The Constitutionality of Prison Privatization: An Analysis of Prison Privatization in the United States and Israel

This note analyzes the constitutionality of the current state of prison privatization in the United States under the non-delegation doctrine and the due process clause. Furthermore, this note analyzes the Israeli Supreme Court\u27s ruling holding prison privatization as unconstitutional under the Basic Law of the Right to Human Dignity and Liberty. Subsequently, an argument is made that the current authority for the utilization of private prisons in the United States is insufficient to establish the use of private prisons as constitutional. As such, this note argues that the overall scheme of privatization should provide for more detailed contracts--similar to those proposed under the Israel privatization authority--to include outcome-based goals, rehabilitative efforts, and proper supervisory oversight by the governmental authority to ensure compliance. If such reforms are made, then the utilization of private prisons in the United States would become a constitutional method to manage the prison population in the United States

The Constitutionality of Prison Privatization: An Analysis of Prison Privatization in the United States and Israel

This note analyzes the constitutionality of the current state of prison privatization in the United States under the non-delegation doctrine and the due process clause. Furthermore, this note analyzes the Israeli Supreme Court\u27s ruling holding prison privatization as unconstitutional under the Basic Law of the Right to Human Dignity and Liberty. Subsequently, an argument is made that the current authority for the utilization of private prisons in the United States is insufficient to establish the use of private prisons as constitutional. As such, this note argues that the overall scheme of privatization should provide for more detailed contracts--similar to those proposed under the Israel privatization authority--to include outcome-based goals, rehabilitative efforts, and proper supervisory oversight by the governmental authority to ensure compliance. If such reforms are made, then the utilization of private prisons in the United States would become a constitutional method to manage the prison population in the United States

Insulin secretion in health and disease: nutrients dictate the pace.

Insulin is a key hormone controlling metabolic homeostasis. Loss or dysfunction of pancreatic β-cells lead to the release of insufficient insulin to cover the organism needs, promoting diabetes development. Since dietary nutrients influence the activity of β-cells, their inadequate intake, absorption and/or utilisation can be detrimental. This review will highlight the physiological and pathological effects of nutrients on insulin secretion and discuss the underlying mechanisms. Glucose uptake and metabolism in β-cells trigger insulin secretion. This effect of glucose is potentiated by amino acids and fatty acids, as well as by entero-endocrine hormones and neuropeptides released by the digestive tract in response to nutrients. Glucose controls also basal and compensatory β-cell proliferation and, along with fatty acids, regulates insulin biosynthesis. If in the short-term nutrients promote β-cell activities, chronic exposure to nutrients can be detrimental to β-cells and causes reduced insulin transcription, increased basal secretion and impaired insulin release in response to stimulatory glucose concentrations, with a consequent increase in diabetes risk. Likewise, suboptimal early-life nutrition (e.g. parental high-fat or low-protein diet) causes altered β-cell mass and function in adulthood. The mechanisms mediating nutrient-induced β-cell dysfunction include transcriptional, post-transcriptional and translational modifications of genes involved in insulin biosynthesis and secretion, carbohydrate and lipid metabolism, cell differentiation, proliferation and survival. Altered expression of these genes is partly caused by changes in non-coding RNA transcripts induced by unbalanced nutrient uptake. A better understanding of the mechanisms leading to β-cell dysfunction will be critical to improve treatment and find a cure for diabetes

Postnatal β-cell maturation is associated with islet-specific microRNA changes induced by nutrient shifts at weaning.

Glucose-induced insulin secretion is an essential function of pancreatic β-cells that is partially lost in individuals affected by Type 2 diabetes. This unique property of β-cells is acquired through a poorly understood postnatal maturation process involving major modifications in gene expression programs. Here we show that β-cell maturation is associated with changes in microRNA expression induced by the nutritional transition that occurs at weaning. When mimicked in newborn islet cells, modifications in the level of specific microRNAs result in a switch in the expression of metabolic enzymes and cause the acquisition of glucose-induced insulin release. Our data suggest microRNAs have a central role in postnatal β-cell maturation and in the determination of adult functional β-cell mass. A better understanding of the events governing β-cell maturation may help understand why some individuals are predisposed to developing diabetes and could lead to new strategies for the treatment of this common metabolic disease

Initiatives communautaires de redevabilité pour revendiquer les droits fonciers en Afrique sub-saharienne

Ces dernières années, les communautés sont confrontées de plus en plus aux accaparements de terres tant au niveau urbain et périurbain qu’au niveau rural facilités par la complicité des élites et les dysfonctionnements administratifs, en particulier en « omettant » d’appliquer les droits fonciers coutumiers pourtant reconnu dans le Code Domanial et Foncier (CDF) du Mali. Cette injustice a créé de nombreux conflits fonciers. Ce sont des territoires, des écosystèmes, des identités communautaires, la souveraineté alimentaire voire nationale qui sont menacés. La Convergence Malienne contre les Accaparements de Terres (CMAT), composée de 5 structures d’envergures nationales (AOPP, CAD-MALI, CNOP, LJDH et l’UACDDDD), travaille avec les communautés des villages Fonsira et Dalla pour trouver des solutions concrètes tant sur le terrain qu’au niveau des textes législatifs, en s’appuyant notamment sur les directives des régimes fonciers du CSA de la FAO

Tout ce qui est décidé pour nous mais sans nous, est contre nous : l’application des droits fonciers coutumiers au Mali en s’appuyant sur les directives pour la gouvernance foncière de la FAO

Ces dernières années, les communautés sont confrontées de plus en plus aux accaparements de terres tant au niveau urbain et périurbain qu’au niveau rural facilités par la complicité des élites et les dysfonctionnements administratifs, en particulier en « omettant » d’appliquer les droits fonciers coutumiers pourtant reconnu dans le Code Domanial et Foncier (CDF) du Mali. Cette injustice a créé de nombreux conflits fonciers. Ce sont des territoires, des écosystèmes, des identités communautaires, la souveraineté alimentaire voire nationale qui sont menacés. La Convergence Malienne contre les Accaparements de Terres (CMAT), composée de 5 structures d’envergures nationales (AOPP, CAD-MALI, CNOP, LJDH et l’UACDDDD), travaille avec les communautés des villages Fonsira et Dalla pour trouver des solutions concrètes tant sur le terrain qu’au niveau des textes législatifs, en s’appuyant notamment sur les directives des régimes fonciers du CSA de la FAO

Roles of Noncoding RNAs in Islet Biology.

The discovery that most mammalian genome sequences are transcribed to ribonucleic acids (RNA) has revolutionized our understanding of the mechanisms governing key cellular processes and of the causes of human diseases, including diabetes mellitus. Pancreatic islet cells were found to contain thousands of noncoding RNAs (ncRNAs), including micro-RNAs (miRNAs), PIWI-associated RNAs, small nucleolar RNAs, tRNA-derived fragments, long non-coding RNAs, and circular RNAs. While the involvement of miRNAs in islet function and in the etiology of diabetes is now well documented, there is emerging evidence indicating that other classes of ncRNAs are also participating in different aspects of islet physiology. The aim of this article will be to provide a comprehensive and updated view of the studies carried out in human samples and rodent models over the past 15 years on the role of ncRNAs in the control of α- and β-cell development and function and to highlight the recent discoveries in the field. We not only describe the role of ncRNAs in the control of insulin and glucagon secretion but also address the contribution of these regulatory molecules in the proliferation and survival of islet cells under physiological and pathological conditions. It is now well established that most cells release part of their ncRNAs inside small extracellular vesicles, allowing the delivery of genetic material to neighboring or distantly located target cells. The role of these secreted RNAs in cell-to-cell communication between β-cells and other metabolic tissues as well as their potential use as diabetes biomarkers will be discussed. © 2020 American Physiological Society. Compr Physiol 10:893-932, 2020

Contribution of Intronic miR-338-3p and Its Hosting Gene AATK to Compensatory β-Cell Mass Expansion.

The elucidation of the mechanisms directing β-cell mass regeneration and maintenance is of interest, because the deficit of β-cell mass contributes to diabetes onset and progression. We previously found that the level of the microRNA (miRNA) miR-338-3p is decreased in pancreatic islets from rodent models displaying insulin resistance and compensatory β-cell mass expansion, including pregnant rats, diet-induced obese mice, and db/db mice. Transfection of rat islet cells with oligonucleotides that specifically block miR-338-3p activity increased the fraction of proliferating β-cells in vitro and promoted survival under proapoptotic conditions without affecting the capacity of β-cells to release insulin in response to glucose. Here, we evaluated the role of miR-338-3p in vivo by injecting mice with an adeno-associated viral vector permitting specific sequestration of this miRNA in β-cells. We found that the adeno-associated viral construct increased the fraction of proliferating β-cells confirming the data obtained in vitro. miR-338-3p is generated from an intron of the gene coding for apoptosis-associated tyrosine kinase (AATK). Similarly to miR-338-3p, we found that AATK is down-regulated in rat and human islets and INS832/13 β-cells in the presence of the cAMP-raising agents exendin-4, estradiol, and a G-protein-coupled Receptor 30 agonist. Moreover, AATK expression is reduced in islets of insulin resistant animal models and selective silencing of AATK in INS832/13 cells by RNA interference promoted β-cell proliferation. The results point to a coordinated reduction of miR-338-3p and AATK under insulin resistance conditions and provide evidence for a cooperative action of the miRNA and its hosting gene in compensatory β-cell mass expansion

Identification of particular groups of microRNAs that positively or negatively impact on beta cell function in obese models of type 2 diabetes.

AIMS/HYPOTHESIS: MicroRNAs are key regulators of gene expression involved in health and disease. The goal of our study was to investigate the global changes in beta cell microRNA expression occurring in two models of obesity-associated type 2 diabetes and to assess their potential contribution to the development of the disease. METHODS: MicroRNA profiling of pancreatic islets isolated from prediabetic and diabetic db/db mice and from mice fed a high-fat diet was performed by microarray. The functional impact of the changes in microRNA expression was assessed by reproducing them in vitro in primary rat and human beta cells. RESULTS: MicroRNAs differentially expressed in both models of obesity-associated type 2 diabetes fall into two distinct categories. A group including miR-132, miR-184 and miR-338-3p displays expression changes occurring long before the onset of diabetes. Functional studies indicate that these expression changes have positive effects on beta cell activities and mass. In contrast, modifications in the levels of miR-34a, miR-146a, miR-199a-3p, miR-203, miR-210 and miR-383 primarily occur in diabetic mice and result in increased beta cell apoptosis. These results indicate that obesity and insulin resistance trigger adaptations in the levels of particular microRNAs to allow sustained beta cell function, and that additional microRNA deregulation negatively impacting on insulin-secreting cells may cause beta cell demise and diabetes manifestation. CONCLUSIONS/INTERPRETATION: We propose that maintenance of blood glucose homeostasis or progression toward glucose intolerance and type 2 diabetes may be determined by the balance between expression changes of particular microRNAs

Scrt1, a transcriptional regulator of β-cell proliferation identified by differential chromatin accessibility during islet maturation.

Glucose-induced insulin secretion, a hallmark of mature β-cells, is achieved after birth and is preceded by a phase of intense proliferation. These events occurring in the neonatal period are decisive for establishing an appropriate functional β-cell mass that provides the required insulin throughout life. However, key regulators of gene expression involved in functional maturation of β-cells remain to be elucidated. Here, we addressed this issue by mapping open chromatin regions in newborn versus adult rat islets using the ATAC-seq assay. We obtained a genome-wide picture of chromatin accessible sites (~ 100,000) among which 20% were differentially accessible during maturation. An enrichment analysis of transcription factor binding sites identified a group of transcription factors that could explain these changes. Among them, Scrt1 was found to act as a transcriptional repressor and to control β-cell proliferation. Interestingly, Scrt1 expression was controlled by the transcriptional repressor RE-1 silencing transcription factor (REST) and was increased in an in vitro reprogramming system of pancreatic exocrine cells to β-like cells. Overall, this study led to the identification of several known and unforeseen key transcriptional events occurring during β-cell maturation. These findings will help defining new strategies to induce the functional maturation of surrogate insulin-producing cells