay. He had no acute trigger for the retinal detachment and no risk factors besides the cataract surgery performed on both eyes some weeks earlier. Simultaneous bilateral retinal detachments will be more common, due to increasing numbers of cataract surgeries and the demographic development. We conclude that funduscopy should be regularly performed in mydriasis to avoid sight-threatening simultaneous bilateral retinal detachments

Bilateral Simultaneous Retinal Detachment in Pseudophakia

Cataract surgery is the most frequent surgical intervention, with approximately 700,000 operations per year in Germany alone. One of the most serious complications is retinal detachment, with a reported incidence rate of pseudophakic retinal detachment of 0.75-1.65%. We report the case of a patient who suffered from a simultaneous bilateral pseudophakic retinal detachment. Interestingly, the bilateral detachments in the left and the right eye started with only some hours' delay. He had no acute trigger for the retinal detachment and no risk factors besides the cataract surgery performed on both eyes some weeks earlier. Simultaneous bilateral retinal detachments will be more common, due to increasing numbers of cataract surgeries and the demographic development. We conclude that funduscopy should be regularly performed in mydriasis to avoid sight-threatening simultaneous bilateral retinal detachments

The antioxidant Trolox restores mitochondrial membrane potential and Ca2+-stimulated ATP production in human complex I deficiency

Malfunction of mitochondrial complex I caused by nuclear gene mutations causes early-onset neurodegenerative diseases. Previous work using cultured fibroblasts of complex-I-deficient patients revealed elevated levels of reactive oxygen species (ROS) and reductions in both total Ca2+ content of the endoplasmic reticulum (ERCa) and bradykinin(Bk)-induced increases in cytosolic and mitochondrial free Ca2+ ([Ca2+]C; [Ca2+]M) and ATP ([ATP]C; [ATP]M) concentration. Here, we determined the mitochondrial membrane potential (Δψ) in patient skin fibroblasts and show significant correlations with cellular ROS levels and ERCa, i.e., the less negative Δψ, the higher these levels and the lower ERCa. Treatment with 6-hydroxy-2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox) normalized Δψ and Bk-induced increases in [Ca2+]M and [ATP]M. These effects were accompanied by an increase in ERCa and Bk-induced increase in [Ca2+]C. Together, these results provide evidence for an integral role of increased ROS levels in complex I deficiency and point to the potential therapeutic value of antioxidant treatment

Hypofibrinolysis in diabetes: a therapeutic target for the reduction of cardiovascular risk

An enhanced thrombotic environment and premature atherosclerosis are key factors for the increased cardiovascular risk in diabetes. The occlusive vascular thrombus, formed secondary to interactions between platelets and coagulation proteins, is composed of a skeleton of fibrin fibres with cellular elements embedded in this network. Diabetes is characterised by quantitative and qualitative changes in coagulation proteins, which collectively increase resistance to fibrinolysis, consequently augmenting thrombosis risk. Current long-term therapies to prevent arterial occlusion in diabetes are focussed on anti-platelet agents, a strategy that fails to address the contribution of coagulation proteins to the enhanced thrombotic milieu. Moreover, antiplatelet treatment is associated with bleeding complications, particularly with newer agents and more aggressive combination therapies, questioning the safety of this approach. Therefore, to safely control thrombosis risk in diabetes, an alternative approach is required with the fibrin network representing a credible therapeutic target. In the current review, we address diabetes-specific mechanistic pathways responsible for hypofibrinolysis including the role of clot structure, defects in the fibrinolytic system and increased incorporation of anti-fibrinolytic proteins into the clot. Future anti-thrombotic therapeutic options are discussed with special emphasis on the potential advantages of modulating incorporation of the anti-fibrinolytic proteins into fibrin networks. This latter approach carries theoretical advantages, including specificity for diabetes, ability to target a particular protein with a possible favourable risk of bleeding. The development of alternative treatment strategies to better control residual thrombosis risk in diabetes will help to reduce vascular events, which remain the main cause of mortality in this condition

Neuromyelitis optica and pregnancy during therapeutic B cell depletion: infant exposure to anti-AQP4 antibody and prevention of rebound relapses with low-dose rituximab postpartum

Neuromyelitis optica (NMO) predominantly affects women, some in childbearing age, and requires early therapeutic intervention to prevent disabling relapses. We report an anti-AQP4 antibody-seropositive patient who became pregnant seven months after low-dose (100 mg) rituximab application. Pregnancy showed no complications, and low-dose rituximab restarted two days after delivery resulted in neurological stability for 24 months. Remarkably, her otherwise healthy newborn presented with anti-AQP4 antibody and reduced B lymphocyte counts in umbilical cord blood, which normalized three months later. Confirming and extending previous reports, our case suggests that low-dose rituximab might be compatible with pregnancy and prevent rebound NMO disease activity postpartum

Liver function predicts survival in patients undergoing extracorporeal membrane oxygenation following cardiovascular surgery

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) represents a valuable and rapidly evolving therapeutic option in patients with severe heart or lung failure following cardiovascular surgery. However, despite significant advances in ECMO techniques and management, prognosis remains poor and accurate risk stratification challenging. We therefore evaluated the predictive value of liver function variables on all-cause mortality in patients undergoing venoarterial ECMO support after cardiovascular surgery. METHODS: We included into our single-center registry a total of 240 patients undergoing venoarterial ECMO therapy following cardiovascular surgery at a university-affiliated tertiary care center. RESULTS: The median follow-up was 37 months (interquartile range 19–67 months), and a total of 156 patients (65 %) died. Alkaline phosphatase and total bilirubin were the strongest predictors for 30-day mortality, with adjusted hazard ratios (HRs) per 1–standard deviation increase of 1.36 (95 % confidence interval [CI] 1.10–1.68; P = 0.004) and 1.22 (95 % CI 1.07–1.40; P = 0.004), respectively. The observed associations persisted for long-term mortality, with adjusted HRs of 1.27 (95 % CI 1.03–1.56; P = 0.023) for alkaline phosphatase and 1.22 (95 % CI 1.07–1.39; P = 0.003) for total bilirubin. CONCLUSIONS: The present study demonstrates that elevated values of alkaline phosphatase and total bilirubin are sensitive parameters for predicting the short-term and long-term outcomes of ECMO patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13054-016-1242-4) contains supplementary material, which is available to authorized users

Impact of genetic and non-genetic factors on phenotypic diversity in NBAS-associated disease

Biallelic pathogenic variants in neuroblastoma-amplified sequence (NBAS) cause a pleiotropic multisystem disorder. Three clinical subgroups have been defined correlating with the localisation of pathogenic variants in the NBAS gene; variants affecting the C-terminal region of NBAS result in SOPH syndrome (short stature, optic atrophy, Pelger-Huët anomaly), variants affecting the Sec 39 domain are associated with infantile liver failure syndrome type 2 (ILFS2) and variants affecting the ß-propeller domain give rise to a combined phenotype. However, there is still unexplained phenotypic diversity across the three subgroups, challenging the current concept of genotype-phenotype correlations in NBAS-associated disease. Therefore, besides examining the genetic influence, we aim to elucidate the potential impact of pre-symptomatic diagnosis, emergency management and other modifying variables on the clinical phenotype. We investigated genotype-phenotype correlations in individuals sharing the same genotypes (n = 30 individuals), and in those sharing the same missense variants with a loss-of-function variant in trans (n = 38 individuals). Effects of a pre-symptomatic diagnosis and emergency management on the severity of acute liver failure (ALF) episodes also were analysed, comparing liver function tests (ALAT, ASAT, INR) and mortality. A strong genotype-phenotype correlation was demonstrated in individuals sharing the same genotype; this was especially true for the ILFS2 subgroup. Genotype-phenotype correlation in patients sharing only one missense variant was still high, though at a lower level. Pre-symptomatic diagnosis in combination with an emergency management protocol leads to a trend of reduced severity of ALF. High genetic impact on clinical phenotype in NBAS-associated disease facilitates monitoring and management of affected patients sharing the same genotype. Pre-symptomatic diagnosis and an emergency management protocol do not prevent ALF but may reduce its clinical severity