Are Remittances Insurance? Evidence from Rainfall Shocks in the Philippines

Do remittances sent by overseas migrants serve as insurance for recipient households? This paper examines how remittances sent by overseas migrants respond to income shocks experienced by Philippine households. Because household income and remittances are jointly determined, we exploit rainfall shocks as instrumental variables for income changes. In households with overseas migrants, we find that exogenous changes in income lead to changes in remittances of the opposite sign, consistent with an insurance motivation for remittances. In such households, we cannot reject the null hypothesis of full insurance: on average, essentially all of exogenous declines in income are replaced by remittance inflows from overseas. By contrast, changes in household income have no effect on remittance receipts in households without overseas migrants. Remittance receipts may also be partly shared with others: in migrant households, net gifts to other households move in the same direction as remittance receipts in response to income shocks.remittances, migration, insurance, risk, instrumental variables, rainfall, Philippines

Randomizing religion: the impact of Protestant evangelism on economic outcomes

We study the causal impact of religiosity through a randomized evaluation of an evangelical Protestant Christian values and theology education program delivered to thousands of ultrapoor Filipino households. Six months after the program ended, treated households have higher religiosity and income; no statistically significant differences in total labor supply, consumption, food security, or life satisfaction; and lower perceived relative economic status. Exploratory analysis suggests that the income treatment effect may operate through increasing grit. Thirty months after the program ended, significant differences in the intensity of religiosity disappear, but those in the treatment group are less likely to be Catholic and more likely to be Protestant, and there is some mixed evidence that their consumption and perceived relative economic status are higher

Local probing of the field emission stability of vertically aligned multiwalled carbon nanotubes

Metallic cantilever in high vacuum atomic force microscope has been used as anode for field emission experiments from densely packed vertically aligned multi-walled carbon nanotubes. The high spatial resolution provided by the scanning probe technique allowed precise setting of the tip-sample distance in the submicron region. The dimension of the probe (curvature radius below 50nm) allowed to measure current contribution from sample areas smaller than 1um^2. The study of long-term stability evidenced that on these small areas the field emission current remains stable (within 10% fluctuations) several hours (at least up to 72 hours) at current intensities between 10-5A and 10-8A. Improvement of the current stability has been observed after performing long-time Joule heating conditioning to completely remove possible adsorbates on the nanotubes.Comment: 15 pages, 7 figure

Hecke-type double sums, Appell-Lerch sums, and mock theta functions (I)

By developing a connection between partial theta functions and Appell-Lerch sums, we find and prove a formula which expresses Hecke-type double sums in terms of Appell-Lerch sums and theta functions. Not only does our formula prove classical Hecke-type double sum identities such as those found in work Kac and Peterson on affine Lie Algebras and Hecke modular forms, but once we have the Hecke-type forms for Ramanujan's mock theta functions our formula gives straightforward proofs of many of the classical mock theta function identities. In particular, we obtain a new proof of the mock theta conjectures. Our formula also applies to positive-level string functions associated with admissable representations of the affine Lie Algebra $A_1^{(1)}$ as introduced by Kac and Wakimoto

The one-message-per-cell-cycle rule: A conserved minimum transcription level for essential genes

The inherent stochasticity of cellular processes leads to significant cell-to-cell variation in protein abundance. Although this noise has already been characterized and modeled, its broader implications and significance remain unclear. In this paper, we revisit the noise model and identify the number of messages transcribed per cell cycle as the critical determinant of noise. In yeast, we demonstrate that this quantity predicts the non-canonical scaling of noise with protein abundance, as well as quantitatively predicting its magnitude. We then hypothesize that growth robustness requires an upper ceiling on noise for the expression of essential genes, corresponding to a lower floor on the transcription level. We show that just such a floor exists: a minimum transcription level of one message per cell cycle is conserved between three model organisms: Escherichia coli, yeast, and human. Furthermore, all three organisms transcribe the same number of messages per gene, per cell cycle. This common transcriptional program reveals that robustness to noise plays a central role in determining the expression level of a large fraction of essential genes, and that this fundamental optimal strategy is conserved from E. coli to human cells.Comment: 18 pages, 11 figure

A socioecological framework for research on work and obesity in diverse urban transit operators based on gender, race, and ethnicity

Urban transit (bus and rail) operators, totaling nearly 700,000 persons, are one of the heaviest occupational groups in the United States (US). Little is known about occupational risk factors for weight gain and obesity and their interrelationship with health-related behaviors, particularly among female minority (African Americans and Hispanics) transit operators who are at greater risk for obesity. As a step towards developing successful obesity interventions among urban transit operators, this paper aims to present a new socioecological framework for studying working conditions, chronic strain, health-related behaviors, weight gain/obesity, and obesity disparity in diverse urban transit operators based on gender, race, and ethnicity. Our framework is a synthesis of several different theories and disciplines: the resource-work load model (work stress), occupational ergonomics, the theory of intersectionality, and worksite health promotion. The framework was developed utilizing an extensive literature review, results from our on-going research on obesity, input from focus groups conducted with Los Angeles transit operators as well as interviews and meetings with transit operator stakeholders (management, unions, and worksite transit wellness program), and ride-along observations. Our hypotheses highlighted in the framework (see Fig. 1) are that adverse working conditions, largely characterized as a combination of high demands and low resources, will increase the risk for weight gain/obesity among transit operators directly through chronic strain and hypothalamic dysfunction (hyper-and hypo-activations), and indirectly through health-related behaviors and injuries/chronic severe pain. We also hypothesize that the observed increase in adiposity among female minority operators is due to their greater exposure to adverse occupational and non-occupational conditions that reflect their intersecting social identities of lower social class and being a minority woman in the US. Our proposed framework could greatly facilitate future transit worksite obesity studies by clarifying the complex and important roles of adverse working conditions in the etiology of weight gain/obesity and obesity disparity among transit operators and other working populations

MYC through miR-17-92 Suppresses Specific Target Genes to Maintain Survival, Autonomous Proliferation, and a Neoplastic State

SummaryThe MYC oncogene regulates gene expression through multiple mechanisms, and its overexpression culminates in tumorigenesis. MYC inactivation reverses turmorigenesis through the loss of distinguishing features of cancer, including autonomous proliferation and survival. Here we report that MYC via miR-17-92 maintains a neoplastic state through the suppression of chromatin regulatory genes Sin3b, Hbp1, Suv420h1, and Btg1, as well as the apoptosis regulator Bim. The enforced expression of miR-17-92 prevents MYC suppression from inducing proliferative arrest, senescence, and apoptosis and abrogates sustained tumor regression. Knockdown of the five miR-17-92 target genes blocks senescence and apoptosis while it modestly delays proliferative arrest, thus partially recapitulating miR-17-92 function. We conclude that MYC, via miR-17-92, maintains a neoplastic state by suppressing specific target genes