Vincentian Pragmatism: Toward a Method for Systemic Change

Scott Kelley creates the term Vincentian Pragmatism and defines it as “Vincent [de Paul]’s way of proceeding . . . [it is] an integrated and holistic way of knowing that is capable of systemic change.” He writes, “Vincentian Pragmatism must also inform the way we engage, identify, explore, interpret, and decide in response to the complex systems that exacerbate poverty. It must unite action and contemplation.” Kelley identifies questions we must ask to pursue Vincentian epistemology and explains how Vincent developed it from his own experience. The process of overcoming our biases and forming a Vincentian worldview is also examined. Vincentian Pragmatism has five components of action: “begin attentively, explore openly, interpret imaginatively, decide responsibly, and act courageously.” These are discussed in detail. Together, they are a way of truly understanding the causes and nature of poverty and strategizing for effective solutions. Different aspects of strategy are described

Emergent Catholicity: Forming the Mind of Vincent

Vincent de Paul has been perceived as anti-intellectual for reasons that are discussed in this article, but his two degrees, especially the one from the University of Toulouse, profoundly influenced his thinking. His education developed his logic, making him “a formidable theologian,” an excellent organizer, and an effective advocate for poor persons. The article traces the medieval university’s influence on Vincent’s university experience. Logic’s importance in the theology curriculum and the way it was taught are described. Since Vincent’s degree allowed him to teach from the seminal Book II of Peter Lombard’s Sentences, Lombard’s writings are contextualized within those of two other scholastic thinkers, Peter Abelard and Thomas Aquinas. Scholasticism examined disparate perspectives with the goal of integrating them into a whole truth. This was a step toward understanding complete truth of God. Vincent’s application of the scholastic method is illustrated with issues he faced in his work and with his response to Jansenism. His education gave him “a comprehensive understanding of Catholic theology, the capacity to engage viewpoints different from his own, and the . . . intellectual mastery required to articulate sophisticated concepts in ways that were understandable to people who did not have his educational background.

Subsidiarity and Global Poverty: Development from Below Upwards

Scott Kelley raises the question of what a Catholic, Vincentian perspective brings to poverty studies that is unique. He answers it by exploring the debate between the developmental economists Jeffrey Sachs and William Easterly, examining the principle of subsidiarity in Catholic social teaching, and describing Frederic Ozanam’s approach to poverty alleviation. Contemporary solutions for poverty reduction are also discussed. The Sachs-Easterly debate is about whether wealthy nations should end world poverty through aid efforts to foreign governments (as Sachs contends), or whether better results come from working toward smaller goals with poor persons themselves (which is Easterly’s perspective). Easterly points out that, among other problems, foreign aid is often inefficiently managed or even pocketed by corrupt governments. Since it is not administered with input from poor persons relative to their needs, it perpetuates colonialism. Catholic social teaching advocates three principles that make up the greater idea of subsidiarity: non-arrogation, empowerment, and collaborative pluralism. These terms are all defined in detail. Taken together, they affirm the state’s obligation to help the poor but also the need for “sub-political groups” that are “intermediate between person and state” to act in partnership with poor persons. Subsidiarity is rooted in Ozanam’s work

The Gut Microbiome Is Altered in a Letrozole-Induced Mouse Model of Polycystic Ovary Syndrome.

Women with polycystic ovary syndrome (PCOS) have reproductive and metabolic abnormalities that result in an increased risk of infertility, diabetes and cardiovascular disease. The large intestine contains a complex community of microorganisms (the gut microbiome) that is dysregulated in humans with obesity and type 2 diabetes. Using a letrozole-induced PCOS mouse model, we demonstrated significant diet-independent changes in the gut microbial community, suggesting that gut microbiome dysbiosis may also occur in PCOS women. Letrozole treatment was associated with a time-dependent shift in the gut microbiome and a substantial reduction in overall species and phylogenetic richness. Letrozole treatment also correlated with significant changes in the abundance of specific Bacteroidetes and Firmicutes previously implicated in other mouse models of metabolic disease in a time-dependent manner. Our results suggest that the hyperandrogenemia observed in PCOS may significantly alter the gut microbiome independently of diet

Current Perspective on the Location and Function of Gamma- Aminobutyric Acid (GABA) and its Metabolic Partners in the Kidney.

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter located in the mammalian central nervous system, which binds to GABAA and GABAB receptors to mediate its neurological effects. In addition to its role in the CNS, an increasing number of publications have suggested that GABA might also play a role in the regulation of renal function. All three enzymes associated with GABA metabolism; glutamic acid decarboxylase, GABA ?-oxoglutarate transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSADH) have been localised to the kidney providing the necessary machinery for localised GABA synthesis and metabolism. Moreover GABA receptors have been localised to both tubular and vascular structures in the kidney, and GABA is excreted in urine (~3 ?M) in humans. Despite the collective evidence describing the presence of a GABA system in the kidney, the precise function of such a system requires further clarification. Here we provide an overview of the current renal GABA literature and provide novel data that indicates GABA can act at contractile pericyte cells located along vasa recta capillaries in the renal medulla to potentially regulate medullary blood flow

Letrozole treatment of pubertal female mice results in activational effects on reproduction, metabolism and the gut microbiome.

Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-aged women that is comprised of two out of the following three features: hyperandrogenism, oligo- or amenorrhea, or polycystic ovaries. In addition to infertility, many women with PCOS have metabolic dysregulation that increases the risk of developing type 2 diabetes, hypertension, and non-alcoholic fatty liver disease. Changes in the gut microbiome are associated with PCOS and gut microbes may be involved in the pathology of this disorder. Since PCOS often manifests in the early reproductive years, puberty is considered to be a critical time period for the development of PCOS. Exposure to sex steroid hormones during development results in permanent, organizational effects, while activational effects are transient and require the continued presence of the hormone. Androgens exert organizational effects during prenatal or early post-natal development, but it is unclear whether androgen excess results in organizational or activational effects during puberty. We recently developed a letrozole-induced PCOS mouse model that recapitulates both reproductive and metabolic phenotypes of PCOS. In this study, we investigated whether letrozole treatment of pubertal female mice exerts organizational or activational effects on host physiology and the gut microbiome. Two months after letrozole removal, we observed recovery of reproductive and metabolic parameters, as well as diversity and composition of the gut microbiome, indicating that letrozole treatment of female mice during puberty resulted in predominantly activational effects. These results suggest that if exposure to excess androgens during puberty leads to the development of PCOS, reduction of androgen levels during this time may improve reproductive and metabolic phenotypes in women with PCOS. These results also imply that continuous letrozole exposure is required to model PCOS in pubertal female mice since letrozole exerts activational rather than organizational effects during puberty

The Multiple Meanings of Global Health Governance: A Call for Conceptual Clarity

Background The term global health governance (GHG) is now widely used, with over one thousand works published in the scholarly literature, almost all since 2002. Amid this rapid growth there is considerable variation in how the term is defined and applied, generating confusion as to the boundaries of the subject, the perceived problems in practice, and the goals to be achieved through institutional reform. Methodology This paper is based on the results of a separate scoping study of peer reviewed GHG research from 1990 onwards which undertook keyword searches of public health and social science databases. Additional works, notably books, book chapters and scholarly articles, not currently indexed, were identified through Web of Science citation searches. After removing duplicates, book reviews, commentaries and editorials, we reviewed the remaining 250 scholarly works in terms of how the concept of GHG is applied. More specifically, we identify what is claimed as constituting GHG, how it is problematised, the institutional features of GHG, and what forms and functions are deemed ideal. Results After examining the broader notion of global governance and increasingly ubiquitous term “global health”, the paper identifies three ontological variations in GHG scholarship - the scope of institutional arrangements, strengths and weaknesses of existing institutions, and the ideal form and function of GHG. This has produced three common, yet distinct, meanings of GHG that have emerged – globalisation and health governance, global governance and health, and governance for global health. Conclusions There is a need to clarify ontological and definitional distinctions in GHG scholarship and practice, and be critically reflexive of their normative underpinnings. This will enable greater precision in describing existing institutional arrangements, as well as serve as a prerequisite for a fuller debate about the desired nature of GHG

A Rare Case of Secondary Bacterial Peritonitis from Clostridium perfringens in an Adult Patient with Noncirrhotic Ascites and a Krukenberg Tumor: Report of a Case

Secondary bacterial peritonitis, in comparison to spontaneous, presents with a surgically treatable intraabdominal source for infection such as a gastrointestinal perforation or abscess and is nearly always polymicrobial. We present a rare case of secondary bacterial peritonitis from Clostridium perfringens in an adult patient with noncirrhotic ascites and a Krukenberg tumor

Cortactin Is a Substrate of Activated Cdc42-Associated Kinase 1 (ACK1) during Ligand-induced Epidermal Growth Factor Receptor Downregulation

Background Epidermal growth factor receptor (EGFR) internalization following ligand binding controls EGFR downstream pathway signaling activity. Internalized EGFR is poly-ubiquitinated by Cbl to promote lysosome-mediated degradation and signal downregulation. ACK1 is a non-receptor tyrosine kinase that interacts with ubiquitinated EGFR to facilitate EGFR degradation. Dynamic reorganization of the cortical actin cytoskeleton controlled by the actin related protein (Arp)2/3 complex is important in regulating EGFR endocytosis and vesicle trafficking. How ACK1-mediated EGFR internalization cooperates with Arp2/3-based actin dynamics during EGFR downregulation is unclear. Methodology/Principal Findings Here we show that ACK1 directly binds and phosphorylates the Arp2/3 regulatory protein cortactin, potentially providing a direct link to Arp2/3-based actin dynamics during EGFR degradation. Co-immunoprecipitation analysis indicates that the cortactin SH3 domain is responsible for binding to ACK1. In vitro kinase assays demonstrate that ACK1 phosphorylates cortactin on key tyrosine residues that create docking sites for adaptor proteins responsible for enhancing Arp2/3 nucleation. Analysis with phosphorylation-specific antibodies determined that EGFR-induced cortactin tyrosine phosphorylation is diminished coincident with EGFR degradation, whereas ERK1/2 cortactin phosphorylation utilized in promoting activation of the Arp2/3 regulator N-WASp is sustained during EGFR downregulation. Cortactin and ACK1 localize to internalized vesicles containing EGF bound to EGFR visualized by confocal microscopy. RNA interference and rescue studies indicate that ACK1 and the cortactin SH3 domain are essential for ligand-mediated EGFR internalization. Conclusions/Significance Cortactin is a direct binding partner and novel substrate of ACK1. Tyrosine phosphorylation of cortactin by ACK1 creates an additional means to amplify Arp2/3 dynamics through N-WASp activation, potentially contributing to the overall necessary tensile and/or propulsive forces utilized during EGFR endocytic internalization and trafficking involved in receptor degradation