Strengthening the M&E system of Peace Corps Colombia

In 1961, when the Peace Corps was established, Colombia was the first country chosen to receive volunteers. The program ran for 20 years, with volunteers working all over the country in various sectors. Then in 1981, due to the increasing violence from the guerilla civil war, the US government decided to withdraw the volunteers and suspend the Colombia program. After a 29-year hiatus, at the request of the Colombian government, the Peace Corps was invited back to Colombia in 2010. The Peace Corps Colombia post currently has two programs, Practical English for Success (PES), established first; and, Community Economic Development (CED), started as a pilot project in 2016. Both of these programs are subject to monitoring and evaluations (M&E) scrutiny, which has increased substantially since the earlier Peace Corps programs in the country. For M&E purposes, project framework and indicators for the PES program are already established. Indicators for the CED program are still under review. Both programs are impacted by the need for increasingly precise data on volunteer programs and expectations of more intensive M&E reporting. This has proved to be difficult for the post due to, among other things, limited staffing. Interest in this situation spawned my research question for this paper: how might the M&E system of Peace Corps Colombia be strengthened? I have used reviews of M&E best practices and potential pitfalls for similar organizations, comparison of these standards to the process at Peace Corps Colombia, and candid staff interviews to assess challenges to the current M&E activities and suggest strategies for improvement

Theoretical and experimental considerations of selective vulnerability In Parkinson's disease

Les maladies neurodégénératives sont typiquement caractérisées en fonction de leurs symptômes et des observations pathologiques effectuées après le décès. Les symptômes spécifiques à la maladie sont également normalement associés aux dysfonctionnements et à la dégénérescence de certaines sous- populations spécifiques de neurones dans le système nerveux. La maladie de Parkinson (MP) est une maladie neurodégénérative principalement caractérisée par des symptômes moteurs dus à la dégénérescence spécifique des neurones dopaminergiques (DA) de la substantia nigra pars compacta (SNpc/SNc). Il semble cependant que les neurones DA de la SNc ne soient pas la seule population de neurones qui dégénère dans la MP. L'analyse post-mortem, l'imagerie in vivo et les symptômes cliniques démontrent que le dysfonctionnement et la dégénérescence se produisent dans plusieurs autres régions du système nerveux, incluant par exemple des neurones noradrénergiques (NA) du locus coeruleus (LC), des neurones sérotoninergiques des noyaux du raphé et des neurones cholinergiques du noyau moteur dorsal du nerf vague (DMV) et du noyau pédonculopontin. Comme d'autres maladies neurodégénératives, la MP est causée par plusieurs facteurs, tant génétiques qu'environnementaux. De nombreuses observations suggèrent que ces facteurs soient associés au dysfonctionnement de plusieurs systèmes ou fonctions cellulaires incluant la production d’énergie par la mitochondrie, l’élimination de protéines dysfonctionnelles par le protéasome et le lysosome, la régulation de l’équilibre entre la production d'espèces oxydatives réactives et les mécanismes antioxydants, la régulation des niveaux de calcium intracellulaire et l’inflammation. Il semble donc que le dysfonctionnement de ces facteurs converge pour provoquer la dégénérescence neuronale dans le contexte du vieillissement. Ce qui rend les neurones de certaines régions du système nerveux intrinsèquement plus vulnérables aux facteurs associés à la MP est une question fondamentale qui n’est pas résolue pour le moment. Les travaux de cette thèse sont basés sur l’hypothèse proposant que cette vulnérabilité sélective découle de propriétés communes retrouvées chez les neurones vulnérables. En particulier, les neurones vulnérables auraient en commun d’être des neurones de projections dotés d’un axone complexe qui projette sur de longues distances, formant un nombre très élevé de terminaisons axonales sur de vastes territoires du système nerveux. De plus, ces neurones présenteraient des propriétés physiologiques distinctives, incluant notamment une décharge autonome (pacemaker). Ensemble, ces caractéristiques pourraient contribuer à placer ces neurones dans des conditions de fonctionnement aux limites de leur capacités bioénergétiques et homéostatiques, rendant difficile toute adaptation aux dysfonctionnements cellulaires associés au vieillissement et causés par les facteurs de risques de la MP. Dans cette thèse, je présenterai une revue systématique de la littérature sur la perte de neurones dans le cerveau des personnes atteintes de la maladie de Parkinson, montrant que l'identité neurochimique précise des neurones qui dégénèrent dans la maladie de Parkinson, et l'ordre temporel dans lequel cela se produit, n’est pas clair. Cependant, en analysant les points de vue présentés dans les publications citant cette revue, nous avons remarqué que la majorité de ceux-ci ne reflètent pas le message central de notre publication. Puisque l’identification de l’identité des neurones vulnérables et non vulnérables à la MP est fondamentale pour le développement de théories et hypothèses sur les causes de la MP, nous suivons cette première publication avec une lettre réaffirmant l'importance de faire face aux problèmes identifiés dans notre revue. Nous présentons ensuite des données in vitro montrant que les neurones vulnérables à la MP, comparés à ceux qui sont moins vulnérables, ont une capacité intrinsèque à développer des champs axonaux plus importants et plus complexes, avec un nombre plus élevé de sites actifs de libération de neurotransmetteurs. De plus, nous constatons que ces observations sont corrélées à une vulnérabilité plus élevée face à un stress oxydatif pertinent pour la MP. Ces données sont en accord avec l'hypothèse selon laquelle le domaine axonal, et en particulier le nombre de sites de libération de neurotransmetteurs par neurone, est un facteur important qui contribue à rendre un neurone sélectivement vulnérable dans le contexte de la MP. Enfin, nous présentons une méthode d’analyse d’image open-source visant à aider les biologistes et les neuroscientifiques à automatiser la quantification du nombre de neurones dans des cultures primaires de neurones, telle qu’utilisée dans les travaux de cette thèse. Nous proposons que cet algorithme simple — mais robuste — permettra aux biologistes d'automatiser le comptage des neurones avec une grande précision, quelque chose de difficile à effectuer avec les autres approches open-source disponibles présentement. Nous espérons que les travaux présentés dans cette thèse permettront de contribuer à raffiner les théories visant à expliquer l’origine de la MP et à terme, de développer de nouvelles approches thérapeutiques.Neurodegenerative diseases are typically characterized based on their symptoms, and pathological factors identified after death. The disease-specific symptoms are due to the dysfunction and degeneration of specific subpopulations of neurons, which cause dysfunction in particular brain functions. Parkinson's disease (PD) is a neurodegenerative disease primarily characterized by motor symptoms due to the specific degeneration of dopamine (DA) neurons of the substantia nigra pars compacta (SNpc/SNc): a population of neurons essential for motor control. SNc DA neurons are, however, not the only population of neurons that degenerate in PD. Post-mortem analysis, in vivo imaging, and clinical symptoms demonstrate that dysfunction and degeneration occur in several other neuronal nuclei. These include, but are not limited to, noradrenergic (NA) locus coeruleus (LC) neurons, serotonin neurons of the raphe nuclei, and cholinergic neurons of the dorsal motor nucleus of the vagus (DMV) and pedunculopontine nucleus. Like other neurodegenerative diseases, PD is linked to several risk factors, both genetic and environmental. The evidence suggests that these risk factors are associated with the dysfunction in systems of cellular bioenergetics (including mitochondrial function); proteostatic homeostasis; endolysosomal function; an imbalance between the production of reactive oxidative species (ROS), and antioxidant mechanisms; calcium homeostasis; alpha-synuclein misfolding; and neuroinflammation. Consequently, together with aging, these risk factors converge on causing the selective degeneration of "PD-vulnerable" nuclei. What makes these neurons intrinsically vulnerable to PD-associated risk factors is a fundamental question — and understanding these neurons will reveal biological mechanisms that we can target to protect these cells from degeneration. Our best hypotheses to explain why these neurons are based on the observations that most PD- vulnerable neurons are long-range projection neuromodulatory neurons sharing common characteristics: projecting to voluminous territories, having very long and highly branched unmyelinated axonal domains with vast numbers of neurotransmitter release sites, and exhibiting a unique physiology such as pacemaker firing. Taken together, this suggests that these neurons function at the tail-end of their bioenergetic and homeostatic capacity, unable to tolerate any further demands, such as those incurred in the presence of risk factors associated with PD. In this thesis, I will present a systematic review on the literature on purported cell loss in PD brains, showing that — given the actual primary evidence — the precise neurochemical identity of neurons that degenerate in PD, and the temporal order of this degeneration, is far less clear than described by most publications. This review — at the time of writing — has gone on to be highly cited. However, analyzing the claims made in publications citing this review, we discover that the majority of claims do not reflect the core message of our publication. Since the identity of PD-vulnerable and non-PD-vulnerable neurons is fundamental to theory and hypotheses when trying to understand PD, we follow this first publication with a letter restating the importance to address our observations. We then present in vitro data showing that classically PD-vulnerable neurons, when compared to non-PD vulnerable neurons, have an intrinsic capacity to develop larger and more complex axonal domains, with higher numbers of active neurotransmitter release sites. Moreover, we find that these observations correlate to elevated vulnerability to PD-relevant stress assays. These data provide additional support for the hypothesis that the axonal domain — and in particular — the number of active neurotransmitter sites per neuron, is a cell-autonomous factor rendering a neuron selectively vulnerable in the context of PD. Finally, we present an open-source tool to support biologists and neuroscientists in automating the quantification of neuron numbers in medium-throughput primary cell cultures. Where the application of other open-source solutions is either too simplistic for the use-case or technically challenging to implement, this simple — yet robust algorithm — allows biologists with limited computational nous to automate neuron counting with high precision. We hope that the work presented in this thesis will contribute to the refinement of theories aimed at explaining the origin of PD and, ultimately, to the development of new therapeutic approaches

Synthesis of a photo-activated analog of the antitumor antibiotic FR 900482

1997 Fall.Includes bibliographical references.A novel synthetic route to the benzazocine framework of the antitumor antibiotic FR 900482 is presented. The synthesis of the benzazocine ring is characterized by a convergent asymmetric strategy. Although the benzazocine ring was not elaborated into the bicyclic skeleton of the natural product, synthesis of a hitherto unknown class of latent mitosenes was accomplished. Acylation of the benzazocine nitrogen with a photo cleavable protecting group allowed for the formation of the highly reactive mitosene under non-reductive conditions

Rigid Body Dynamics of Ship Hulls via Hydrostatic Forces Calculated From FFT Ocean Height Fields

An art tool is presented that utilizes a method for simulating the motion of ships in response to hydrostatic forces on the hull from a height-field representation of an ocean surface. Other forces modeled as a PID controller aid to steer the ship and stabilize the motion. The algorithms described can be applied to 3D models of arbitrary shapes composed of polygons floating on height fields generated from a myriad of additional spectra. The performance of the method is demonstrated in simple and complex ships, and ocean surfaces of at, medium, and large waveheights

Transparency of Land-based Investments: Cameroon Country Snapshot

Despite a recent transparency law and participation in transparency initiatives, Cameroon’s investment environment remains plagued by poor transparency. In a new report focusing on agribusiness projects in Cameroon, CCSI and the Centre pour l’Environnement et le Développement (CED) find that: Communities continue to be excluded from decision-making around investments. The government pursues a top-down approach to concession allocation and remains reluctant to recognize all legitimate tenure rights. The government faces threats to its legitimacy as the grievances of citizens and investors alike lead to the barring of roads by communities and investor withdrawals. CCSI and CED therefore call for: A new law concerning the governance of land and land-based investment in Cameroon, to be developed in close consultation and collaboration with communities, Indigenous groups, and other actors. The law should respond to the transparency needs of affected communities, enable increased funding for technical support to communities, and facilitate the recognition of all legitimate customary land rights, with specific attention to Indigenous communities and women and girls. A national moratorium on any new approvals for large-scale agribusiness and other land-based investment projects until Cameroon’s legal and policy landscape has been reformed. This research forms part of a broader portfolio of research conducted by CCSI on a demand-driven approach to land investment transparency, focusing on the transparency needs of project-affected communities and host governments. This project was funded with UK aid from the UK government; however, the views expressed do not necessarily reflect the UK government’s official policies

Local variations in spatial synchrony of influenza epidemics

Background: Understanding the mechanism of influenza spread across multiple geographic scales is not complete. While the mechanism of dissemination across regions and states of the United States has been described, understanding the determinants of dissemination between counties has not been elucidated. The paucity of high resolution spatial-temporal influenza incidence data to evaluate disease structure is often not available. Methodology and Findings: We report on the underlying relationship between the spread of influenza and human movement between counties of one state. Significant synchrony in the timing of epidemics exists across the entire state and decay with distance (regional correlation = 62%). Synchrony as a function of population size display evidence of hierarchical spread with more synchronized epidemics occurring among the most populated counties. A gravity model describing movement between two populations is a stronger predictor of influenza spread than adult movement to and from workplaces suggesting that non-routine and leisure travel drive local epidemics. Conclusions: These findings highlight the complex nature of influenza spread across multiple geographic scales. © 2012 Stark et al

A Literature Review of Studies Evaluating Rotator Cuff Activation during Early Rehabilitation Exercises for Post-Op Rotator Cuff Repair

Despite the modern advancement of surgical repair equipment and techniques, many rotator cuff repairs do not clinically heal. Prescribed rehabilitative exercises must appropriately load the repaired muscle-tendon complex to promote healing and prevent capsular adhesions without damaging the repair. The clinician must possess an understanding of the anatomy and physiology of the healing rotator cuff, and understand the importance of the plane of movement, speed of the movement, position of the extremity, level of assistance, and type of resistance used. Electromyography (EMG) provides a useful means to determine muscle activation levels during specific exercises. Descriptions of specific exercises and EMG activation as they relate to the rotator cuff muscles are described. The specific performance of the exercises, the reliability of such EMG measures, and the descriptive figures are described. Practicing clinicians will benefit from the correct interpretation of the EMG data, and how it can be used in the exercise prescription when formulating a treatment plan

Note and Comment

Attendance at the Law School; An Extreme Case in the Application of the Safety Appliance Act; Advisory Opinions; Refusal of Specific Performance Where Subsequent Unexpected Events Render it Inequitable; Is Vasectomy a Cruel Punishmen

Huntingtin disrupts lipid bilayers in a polyQ-length dependent manner

AbstractHuntington's Disease (HD) is a neurodegenerative disorder that is defined by the accumulation of nanoscale aggregates comprised of the huntingtin (htt) protein. Aggregation is directly caused by an expanded polyglutamine (polyQ) domain in htt, leading to a diverse population of aggregate species, such as oligomers, fibrils, and annular aggregates. Furthermore, the length of this polyQ domain is directly related to onset and severity of disease. The first 17 N-terminal amino acids of htt have been shown to further modulate aggregation. Additionally, these 17 amino acids appear to have lipid binding properties as htt interacts with a variety of membrane-containing structures present in cells, such as organelles, and interactions with these membrane surfaces may further modulate htt aggregation. To investigate the interaction between htt exon1 and lipid bilayers, in situ atomic force microscopy (AFM) was used to directly monitor the aggregation of htt exon1 constructs with varying Q-lengths (35Q, 46Q, 51Q, and myc-53Q) on supported lipid membranes comprised of total brain lipid extract. The exon1 fragments accumulated on the lipid membranes, causing disruption of the membrane, in a polyQ dependent manner. Furthermore, the addition of an N-terminal myc-tag to the htt exon1 fragments impeded the interaction of htt with the bilayer