Tenure Security and Urban Social Protection Links: India

Guaranteeing tenure security to the households living in informal settlements (slums) has not seen any progress in urban India. This is because the policymakers have failed to see land tenure status as a continuum from insecure tenure to a legal status. In general, the poor in the cities move from informal to quasi?legal ( de facto ) tenure through various processes, and then to legal tenure ( de jure ) in cases of a public policy intervention that confers property title on them. In the absence of such a policy, the urban poor and low?income migrants can seek to consolidate their urban citizenship through political citizenship in an electoral democracy, through welfare interventions by the state and above all, through their own subversions of urban legalities. This article first illustrates the existence of a continuum of tenure status in informal settlements in Ahmedabad City. It explains the factors that give a slum settlement a particular level of tenure status; and then through quantitative data, links the level of tenure security to social protection outcomes. The article shows that through small public actions, it is possible to improve access of the urban poor to social protection measures and that it is not necessary to leapfrog to extending property rights to the dwellers of these informal settlements. It is essential to realise that if land titles are given in a society where other rights are not present, the poor will not be able to retain them

Developmental plasticity and circuit mechanisms of dopamine-modulated aggression

Aggression and violence pose a significant public health concern to society. Aggression is a highly conserved behavior that shares common biological correlates across species. While aggression developed as an evolutionary adaptation to competition, its untimely and uncontrolled expression is maladaptive and presents itself in a number of neuropsychiatric disorders. A mechanistic hypothesis for pathological aggression links aberrant behavior with heightened dopamine function. However, while dopamine hyper-activity is a neural correlate of aggression, the developmental aspects and circuit level contributions of dopaminergic signaling have not been elucidated. In this dissertation, I aim to address these questions regarding the specifics of dopamine function in a murine model of aggressive behavior. In chapter I, I provide a review of the literature that describes the current state of research on aggression. I describe the background elements that lay the foundation for experimental questions and original data presented in later chapters. I introduce, in detail, published studies that describe the clinical manifestation and epidemiological spread, the dominant categories, the anatomy and physiology, and the pharmacology of aggression, with a particular emphasis on the dopaminergic system. Finally, I describe instances of genetic and environmental risk factors impacting aggression, concluding with studies revealing an important role for interactions among genetics, environmental factors, and age in the development of aggression. In chapter II, I investigate the developmental origins of aggression by examining sensitive periods during which perturbations to the dopaminergic system impact adult aggressive behavior. Previous work in our laboratory has concluded that periadolescent (postnatal days 22-41) elevation in dopamine, via transient dopamine transporter blockade, leads to increased adult aggression and heightened response to amphetamine. I expanded on these findings by temporally refining the opening and closing of this window of sensitivity, specifically to postnatal days 32 to 41, during which increases in dopaminergic tone increase adult aggression and behavioral sensitivity to psychostimulants. The potentiated response to amphetamine indicated to us a state of altered dopaminergic physiology. We next validated this hypothesis and found increased firing rate (in vitro), and increased bursting and population activity (in vivo) at baseline. These data indicate that elevated periadolescent dopamine impacts maturation of the dopamine system, leading to a hyper-active dopaminergic and aggressive predisposition. In conclusion, this chapter introduces a developmental component to the hyper-dopaminergic model of aggression. In chapter III, I report a series of experiments exploring the direct and causal involvement of dopamine in driving aggression. While dopamine hyper-activity is a neural correlate of aggression, the precise brain circuits involved have not been elucidated. Using optogenetics, I established a causal role for the ventral tegmental area (a key source of dopamine) in aggression modulation. I further advanced this finding by demonstrating that the modulatory role of dopamine, is population- and projection-specific. I found that activity of ventral tegmental area, but not substantia nigra, dopamine neurons promotes aggression. Furthermore, controlled stimulation of ventral tegmental area dopaminergic terminals in the lateral septum, but not the nucleus accumbens, mediates increased aggression. I selectively traced connectivity between the lateral septum and the ventral tegmental area using a Cre-driven, population-specific viral vector. I used this virus to show that anatomically distinct clusters of ventral tegmental area dopamine cells send projections to the lateral septum and the nucleus accumbens, thereby dissociating the two target sites both behaviorally and anatomically. Furthermore, I found that while local dopamine release in the lateral septum increases aggression, it has no bearing on reward behaviors thus indicating a stronger association with impulsive, and not motivated, aggression. In conclusion, this chapter offers causal evidence for dopamine’s role in modulating impulsive aggression by identifying a distinct pathway from the ventral tegmental area to the lateral septum that controls aggression. In the work described in chapter IV, my aim was to determine the mechanism underlying ventral tegmental area to lateral septum dopamine-mediated aggression. I first characterized the expression of dopamine receptors in the lateral septum and found that D2 receptors heavily colocalize with the dominant population of neurons in the lateral septum, i.e. GABAergic cells. Moreover, the D2 receptors are perfectly aligned with incoming dopamine afferents. Next we investigated, in acute brain slices, how D2 signaling affects lateral septum function. We revealed that activating D2 receptors hyperpolarizes D2-expressing lateral septum neurons. This effect was abolished with bath application of the D2 receptor antagonist, sulpiride. We validated the functional involvement of post-synaptic D2 signaling in a behavioral test, and found that the aggression induced by direct terminal release of dopamine at the lateral septum is reversed by acutely blocking local D2 receptor signaling. In conclusion, this chapter demonstrates that the ventral tegmental area to lateral septum dopamine pathway, via D2-mediated inhibition of GABAergic lateral septum neurons, is necessary to drive ventral tegmental area-triggered aggression. In chapter V, I engage in a general discussion addressing how the findings from each chapter can be linked to provide a more comprehensive outlook on environmental and genetic risk factors that can modulate ventral tegmental area-triggered aggression. I discuss possible pre- and post-synaptic mechanisms that could impact the functionality of the identified dopaminergic ventral tegmental area to lateral septum pathway. Moreover, in distinguishing this specific dopamine circuit and lateral septum D2 signaling as an underlying correlate of violent pathology, this dissertation aims to evoke deeper understanding of the mechanism of current antipsychotics used to manage aggression. I end this dissertation by proposing new empirical questions, techniques and lines of research that could further develop my findings as well strengthen the links between dominant models of aggression that exist in the field today

Regulation of health professions in Ontario: self-regulation with statutory- based public accountability

The paper explores the model of regulation of health professionals in Ontario, Canada; a self-regulation model built around a detailed statutory scheme. The core of the paper consists of a discussion of Ontario’s Regulated Health Professions Act and of the key components of 26 specific health profession acts that have been enacted under its umbrella. The paper explores the role of the regulatory colleges, the role of the Ministry of Health in determining scope of practice and other components of medical practice, and the disciplinary and appeal procedures. Some other specific issues are also briefly touched upon, such as the integration into the profession of internationally trained physicians, and the government’s role in ensuring access to specialists across the province. A final section looks at the challenges and the limitations of the Ontario model, through a number of health professions-related controversies that reveal gaps in self-regulation, including: failure to set and enforce proper educational and practice standards in specific areas; failure to conduct timely investigations into potential misconduct by professionals; and failure to question professionals in a position of power. The paper also discusses briefly the implications of recognizing through legal regulation some alternative and complementary medical practices, and the challenge of regulating indigenous health care practitioners. It concludes that the primary limitations of the regulatory model arise on account of professional self-interest and power-relations impacting procedural issues, and the complexity of the regulatory model that may potentially undermine quality control. Este artigo explora o modelo de regulação dos profissionais de saúde em Ontário, Canadá, um modelo de autorregulação construído em torno de um regime estatutário específico. O foco central do trabalho é a discussão sobre a Lei de Regulamentação das Profissões de Saúde de Ontário e os principais componentes de 26 leis que foram promulgadas sob sua égide para regulamentar profissões de saúde específicas. O artigo explora a função dos colegiados regulatórios, o papel do Ministério da Saúde na determinação de escopos de prática e de outros elementos da atividade médica, e os procedimentos disciplinares e de recurso. Outras questões específicas também são brevemente abordadas como a adequação profissional de médicos treinados no exterior e a atribuição do governo de garantir o acesso a especialistas em toda a província. A seção final analisa os desafios e as limitações do modelo, levantando uma série de controvérsias relacionadas às profissões de saúde que revelam lacunas na autorregulação, incluindo: incapacidade de estabelecer e aplicar padrões educacionais e práticos adequados em áreas específicas; falha na condução de investigações em tempo hábil sobre possíveis desvios de conduta por parte dos profissionais; e falha em questionar profissionais em posições de poder. O artigo discute ainda o desafio de regular os profissionais de saúde indígenas. Conclui-se que as principais limitações do modelo regulatório surgem em razão de interesses profissionais individualistas e de relações de poder que afetam questões processuais, bem como da complexidade do modelo regulatório, que pode potencialmente prejudicar o controle de qualidade.&nbsp

Introduction. Safe and inclusive cities: contesting violence

Introduction. Safe and inclusive cities: contesting violenc