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Genebanks play an essential role in a world where agricultural biodiversity has been lost from farming habitats, malnutrition persists as global population continues to rise, and farm productivity is vulnerable to climate change. We demonstrate the importance of the genebank of the International Center for Tropical Agriculture (CIAT) to the development of seven iron-biofortified varieties of climbing bean and the impact of their adoption on farm households in Rwanda. First, we link iron-biofortified varieties of climbing beans directly to the genebank through pedigree analysis and key informant interviews with the breeders who developed them. Second, we apply various econometric models to test the impact of adoption on yield, consumption, and purchase of beans by farming households in Rwanda, building upon previous research on bush beans. We based the analysis on a dataset of nearly 1400 households, collected in 2015 by HarvestPlus. We found that the scope of the genetic diversity housed in the bean collection at CIAT was fundamental to developing successful iron-biofortified beans. We found significant positive effects of climbing varieties on yields; however, we did not find significant effects on the amounts of beans consumed by households or bean purchases. Our results suggest that it is possible to trace the journey of an accession from its introduction in the genebank to its final use by farmers and consumers. Positive effects on yield generate incentives for adoption of iron-biofortified bean varieties, potentially boosting micronutrient consumption. Further research is needed to understand the factors affecting the adoption and impacts of climbing bean varieties.

Identifying the determinants of human behavior is useful to adjust interventions and lead the civil society toward a stronger commitment to climate change (CC) mitigation and adaptation objectives, achieving greater support for successfully implementing environmental policies. Existing research has largely focused on case studies of pro-environmental behaviors (PEBs) in developed economies but there is very little evidence for developing countries. This study provides estimations of the effect of internal factors, such as sociodemographic variables, and four psychological dimensions (CC knowledge, environmental attitudes, self-efficacy, and trust in sources of environmental information) on PEBs. Data were obtained through a survey applied with future decision makers – university students – from Colombia (n = 4,769) and Nicaragua (n = 2,354). Indices were generated for PEBs and the psychological dimensions using z-scores and Principal Component Analysis (PCA). Partial correlations were evaluated through the Ordinary Least Squares (OLS) method. Our results suggest that, in order to reach the planned emission reduction targets, policy approaches should more strongly focus on educating and motivating citizens and prepare them for contributing to the environmental cause, as well as provide individual solutions to combat CC, rather than providing only information on its causes and consequences.

Tissue-type transglutaminases constitute a family of enzymes having a dual role. They catalyze the post-translational modification of proteins and play a role in signal transduction pathways, several isoforms have been cloned in the brain. Many in vitro experiments and post-mortem studies have claimed that the enzyme plays a central role in the development of neurodegenerative disorders, especially in CAG-triplet diseases. In the present investigation, we conducted an immunocytochemical study using two different antibodies raised against tissue-type transglutaminase. To confirm the enzyme expression, non-radioactive in situ hybridization was performed on adjacent sections. The study was completed by analyzing the ultrastructural localization of the enzyme by electron microscopy. Tissue-type transglutaminase was widely expressed in both the human and rat brain. Many positive cells exhibiting neuronal features were found in the brain and cerebellum. There was a preferential expression in elements of pyramidal and extrapyramidal pathways with less expression in the somatosensory system. The mRNA detection confirmed the distribution of the enzyme. The ultrastructural approach revealed the presence of the enzyme in all neuronal compartments. Light and electron microscopy studies showed the ubiquitous nature of the enzyme and its putative role in functional as well as putative pathological processes.

Nerve growth factor (NGF), an essential peptide for sensory neurons, seems to have opposite effects when administered peripherally or directly to the central nervous system. We investigated the effects of 7-days intrathecal (i.t.) infusion of NGF on neuronal and glial spinal markers relevant to neuropathic behavior induced by chronic constriction injury (CCI) of the sciatic nerve. Allodynic and hyperalgesic behaviors were investigated by Von Frey and thermal Plantar tests, respectively. NGF-treated animals showed reduced allodynia and thermal hyperalgesia, compared to control animals. We evaluated on lumbar spinal cord the expression of microglial (ED-1), astrocytic (GFAP and S-100β), and C- and Aδ-fibers (SubP, IB-4 and Cb) markers. I.t. NGF treatment reduced reactive astrocytosis and the density of SubP, IB4 and Cb positive fibers in the dorsal horn of injured animals. Morphometric parameters of proximal sciatic nerve stump fibers and cells in DRG were also analyzed in CCI rats: myelin thickness was reduced and DRG neurons and satellite cells appeared hypertrophic. I.t. NGF treatment showed a beneficial effect in reversing these molecular and morphological alterations. Finally, we analyzed by immunohistochemistry the expression pattern of neurotrophin receptors TrkA, pTrkA, TrkB and p75NTR. Substantial alterations in neurotrophin receptors expression were observed in the spinal cord of CCI and NGF-treated animals. Our results indicate that i.t. NGF administration reverses the neuro-glial morphomolecular changes occurring in neuropathic animals paralleled by alterations in neurotrophin receptors ratio, and suggest that NGF is effective in restoring homeostatic conditions in the spinal cord and maintaining analgesia in neuropathic pain. © 2009 Springer Science+Business Media, LLC.

Reactive astrocytosis seems to be strongly implicated in the development and maintenance of inflammatory and neurodegenerative disorders. We design a new toxic model treatment with 3-nitropropionic acid (3-NP), a mitochondrial complex II irreversible inhibitor, to induce in rats Huntington's disease (HD) like syndrome, characterized by hindlimb dystonia, involuntary choreiform movements and reduced global activity. In an attempt to find out whether molecular and morphological changes in the neuro-glial network could be involved in the pathogenesis of this disease, we developed a protocol of subchronic intra-peritoneal 3-NP intoxication. Moreover we set up specific, highly discriminative, behavioral tests to detect very early mild motor disabilities in 3-NP treated rats. This treatment did not cause severe cell death. However, in the Caudate-Putamen (CPu) of all 3-NP treated animals we found a massive astrogliosis, revealed by increased GFAP levels, paralleled by changes of the glial glutamate transporter GLAST distribution. To these glial changes we detected a transcriptional upregulation of c-fos and Sub-P in the striatal medium spiny neurons (MSN). We propose that this model of 3-NP intoxication along with the designed set of behavioral analyses allow to unmask in a very early phase the motor deficits and the underlying morpho-molecular changes associated to the onset of motor disabilities in the HD-like syndrome. Therefore this model unveil the key role played by the different components of the tripartite synapse in the pathogenesis of the HD, a putative non-cell-autonomous disease.

Voltage-dependent K(+) channels play a pivotal role in controlling cellular excitability within the nervous system. The aim of the present study was to investigate the expression in the adult rat brain of the three ether-a-gogo-related gene (ERG) family members ERG1, ERG2, and ERG3, encoding for K(+) channel subunits. To this aim, the distribution of ERG transcripts was studied by means of reverse-transcription polymerase chain reaction (RT-PCR) and nonradioactive in situ hybridization histochemistry (NR-ISH). Furthermore, ERG1 subunit distribution was studied by immunohistochemical analysis. RT-PCR analysis revealed ERG1, ERG2, and ERG3 expression in the olfactory bulb, cerebral cortex, hippocampus, hypothalamus, and cerebellum. NR-ISH experiments detected transcripts encoded by all three ERG genes in the cerebral cortex and in all CA subfields and in the granular cell layer of the dentate gyrus of the hippocampus; strong ERG1 signals were also detected in scattered large elements throughout the oriens, pyramidal, and radiatum layers, and in the hilus of the dentate gyrus. In the thalamus, positively labeled neurons were detected in the reticular nucleus with ERG1 and ERG3 and in the anterodorsal nucleus with ERG2 riboprobes. Transcripts for ERG1 and, to a lesser degree, also for ERG3, were detected in the basal ganglia and in several brainstem nuclei. All three ERG genes appeared to be expressed in cerebellar Purkinje cells. Finally, ERG1 expression was also revealed in non-neuronal elements such as ependymal and subependymal cells along the ventricular walls and hippocampal astrocytes. These results suggest that the K(+) channel isoforms of the ERG family appear to be expressed in different central nervous system regions where they might differentially control the firing of neurons engaged in several networks.

In the central nervous system (CNS), the Na+-Ca2+ exchanger plays a fundamental role in controlling the changes in the intracellular concentrations of Na+ and Ca2+ ions. These cations are known to regulate neurotransmitter release, cell migration and differentiation, gene expression, and neurodegenerative processes. In the present study, nonradioactive in situ hybridization and light immunohistochemistry were carried out to map the regional and cellular distribution for both transcripts and proteins encoded by the three known Na+-Ca2+ exchanger genes NCX1, NCX2, and NCX3. NCX1 transcripts were particularly expressed in layers III-V of the motor cortex, in the thalamus, in CA3 and the dentate gyrus of the hippocampus, in several hypothalamic nuclei, and in the cerebellum. NCX2 transcripts were strongly expressed in all hippocampal subregions, in the striatum, and in the paraventricular thalamic nucleus. NCX3 mRNAs were mainly detected in the hippocampus, in the thalamus, in the amygdala, and in the cerebellum. Immunohistochemical analysis revealed that NCX1 protein was mainly expressed in the supragranular layers of the cerebral cortex, in the hippocampus, in the hypothalamus, in the substantia nigra and ventral tegmental area, and in the granular layer of the cerebellum. The NCX2 protein was predominantly expressed in the hippocampus, in the striatum, in the thalamus, and in the hypothalamus. The NCX3 protein was particularly found in the CA3 subregion, and in the oriens, radiatum, and lacunoso-moleculare layers of the hippocampus, in the ventral striatum, and in the cerebellar molecular layer. Collectively, these results suggest that the different Na+-Ca2+ exchanger isoforms appear to be selectively expressed in several CNS regions where they might underlie different functional roles. J. Comp. Neurol. 461:31–48, 2003. © 2003 Wiley-Liss, Inc.

In the central nervous system, the Na(+)/Ca(2+) exchanger plays a fundamental role in controlling changes in the intracellular concentrations of Na(+) and Ca(2+) ions that occur in physiologic conditions such as neurotransmitter release, cell migration and differentiation, gene expression, as well as neuro-degenerative processes. Three genes, NCX1, NCX2, and NCX3, encoding for Na(+)/Ca(2+) exchanger isoforms have been cloned. In this review, by using non-radioactive in situ hybridization and light immunohistochemistry with NCX isoform-specific riboprobes and antibodies, respectively, a systematic brain mapping for both transcripts and proteins encoded by all three NCX genes is described. Intense expression of NCX transcripts and proteins was detected in the cerebral cortex, hippocampus, thalamus, metathalamus, hypothalamus, brainstem, spinal cord, and cerebellum. In these areas, NCX transcripts and proteins were often found with an overlapping distribution pattern, although specific brain areas displaying a peculiar expression of each exchanger isoform were also found. Furthermore, immunoelectron and confocal microscopy revealed the expression of the NCX1 isoform of the exchanger at both pre- and postsynaptic sites as well as in association with membranes of the endoplasmic reticulum. Collectively, these data suggest that the different isoforms of the Na(+)/Ca(2+) exchanger appear to be selectively expressed in several CNS regions where they might underlie different functional roles.

Remodeling of neural networks in the anterior forebrain of an animal model of hyperactivity and attention deficits as monitored by molecular imaging probes. These studies report on the remodeling of neural networks which are likely to be the consequences of the segmental defect in the anterior forebrain of an animal model of hyperactivity and attention-deficit, the juvenile prehypertensive male spontaneously hypertensive rat (SHR). Molecular biology and microscope imaging techniques were used such as: (i) dopamine (DA) D-1 and D-2 receptors by radioligand binding studies; (ii) the Ca2+/Calmodulin-dependent protein kinase II (CaMKII); (iii) transcription factors (TF) such as c-FOS by Immunocytochemistry; and (iv) the respiratory chain enzyme cytochrome-oxidase (C.O.), as markers of neuronal activity in the anterior forebrain of SHR and Wistar Kyoto normotensive (WKY) controls rats. Microcomputer-assisted high-resolution image analysis using DA receptor binding and C.O., as probes revealed by cross-correlations among different regions within brain an altered cross-talk in the anterior forebrain of the SHR as compared to the controls. In particular, an altered cross-talk was also observed within the amygdala complex in the SHR by CaMKII and c-FOS expression. Therefore, the hypothesized segmental defect in the anterior forebrain of the SHR produces network consequences leading to behavioral alteration in the attentional activity and emotional domains. Subchronic treatment with metilphenidate (MP) that is known to block the reuptake of biogenic amines (mainly DA) produced network remodeling which are known to be paralleled by behavioral modifications in the attentive activity and emotional domains. Imperspective, the results from this model system that features the main aspects of attention-deficit hyperactivity disorder (ADHD), can be useful for the understanding of the neural substrates of hyperactivity and attention deficits and possibly for an early diagnosis and appropriate treatment of ADHD children.

Infiltration of the nonobese diabetic (NOD) mouse's Harderian gland (HG) was studied in 1–30-week-old animals. A mononuclear cell invasion of this gland is first seen in 8-week-old female mice (i.e., at a slightly later age than that for the onset of infiltration of pancreatic islets). Infiltrating elements are mainly located at the hilus of the gland or at one or two foci (periacinar infiltration) within the parenchyma. In the latter case, a few elements infiltrate the fibrous connective tissue surrounding the acini (one or more) without damaging them. The most severe histopathological lesion was observed in 16-week-old animals; at this time infiltration ranges from a still focal lesion to complete acinar destruction of the gland. Ultrastructural observations confirm that in several cases acinar cells are destroyed and the HG parenchyma is substituted with infiltrating elements, fibroblasts, and connective tissue. HG infiltration is comparable to the pancreatic inflammatory infiltration; the two processes are very similar, though insulitis starts slightly earlier than HG infiltration. Furthermore, as for insulitis and diabetes incidence, HG infiltration affects NOD males less than females. Moreover, immunocytochemistry has shown that T lymphocytes are the prevalent infiltrating element both in pancreatic islets and HGs. Further studies are required to understand the reasons for autoimmune destruction of this gland. © 1996 Wiley-Liss, Inc.

Low-dose streptozocin-treated (LDS) mice were administered an inhibitor of lipid peroxidation, U-83836-E (a derivative of vitamin E), in order to observe its ability to alter the onset of diabetes. Ten or 20 mg/kg body wt. per day of U-83836-E were given to mice for 7 days and they were killed after 21 days. Results revealed that there was a significant increase in glycaemia in treated groups up to day 14 after which no further increase was noticed. Superoxide dismutase (SOD) assay showed that: (1) the LDS treatment significantly reduces SOD activity when compared with untreated controls (P0.005); (2) U-83836-E increases SOD levels (when compared with untreated controls); and (3) U-83836-E counteracts LDS treatment, since SOD activity is significantly higher with respect to that found in LDS-controls (P0.05), and SOD levels were significantly higher with respect to that found in Group 2 animals (P0.05), but significantly lower with respect to those found in groups 3 and 4 (P0.005). Moreover, malondialdehyde (MDA), the end-product of lipoperoxidation, was found at much higher levels in LDS controls than in the other groups and the lowest values were found in U-83836-E controls and in normoglycaemic animals treated with both streptozocin and U-83836-E. Morphological observations demonstrated that islet beta cells were of normal appearance in normoglycaemic animals of the treated groups. In conclusion, the in vivo inhibition of lipid peroxidation by this compound produces a limited but significant prevention of the islet beta cell destruction.