Rural Deposit Mobilization in Asia

Domestic resource mobilization is becoming increasingly important in many developing countries because of the problems they are facing in attaining additional foreign resources and aid. But in many countries systematic disincentives must be removed before the full rural deposit mobilization potential can be realized. This paper presents an analysis of rural deposit mobilization in four Asian countries: Bangladesh, Indonesia, the Philippines and Thailand. With the exception of Bangladesh, there is no clear upward trend in share of rural deposits relative to total deposits. Institutions specializing in rural lending appear to mobilize an even smaller share of their total resources than the rest of the banking system. Determinants of savings behavior are discussed considering incentives for both savers and lenders. Administered interest rates are identified as a problem because they often result in negative real rates on deposits for savers while making rediscount and other government funds cheaper for banks/branches than mobilizing deposits. Efforts to expand banks/branches into rural areas have been thwarted by credit policies which make them unviable. Therefore, reforms in interest rates and other financial policies are often a necessary first step in expanding rural deposit mobilization

An Ethical Inquiry to Personhood as the Standard for Sexbot Ownership: A Response to S. Petersen

In the field of robot ethics, debates about sexbots, their personhood, and their moral status continue. To provide our stance in this debate, we ask the question: Is it unethical for sexbots to be owned? This paper responds to the claims of Steve Petersen’s (2016) paper “Is it good for them too? Ethical concerns for the sexbots”, where he argues that sexbots are not wronged for performing the functions they are designed for. We respond to this claim by arguing for John Danaher’s Theory of Ethical Behaviorism (2020). If ethical behaviorism is correct in claiming that behavior is a sufficient ground for moral status ascription, we see sexbot ownership as unethical. We argue for our claim and show that the moral considerability of the sexbot could be proven under the standards given in our framework for ascribing moral status

Synapsins I and II Are Not Required for Insulin Secretion from Mouse Pancreatic beta-cells

Synapsins are a family of phosphoproteins that modulate the release of neurotransmitters from synaptic vesicles. The release of insulin from pancreatic beta-cells has also been suggested to be regulated by synapsins. In this study, we have utilized a knock out mouse model with general disruptions of the synapsin I and II genes [synapsin double knockout (DKO)]. Stimulation with 20 mM glucose increased insulin secretion 9-fold in both wild-type (WT) and synapsin DKO islets, whereas secretion in the presence of 70 mM K+ and 1mM glucose was significantly enhanced in the synapsin DKO mice compared to WT. Exocytosis in single beta-cells was investigated using patch clamp. The exocytotic response, measured by capacitance measurements and elicited by a depolarization protocol designed to visualize exocytosis of vesicles from the readily releasable pool and from the reserve pool, was of the same size in synapsin DKO and WT beta-cells. The increase in membrane capacitance corresponding to readily releasable pool was approximately 50fF in both genotypes. We next investigated the voltage-dependent Ca2+ influx. In both WT and synapsin DKO beta-cells the Ca2+ current peaked at 0 mV and measured peak current (I-p) and net charge (Q) were of similar magnitude. Finally, ultrastructural data showed no variation in total number of granules (N-v) or number of docked granules (N-s) between the beta-cells from synapsin DKO mice and WT control. We conclude that neither synapsin I nor synapsin II are directly involved in the regulation of glucose-stimulated insulin secretion and Ca-2-dependent exocytosis in mouse pancreatic beta-cells. (Endocrinology 153: 2112-2119, 2012

Misallocation and Productivity in Colombia’S Manufacturing Industries

Following Hsieh and Klenow (2009), this paper studies productivity dispersions in Colombian industrial establishments using the Colombian Annual Manufacturing Survey (AMS) from 1982 to 1998. The United States is used as a benchmark to estimate the reallocation of capital and labor to equalize marginal products across plants in Colombia. Gains are found in manufacturing Total Factor Productivity (TFP) of approximately 3-8 percent and TPF is positively correlated with exporting status, age, size, and location in the central region of the country. There is also suggestive evidence that opening the economy in 1991 is associated with an increase in plant productivity levels for firms that export goods. The 1990 reform that reduced dismissal costs is associated with an increase in productivity, while the reform that increased labor costs in 1993 is associated with a decrease in plants productivity. Further work is needed to establish a causal relation between productivity and policy changes

Reduced insulin secretion correlates with decreased expression of exocytotic genes in pancreatic islets from patients with type 2 diabetes.

Reduced insulin release has been linked to defect exocytosis in β-cells. However, whether expression of genes suggested to be involved in the exocytotic process (exocytotic genes) is altered in pancreatic islets from patients with type 2 diabetes (T2D), and correlate to insulin secretion, needs to be further investigated. Analysing expression levels of 23 exocytotic genes using microarray revealed reduced expression of five genes in human T2D islets (χ(2)=13.25; p<0.001). Gene expression of STX1A, SYT4, SYT7, SYT11, SYT13, SNAP25 and STXBP1 correlated negatively to in vivo measurements of HbA1c levels and positively to glucose stimulated insulin secretion (GSIS) in vitro in human islets. STX1A, SYT4 and SYT11 protein levels correspondingly decreased in human T2D islets. Moreover, silencing of SYT4 and SYT13 reduced GSIS in INS1-832/13 cells. Our data support that reduced expression of exocytotic genes contributes to impaired insulin secretion, and suggest decreased expression of these genes as part of T2D pathogenesis

A circular RNA generated from an intron of the insulin gene controls insulin secretion.

Fine-tuning of insulin release from pancreatic β-cells is essential to maintain blood glucose homeostasis. Here, we report that insulin secretion is regulated by a circular RNA containing the lariat sequence of the second intron of the insulin gene. Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of β-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. The effect of the circular RNA is exerted at the transcriptional level and involves an interaction with the RNA-binding protein TAR DNA-binding protein 43 kDa (TDP-43). The level of this circularized intron is reduced in the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired secretory capacity. The study of this and other circular RNAs helps understanding β-cell dysfunction under diabetes conditions, and the etiology of this common metabolic disorder

A circular RNA generated from an intron of the insulin gene controls insulin secretion

Fine-tuning of insulin release from pancreatic β-cells is essential to maintain blood glucose homeostasis. Here, we report that insulin secretion is regulated by a circular RNA containing the lariat sequence of the second intron of the insulin gene. Silencing of this intronic circular RNA in pancreatic islets leads to a decrease in the expression of key components of the secretory machinery of β-cells, resulting in impaired glucose- or KCl-induced insulin release and calcium signaling. The effect of the circular RNA is exerted at the transcriptional level and involves an interaction with the RNA-binding protein TAR DNA-binding protein 43 kDa&nbsp;(TDP-43). The level of this circularized intron is reduced in the islets of rodent diabetes models and of type 2 diabetic patients, possibly explaining their impaired secretory capacity. The study of this and other circular RNAs helps understanding β-cell dysfunction under diabetes conditions, and the etiology of this common metabolic disorder