Effects of eel (Anguilla anguilla L.) removals from selected sites of a stream on its subsequent densities

We assessed the effect of eel (Anguilla anguilla) removal from three sites of a Cantabrian stream upon its subsequent densities. In the first sample (Sept. 1986) numbers and densities were estimated as 43, 45 and 84 ind and 3490, 3030 and 3750 ind ha ⁻¹. Removal of these eels reduced the subsequent numbers and densities which, except on two occasions, were never reached again during the two years (eleven estimates) of study. Highest densities were recorded in the uppermost site in May and July, 1987, coincident with a strong drought and the lowest densities occurred in 1988 during a normal wet year. We hypothesize first that, because of a selective underground homing behaviour of eels, electro-fishing is inefficient and results in underestimates of the population. Second, seasonal variations of water discharge and droughts may not influence the homing behaviour of'eels until a threshold of dryness is reached. If this occurs, eels abandon their refuges and move towards the stream bottom. It seems that in Arroyo Chabatchos this threshold was exceeded in the summer of 1987 when the highest densities were estimated. The re-colonization of these sites experimentally depleted of eels, is a slow procces that lasts for, at least, two years.     

Land Use Changes and GHG Emissions from Tropical Forest Conversion by Oil Palm Plantations in Riau Province,Indonesia

Increasing prices and demand for biofuel and cooking oil from importer countries have caused a remarkable expansion of oil palm plantations in Indonesia. In this paper, we attempt to monitor the expansion of oil palm plantations on peat land and in tropical forests. We measure the GHG emissions from the land conversion activities at provincial scale. Using Landsat images from three different periods (1990s, 2000s and 2012), we classified LULC of the Riau Province, which is the largest oil palm producing region in Indonesia. A hybrid method of integration, generated by combining automatic processing and manual analysis, yields the best results. We found that the tropical rainforest cover decreased from ∼63% in the 1990s to ∼37% in the 2000s. By 2012, the remaining tropical rainforest cover was only ∼22%. From the 1990s to the 2000s, conversion of forests and peat lands was the primary source of emissions, total CO₂ emitted to the atmosphere was estimated at ∼26.6 million tCO₂.y^-1, with 40.62% and 59.38% of the emissions from conversion of peat lands and forests, respectively. Between 2000 and 2012, the total CO₂ emitted to the atmosphere was estimated at ∼5.2 million tCO₂. y^-1, with 69.94% and 27.62% of the emissions from converted peat lands and converted forests, respectively. The results show that in the Riau Province, the oil palm industry boomed in the period from 1990 to 2000, with transformation of tropical forest and peat land as the primary source of emissions. The decrease of CO₂ emissions in the period from 2000 to 2012 is possibly due to the enforcement of a moratorium on deforestation.     

A Huntingtin Peptide Inhibits PolyQ-Huntingtin Associated Defects

Background

Huntington’s disease (HD) is caused by the abnormal expansion of the polyglutamine tract in the human Huntingtin protein (polyQ-hHtt). Although this mutation behaves dominantly, huntingtin loss of function also contributes to HD pathogenesis. Indeed, wild-type Huntingtin plays a protective role with respect to polyQ-hHtt induced defects.

Methodology/Principal Findings

The question that we addressed here is what part of the wild-type Huntingtin is responsible for these protective properties. We first screened peptides from the Huntingtin protein in HeLa cells and identified a 23 aa peptide (P42) that inhibits polyQ-hHtt aggregation. P42 is part of the endogenous Huntingtin protein and lies within a region rich in proteolytic sites that plays a critical role in the pathogenesis process. Using a Drosophila model of HD, we tested the protective properties of this peptide on aggregation, as well as on different polyQ-hHtt induced neuronal phenotypes: eye degeneration (an indicator of cell death), impairment of vesicular axonal trafficking, and physiological behaviors such as larval locomotion and adult survival. Together, our results demonstrate high protective properties for P42 in vivo, in whole animals. These data also demonstrate a specific role of P42 on Huntington’s disease model, since it has no effect on other models of polyQ-induced diseases, such as spinocerebellar ataxias.

Conclusions/Significance

Altogether our data show that P42, a 23 aa-long hHtt peptide, plays a protective role with respect to polyQ-hHtt aggregation as well as cellular and behavioral dysfunctions induced by polyQ-hHtt in vivo. Our study also confirms the correlation between polyQ-hHtt aggregation and neuronal defects. Finally, these results strongly suggest a therapeutic potential for P42, specific of Huntington’s disease.     

VIP and CRF reduce ADAMTS expression and function in osteoarthritis synovial fibroblasts

ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family is known to play an important role in the pathogenesis of osteoarthritis (OA), working on aggrecan degradation or altering the integrity of extracellular matrix (ECM). Thus, the main purpose of our study was to define the role of vasoactive intestinal peptide (VIP) and corticotrophin‐releasing factor (CRF), as immunoregulatory neuropeptides, on ADAMTS production in synovial fibroblasts (SF) from OA patients and healthy donors (HD). OA‐ and HD‐SF were stimulated with pro‐inflammatory mediators and treated with VIP or CRF. Both neuropeptides decreased ADAMTS‐4, ‐5, ‐7 and ‐12 expressions, aggrecanase activity, glycosaminoglycans (GAG), and cartilage oligomeric matrix protein (COMP) degradation after stimulation with fibronectin fragments (Fn‐fs) in OA‐SF. After stimulation with interleukin‐1β, VIP reduced ADAMTS‐4 and ‐5, and both neuropeptides decreased ADAMTS‐7 production and COMP degradation. Moreover, VIP and CRF reduced Runx2 and β‐catenin activation in OA‐SF. Our data suggest that the role of VIP and CRF on ADAMTS expression and cartilage degradation could be related to the OA pathology since scarce effects were produced in HD‐SF. In addition, their effects might be greater when a degradation loop has been established, given that they were higher after stimulation with Fn‐fs. Our results point to novel OA therapies based on the use of neuropeptides, since VIP and CRF are able to stop the first critical step, the loss of cartilage aggrecan and the ECM destabilization during joint degradation.     

Evidence for new C-terminally truncated variants of α- and β-tubulins

Cellular α-tubulin can bear various carboxy-terminal sequences: full-length tubulin arising from gene neosynthesis is tyrosinated, and two truncated variants, corresponding to detyrosinated and Δ2 α‑tubulin, result from the sequential cleavage of one or two C-terminal residues, respectively. Here, by using a novel antibody named 3EG that is highly specific to the –EEEG C-terminal sequence, we demonstrate the occurrence in neuronal tissues of a new αΔ3‑tubulin variant corresponding to α1A/B‑tubulin deleted of its last three residues (EEY). αΔ3‑tubulin has a specific distribution pattern: its quantity in the brain is similar to that of αΔ2-tubulin around birth but is much lower in adult tissue. This truncated α1A/B-tubulin variant can be generated from αΔ2-tubulin by the deglutamylases CCP1, CCP4, CCP5, and CCP6 but not by CCP2 and CCP3. Moreover, using 3EG antibody, we identify a C‑terminally truncated β-tubulin form with the same –EEEG C-terminal sequence. Using mass spectrometry, we demonstrate that β2A/B-tubulin is modified by truncation of the four C-terminal residues (EDEA). We show that this newly identified βΔ4-tubulin is ubiquitously present in cells and tissues and that its level is constant throughout the cell cycle. These new C-terminally truncated α- and β-tubulin variants, both ending with –EEEG sequence, are expected to regulate microtubule physiology. Of interest, the αΔ3-tubulin seems to be related to dynamic microtubules, resembling tyrosinated-tubulin rather than the other truncated variants, and may have critical function(s) in neuronal development.     

Direct comparison of binding equilibrium, thermodynamic, and rate constants determined by surface- and solution-based biophysical methods

The binding interactions of small molecules with carbonic anhydrase II were used as model systems to compare the reaction constants determined from surface- and solution-based biophysical methods. Interaction data were collected for two arylsulfonamide compounds, 4-carboxybenzenesulfonamide (CBS) and 5-dimethyl-amino-1-naphthalene-sulfonamide (DNSA), binding to the enzyme using surface plasmon resonance, isothermal titration calorimetry, and stopped-flow fluorescence. We demonstrate that when the surface plasmon resonance biosensor experiments are performed with care, the equilibrium, thermodynamic, and kinetic constants determined from this surface-based technique match those acquired in solution. These results validate the use of biosensor technology to collect reliable data on small molecules binding to immobilized macromolecular targets. Binding kinetics were shown to provide more detailed information about complex formation than equilibrium constants alone. For example, although carbonic anhydrase II bound DNSA with twofold higher affinity than CBS, kinetic analysis revealed that CBS had a fourfold slower dissociation rate. Analysis of the binding and transition state thermodynamics also revealed significant differences in the enthalpy and entropy of complex formation. The lack of labeling requirements, high information content, and high throughput of surface plasmon resonance biosensors will make this technology an important tool for characterizing the interactions of small molecules with enzymes and receptors.     

Childhood Symptoms of ADHD Overrule Comorbidity in Relation to Psychosocial Outcome at Age 15: A Longitudinal Study

Objective

Neurodevelopmental problems (NDPs) may influence the transition from childhood to adolescence. Our aim was to study long-term psychosocial outcomes of NDPs, focusing on ADHD.

Method

Data was collected through a telephone interview with parents of twins at ages 9 or 12 years. NDP screen-positive children were clinically assessed at age 15; N = 450. Psychosocial outcome concerning peers, school, internalizing problems, antisocial behavior, alcohol misuse, drug misuse, and impaired daily functioning was examined.

Results

Even after controlling for other NDP comorbidity, screen-positivity for ADHD doubled or tripled the odds of later psychosocial problems. When controlling for parental education level, the significant effect of ADHD remained only for antisocial behavior and impaired daily functioning.

Conclusions

Signs of NDPs as well as other psychiatric diagnoses at ages 9 or 12 years are associated with a more problematic adolescence. However, despite the presence of comorbidity, early ADHD symptoms stand out as the most important risk factor for later antisocial development and impaired daily functioning.     

Impact of hemodialysis on P-wave amplitude, duration, and dispersion

Atrial fibrillation (AF) is a frequent arrhythmia in patients undergoing hemodialysis (HD). P wave duration (PWdu) and P wave dispersion (PWdi) have been shown to be predictors of emerging AF in different clinical conditions. We sought to study the impact of HD on PWdu, PWdi, and P wave amplitude in a cohort of patients undergoing HD. Seventeen patients (8 men, 31+/-10 years) were studied. Echocardiography parameters, the sum of the amplitude of P waves in all 12 ECG leads (SP), mean PWdu, and PWdi, along with a host of other parameters (body weight, heart rate, electrolytes and hemoglobin/hematochrit) were measured 1/2h, before and after, HD. SP increased (11.8+/-3.9 vs 15.3+/-4.0 mm, p = 0.004), mean PWdu remained stable (82.7+/-11.1 vs 81.6+/-10.5 ms, p = 0.606), PWdi decreased (51.7+/-19.1 vs 41.7+/-19.1 ms, p = 0.03), and left atrial dimension decreased (37.96+/-3.90 vs 30.62+/-3.38 mm, p = 0.0001), after HD. The change in PWdi correlated with fluid removed by HD (r = -0.55, p = 0.022). Re-measurements of P-wave parameters in a random group of 11 of the 17 patients revealed augmented SP (p = 0.01), and stable mean PWdu (p = 0.36), and PWdi (p = 0.31), after HD. Fluid removed by HD leads to an increase in SP, a stable mean PWdu, and decrease (or stability on re-measurement in a subgroup of patients) in PWdi. Stability of PWdu may be due to the effects of augmentation of the P-wave amplitude and the reduction of the left atrial volume, cancelling each other. Variability of PWdi may stem from the occasional impossibility to measure PWdu (or measure it correctly) in minute P-waves in certain ECG leads, which in turn profoundly affects the PWdi.