63 research outputs found

    Can Maternity Benefits Have Long-Term Effects on Childbearing? Evidence from Soviet Russia

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    This paper quantifies the effects of Russia’s 1981 expansion in maternity benefits on completed childbearing. The program provided one year of partially paid parental leave and a small cash transfer upon a child’s birth. I exploit the program’s two-stage implementation and find evidence that women had more children as a result of the program. Fertility rates rose immediately by 8.2% over twelve months. The increase in fertility rates not only persisted for the ten-year duration of the program, but it reflected large increases in higher-order births to older women who already had children before the program started

    Essays on Family Policy, Fertility and Children's Outcomes.

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    Governments around the world have long provided financial incentives that encourage and discourage childbearing with a goal of improving children’s outcomes. Empirical evidence concerning the effects of these interventions on childbearing and children’s outcomes is crucial to resolve on-going policy debates about whether to continue providing, expand, or introduce funding for such programs. However, the long-term effectiveness of these incentives remains an open question because of the difficulty of assessing the causal effects of interventions. My dissertation provides credible estimates of the effects of the introduction of various family policies in Russia and in the United States. The first and second chapters use newly-available data from Russian censuses to estimate the effect of introducing a maternity benefit program in Russia on short-term and long-term childbearing as well as on long-term children’s outcomes. The first chapter exploits the program’s two-stage implementation and finds evidence that women had more children as a result of the program. The program induced nearly 5 million births over its duration, where an extra birth cost the government about 1.4 times a year’s average national earnings. The second chapter finds that the program resulted in slightly lower educated cohorts, but had no other influence on many economic and family structure outcomes in adulthood. Thus, the maternity benefit program was able to induce more births, but there is little evidence that it induced extra costs on the government in the longer-term based on outcomes in adulthood of children born after the start of the program. The third chapter uses restricted American census data to estimate the effect of introducing family planning program funding in the United States on children’s economic well-being. This chapter finds that household incomes were 3 percent higher among children born after family planning programs began. These children were also 8 percent less likely to live in poverty and 11 percent less likely to live in households receiving public assistance.PhDEconomicsUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/113490/1/omalkova_1.pd

    Federally funded family planning programs in the United States reduce poverty in childhood and, decades later, in adulthood

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    The Affordable Care Act’s contraceptive mandate has been one of the most hotly debated segments of the already controversial law, but it is by no means the first time the federal government has become involved in family planning. Johannes Norling, Martha J. Bailey, and Olga Malkova examine how federally funded family planning programs begun in the 1960s and 1970s affected childhood and adult poverty rates. They find that parents’ access to affordable contraception is associated with lower poverty rates for their offspring, both during childhood and later in life

    Cellular immune response induced by dna immunization of mice with drug resistant integrases of hiv-1 clade a offers partial protection against growth and metastatic activity of integrase-expressing adenocarcinoma cells

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    Funding Information: Funding: Experiments were supported by the grants of the Russian Science Fund 15-15-30039, Russian Fund for Basic Research 20-04-01034, Latvian Science Fund LZP 2018-2-03-08, and EU-ROPARTNER project “Strengthening and spreading international partnership activities of the Faculty of Biology and Environmental Protection of University of Lodz, Poland, for interdisciplinary research and innovation”. Mobility and method acquisition were supported by Swedish institute PI project 19806/2016TP, and Horizon 2020 project VACTRAIN#692293. MI and BW were supported by Horizon 2020 grant EAVI contract N68113. Funding Information: Experiments were supported by the grants of the Russian Science Fund 15-15-30039, Russian Fund for Basic Research 20-04-01034, Latvian Science Fund LZP 2018-2-03-08, and EU-ROPARTNER project ?Strengthening and spreading international partnership activities of the Faculty of Biology and Environmental Protection of University of Lodz, Poland, for interdisciplinary research and innovation?. Mobility and method acquisition were supported by Swedish institute PI project 19806/2016TP, and Horizon 2020 project VACTRAIN#692293. MI and BW were supported by Horizon 2020 grant EAVI contract N68113. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.Therapeutic DNA-vaccination against drug-resistant HIV-1 may hinder emergence and spread of drug-resistant HIV-1, allowing for longer successful antiretroviral treatment (ART) up-to relief of ART. We designed DNA-vaccines against drug-resistant HIV-1 based on consensus clade A integrase (IN) resistant to raltegravir: IN_in_r1 (L74M/E92Q/V151I/N155H/G163R) or IN_in_r2 (E138K/G140S/Q148K) carrying D64V abrogating IN activity. INs, overexpressed in mammalian cells from synthetic genes, were assessed for stability, route of proteolytic degradation, and ability to induce oxidative stress. Both were found safe in immunotoxicity tests in mice, with no inherent carcinogenicity: their expression did not enhance tumorigenic or metastatic potential of adenocarcinoma 4T1 cells. DNA-immunization of mice with INs induced potent multicytokine T-cell response mainly against aa 209–239, and moderate IgG response cross-recognizing diverse IN variants. DNA-immunization with IN_in_r1 protected 60% of mice from challenge with 4Tlluc2 cells expressing non-mutated IN, while DNA-immunization with IN_in_r2 protected only 20% of mice, although tumor cells expressed IN matching the immunogen. Tumor size inversely correlated with IN-specific IFN-γ/IL-2 T-cell response. IN-expressing tumors displayed compromised metastatic activity restricted to lungs with reduced metastases size. Protective potential of IN immunogens relied on their immunogenicity for CD8+ T-cells, dependent on proteasomal processing and low level of oxidative stress.publishersversionPeer reviewe

    ОСОБЕННОСТИ ФОРМИРОВАНИЯ КОРПОРАТИВНЫХ СТРУКТУР В СИСТЕМЕ ТЕПЛОСНАБЖЕНИЯ РЕГИОНА

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    The article contains the research results of formation and functioning of corporate structures of the regional heat power engineering. A geometrical model of interactions between hierarchy levels of this structure is proposed. The role of the government in an improvement of the effectiveness of the heat supply system of regions is proved.В работе приведены результаты исследования формирования и функционировании создаваемых корпоративных структур региональной теплоэнергетики. Предложена геометрическая модель взаимодействия между уровнями иерархии такой структуры. Обоснование роли государства в повышении эффективности функционирования теплоснабжения регионов

    Defining phenotypic and functional heterogeneity of glioblastoma stem cells by mass cytometry

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    Most patients with glioblastoma (GBM) die within 2 years. A major therapeutic goal is to target GBM stem cells (GSCs), a subpopulation of cells that contribute to treatment resistance and recurrence. Since their discovery in 2003, GSCs have been isolated using single-surface markers, such as CD15, CD44, CD133, and α6 integrin. It remains unknown how these single-surface marker-defined GSC populations compare with each other in terms of signaling and function and whether expression of different combinations of these markers is associated with different functional capacity. Using mass cytometry and fresh operating room specimens, we found 15 distinct GSC subpopulations in patients, and they differed in their MEK/ERK, WNT, and AKT pathway activation status. Once in culture, some subpopulations were lost and previously undetectable ones materialized. GSCs that highly expressed all 4 surface markers had the greatest self-renewal capacity, WNT inhibitor sensitivity, and in vivo tumorigenicity. This work highlights the potential signaling and phenotypic diversity of GSCs. Larger patient sample sizes and antibody panels are required to confirm these findings

    Identification of enhanced IFN-γ signaling in polyarticular juvenile idiopathic arthritis with mass cytometry

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    Polyarticular juvenile idiopathic arthritis (JIA) is among the most challenging of the JIA subtypes to treat. Even with current biologic therapies, the disease remains difficult to control in a substantial subset of patients, highlighting the need for new therapies. The aim of this study was to use the high dimensionality afforded by mass cytometry with phospho-specific antibodies to delineate signaling abnormalities in immune cells from treatment-naive polyarticular JIA patients. Peripheral blood mononuclear cells were isolated from 17 treatment-naive polyarticular JIA patients, 10 of the patients after achieving clinical remission, and 19 healthy controls. Samples were stimulated for 15 minutes with IL-6 or IFN-γ and analyzed by mass cytometry. Following IFN-γ stimulation, increased STAT1 and/or STAT3 phosphorylation was observed in subsets of CD4 T cells and classical monocytes from treatment-naive patients. The enhanced IFN-γ signaling was associated with increased expression of JAK1 and SOCS1 in CD4 T cells. Furthermore, substantial heterogeneity in surface marker expression was observed among the subsets of CD4 T cells and classical monocytes with increased IFN-γ responsiveness. The identification of enhanced IFN-γ signaling in CD4 T cells and classical monocytes from treatment-naive polyarticular JIA patients provides mechanistic support for investigations into therapies that attenuate IFN-γ signaling in this disease

    The state of the Martian climate

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    60°N was +2.0°C, relative to the 1981–2010 average value (Fig. 5.1). This marks a new high for the record. The average annual surface air temperature (SAT) anomaly for 2016 for land stations north of starting in 1900, and is a significant increase over the previous highest value of +1.2°C, which was observed in 2007, 2011, and 2015. Average global annual temperatures also showed record values in 2015 and 2016. Currently, the Arctic is warming at more than twice the rate of lower latitudes

    Genome-wide significant association with seven novel multiple sclerosis risk loci

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    Objective: A recent large-scale study in multiple sclerosis (MS) using the ImmunoChip platform reported on 11 loci that showed suggestive genetic association with MS. Additional data in sufficiently sized and independent data sets are needed to assess whether these loci represent genuine MS risk factors. Methods: The lead SNPs of all 11 loci were genotyped in 10 796 MS cases and 10 793 controls from Germany, Spain, France, the Netherlands, Austria and Russia, that were independent from the previously reported cohorts. Association analyses were performed using logistic regression based on an additive model. Summary effect size estimates were calculated using fixed-effect meta-analysis. Results: Seven of the 11 tested SNPs showed significant association with MS susceptibility in the 21 589 individuals analysed here. Meta-analysis across our and previously published MS case-control data (total sample size n=101 683) revealed novel genome-wide significant association with MS susceptibility (p<5×10−8) for all seven variants. This included SNPs in or near LOC100506457 (rs1534422, p=4.03×10−12), CD28 (rs6435203, p=1.35×10−9), LPP (rs4686953, p=3.35×10−8), ETS1 (rs3809006, p=7.74×10−9), DLEU1 (rs806349, p=8.14×10−12), LPIN3 (rs6072343, p=7.16×10−12) and IFNGR2 (rs9808753, p=4.40×10−10). Cis expression quantitative locus effects were observed in silico for rs6435203 on CD28 and for rs9808753 on several immunologically relevant genes in the IFNGR2 locus. Conclusions: This study adds seven loci to the list of genuine MS genetic risk factors and further extends the list of established loci shared across autoimmune diseases

    Genome-wide significant association with seven novel multiple sclerosis risk loci

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    Objective: A recent large-scale study in multiple sclerosis (MS) using the ImmunoChip platform reported on 11 loci that showed suggestive genetic association with MS. Additional data in sufficiently sized and independent data sets are needed to assess whether these loci represent genuine MS risk factors. Methods: The lead SNPs of all 11 loci were genotyped in 10 796 MS cases and 10 793 controls from Germany, Spain, France, the Netherlands, Austria and Russia, that were independent from the previously reported cohorts. Association analyses were performed using logistic regression based on an additive model. Summary effect size estimates were calculated using fixed-effect meta-analysis. Results: Seven of the 11 tested SNPs showed significant association with MS susceptibility in the 21 589 individuals analysed here. Meta-analysis across our and previously published MS case-control data (total sample size n=101 683) revealed novel genome-wide significant association with MS susceptibility (p<5×10−8) for all seven variants. This included SNPs in or near LOC100506457 (rs1534422, p=4.03×10−12), CD28 (rs6435203, p=1.35×10−9), LPP (rs4686953, p=3.35×10−8), ETS1 (rs3809006, p=7.74×10−9), DLEU1 (rs806349, p=8.14×10−12), LPIN3 (rs6072343, p=7.16×10−12) and IFNGR2 (rs9808753, p=4.40×10−10). Cis expression quantitative locus effects were observed in silico for rs6435203 on CD28 and for rs9808753 on several immunologically relevant genes in the IFNGR2 locus. Conclusions: This study adds seven loci to the list of genuine MS genetic risk factors and further extends the list of established loci shared across autoimmune diseases
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