The Evolution of Collective Land Tenure Regimes in Pastoralist Societies: Lessons from Andean Countries

Much has been said about the importance of pastoralist livelihoods for the effective and sustainable use of drylands around the world. Yet, pastoralist societies are experiencing more pressures to their way of life than ever before. These pressures and changing trends are jeopardising pastoralist livelihoods as well as the sustainability of dryland resources. In the face of this challenging reality, this paper aims to analyse how land tenure regimes of pastoralist societies living in the Andean altiplano have transformed over the last 50 years. It also discusses the implications of these transformations for the sustainability of resource management in these areas, based on the premise that a better understanding of customary land tenure regimes can help to inform public policy and decision making.GRADEELLA projectPractical Actio

No good recommendation without a mechanistic explanation? : the case of higher education governance

In higher education, reforms have long been driven by the theory that system performance depends on governance design; yet it remains far from clear which arrangements can actually deliver results, as shown in the analysis of various streams of research devoted to assessing performance in higher education. We reason that such a question can be better answered if research aims for a mechanistic explanation and operationalizes it to avoid the shortcomings of both \u2018variable-oriented\u2019 and \u2018case-oriented\u2019 strategies. We therefore develop a \u2018diversity-oriented\u2019 mechanistic framework that explains differences in performance by differences in policy tool mixes, which we define as governance regimes. This set of policy tools is meant as a configuration of properties of delivery vehicles, decision-making design, and accountability design. Such an explanatory focus has many advantages: policy tools are manipulable, as they depend on political and administrative decisions; moreover, they are efficient causes, as they trigger mechanisms at the individual level that directly account for both individual and institutional behavior and, hence, performance. Tool-based explanations therefore can more easily allow for policy learning and transfer than can \u2018remote\u2019 constitutional, historical, or cultural accounts

Effects of Delivering Guanidinoacetic Acid or Its Prodrug to the Neural Tissue: Possible Relevance for Creatine Transporter Deficiency

The creatine precursor guanidinoacetate (GAA) was used as a dietary supplement in humans with no adverse events. Nevertheless, it has been suggested that GAA is epileptogenic or toxic to the nervous system. However, increased GAA content in rodents affected by guanidinoacetate methyltransferase (GAMT) deficiency might be responsible for their spared muscle function. Given these conflicting data, and lacking experimental evidence, we investigated whether GAA affected synaptic transmission in brain hippocampal slices. Incubation with 11.5 \ub5M GAA (the highest concentration in the cerebrospinal fluid of GAMT-deficient patients) did not change the postsynaptic compound action potential. Even 1 or 2 mM had no effect, while 4 mM caused a reversible decrease in the potential. Guanidinoacetate increased creatine and phosphocreatine, but not after blocking the creatine transporter (also used by GAA). In an attempt to allow the brain delivery of GAA when there was a creatine transporter deficiency, we synthesized diacetyl guanidinoacetic acid ethyl ester (diacetyl-GAAE), a lipophilic derivative. In brain slices, 0.1 mM did not cause electrophysiological changes and improved tissue viability after blockage of the creatine transporter. However, diacetyl-GAAE did not increase creatine nor phosphocreatine in brain slices after blockage of the creatine transporter. We conclude that: (1) upon acute administration, GAA is neither epileptogenic nor neurotoxic; (2) Diacetyl-GAAE improves tissue viability after blockage of the creatine transporter but not through an increase in creatine or phosphocreatine. Diacetyl-GAAE might give rise to a GAA\u2013phosphoGAA system that vicariates the missing creatine\u2013phosphocreatine system. Our in vitro data show that GAA supplementation may be safe in the short term, and that a lipophilic GAA prodrug may be useful in creatine transporter deficiency

Creatine salts provide neuroprotection even after partial impairment of the creatine transporter

open6Creatine, a compound that is critical for energy metabolism of nervous cells, crosses the blood-brain barrier (BBB) and the neuronal plasma membrane with difficulty, and only using its specific transporter. In the hereditary condition where the creatine transporter is defective (creatine transporter deficiency) there is no creatine in the brain, and administration of creatine is useless lacking the transporter. The disease is severe and incurable. Creatine-derived molecules that could cross BBB and plasma membrane independently of the transporter might be useful to cure this condition. Moreover, such molecules could be useful also in stroke and other brain ischemic conditions. In this paper, we investigated three creatine salts, creatine ascorbate, creatine gluconate and creatine glucose. Of these, creatine glucose was ineffective after transporter block with guanidine acetic acid (GPA) administration. Creatine ascorbate was not superior to creatine in increasing tissue creatine and phosphocreatine content after transporter impairment, however even after such impairment it delayed synaptic failure during anoxia. Finally, creatine gluconate was superior to creatine in increasing tissue content of creatine after transporter block and slowed down PS disappearance during anoxia, an effect that creatine did not have. These findings suggest that coupling creatine to molecules having a specific transporter may be a useful strategy in creatine transporter deficiency. In particular, creatine ascorbate has effects comparable to those of creatine in normal conditions, while being superior to it under conditions of missing or impaired creatine transporter.openAdriano, E; Garbati, P; Salis, A; Damonte, G; Millo, E; Balestrino, MAdriano, ENRICO GIOVANNI; Garbati, Patrizia; Salis, Annalisa; Damonte, Gianluca; Millo, Enrico; Balestrino, Maurizi

Opto-electronic characterization of TiO₂/Metal/TiO₂ multilayers

Transparent conductive oxides (TCOs) play an important role in many optoelectronic devices such as solar cells, organic light emitting diodes, touch panel and efficiency energy applications, heat mirrors and thermoelectric materials. In recent years, many researchers proposed a TCO/metal/TCO multilayer structure with advanced electrical properties, mechanical flexibility, chemical stability and high optical transparency than a TCO single layer. Multilayer films of TiO₂/Cu/TiO₂ and TiO2/Co/TiO2were grown on glass substrate by DC magnetron sputtering technique at low temperature deposition for low cost applications. Copper interlayer was chosen as a possible replacement of Ag due to their comparable electrical conductivity and relativity low cost. Cobalt interlayer is studied for ferromagnetic properties at room temperature because of its potential applications in spintronics. The deposition time was chosen to obtain estimated thickness for layers of 30 nm while metal interlayers of 12, 15 and 18 nm thick were grown. The optical, electrical, structural and morphological properties of these films were characterized by UV-visible spectroscopy, four probe technique, X-rays diffraction patterns and atomic force microscopy (AFM) respectively. Figures of merit (FOM) are determinate for transparent solar cells electrode and others applications.Instituto de Física La Plat

Fibrinogen αC‐regions are not directly involved in fibrin polymerization as evidenced by a "Double‐Detroit" recombinant fibrinogen mutant and knobs‐mimic peptides

Background: Fibrin polymerization, following fibrinopeptides A and B (FpA, FpB) cleavage, relies on newly exposed α‐ and β‐chains N‐termini (GPR, GHR; A‐, B‐knobs, respectively) engaging pre‐existent a and b pockets in other fibrin(ogen) molecules' γ‐ and (B)β‐chains C‐terminal regions. A role for mostly disordered (A)α‐chains C‐terminal regions "bridging" between fibrin molecules/fibrils has been proposed. Objectives: Fibrinogen Detroit is a clinically observed mutation (AαR19→S) with non‐engaging GPS A‐knobs. By analogy, a similar Bβ‐chain mutation, BβR17→S, should produce non‐engaging GHS B‐knobs. A homozygous “Double‐Detroit” mutant (AαR19→S, BβR17→S; DD‐FG) was developed: with A‐a and B‐b engagements endogenously blocked, other interactions would become apparent. Methods: DD‐FG, wild‐type recombinant (WT‐FG), and human plasma (hp‐FG) fibrinogen self‐association was studied by turbidimetry coupled with fibrinopeptides release HPLC/mass spectrometry analyses, and by light‐scattering following size‐exclusion chromatography (SE‐HPLC). Results: In contrast to WT‐FG and hp‐FG, DD‐FG produced no turbidity increase, irrespective of thrombin concentration. The SE‐HPLC profile of concentrated DD‐FG was unaffected by thrombin treatment, and light‐scattering, at lower concentration, showed no intensity and hydrodynamic radius changes. Compared with hp‐FG, both WT‐FG and DD‐FG showed no FpA cleavage difference, while ~50% FpB was not recovered. Correspondingly, SDS‐PAGE/Western‐blots revealed partial Bβ‐chain N‐terminal and Aα‐chain C‐terminal degradation. Nevertheless, ~70% DD‐FG molecules bearing (A)αC‐regions potentially able to associate were available. Higher‐concentration, nearly‐intact hp‐FG with 500‐fold molar excess GPRP‐NH2/GHRP‐NH2 knobs‐mimics experiments confirmed these no‐associations findings. Conclusions: (A)αC‐regions interactions appear too weak to assist native fibrin polymerization, at least without knobs engagement. Their role in all stages should be carefully reconsidered