An equilibrium-conserving taxation scheme for income from capital

Under conditions of market equilibrium, the distribution of capital income follows a Pareto power law, with an exponent that characterizes the given equilibrium. Here, a simple taxation scheme is proposed such that the post-tax capital income distribution remains an equilibrium distribution, albeit with a different exponent. This taxation scheme is shown to be progressive, and its parameters can be simply derived from (i) the total amount of tax that will be levied, (ii) the threshold selected above which capital income will be taxed and (iii) the total amount of capital income. The latter can be obtained either by using Piketty's estimates of the capital/labor income ratio or by fitting the initial Pareto exponent. Both ways moreover provide a check on the amount of declared income from capital.Comment: 4 pages, 2 figure

Vitamin D intake and type 2 diabetes risk: a meta-analysis of prospective cohort studies

Background: The findings form studies on the relationship between vitamin D and type 2 diabetes were inconsistent.Objectives: To elucidate the association between vitamin D consumption and type 2 diabetes risk by conducting a metaanalysis.Methods: We conducted a systematic literature search to identify prospective cohort studies of vitamin D intake and type 2 diabetes risk prior to November 2012. Eligible studies were retrieved via both computer searches and manual review of references. The summary risk estimates were calculated based on the highest versus the lowest categories.Results: Meta-analysis of 4 prospective cohort studies involving 187, 592 participants and 9, 456 incident cases showed an absence of significant association between total vitamin D intake and type 2 diabetes risk. The combined RR was 0.93 (95% CI: 0.85–1.01). The associations were similar for subgroup analyses, a combined RR respectively was 0.94 (95% CI: 0.77-1.08), 0.91 (95% CI: 0.77-1.08), 0.93 (95% CI: 0.84-1.02), and 0.92 (95% CI: 0.84–1.01) for the intake of dietary vitamin D, supplemental vitamin D, total vitamin D in USA and total vitamin D for women only.Conclusions: Our results support that there was no association between vitamin D intake and type 2 diabetes.Keywords: Vitamin D, Diet; Type 2 Diabetes, Meta-analysisAfrican Health Sciences 2013; 13(4): 1130 - 113

Bis(2-hydroxy­imino­methyl-6-methoxy­phenolato-κ2 O 1,N)cobalt(II)

In the title compound, [Co(C8H8NO3)2], the CoII atom lies on a centre of inversion and is coordinated in a slightly distorted square-planar geometry by two N and two O atoms from the 2-hydroxy­imino­methyl-6-methoxy­phenolate ligands. Intra­molecular O—H⋯O hydrogen bonds are formed and the complexes form stacks along the b axis, with an inter­planar separation of 3.332 (1) Å between complexes. Pairs of C—H⋯O contacts are formed between complexes in neighbouring stacks

Life Span Extension by Calorie Restriction Depends on Rim15 and Transcription Factors Downstream of Ras/PKA, Tor, and Sch9

Calorie restriction (CR), the only non-genetic intervention known to slow aging and extend life span in organisms ranging from yeast to mice, has been linked to the down-regulation of Tor, Akt, and Ras signaling. In this study, we demonstrate that the serine/threonine kinase Rim15 is required for yeast chronological life span extension caused by deficiencies in Ras2, Tor1, and Sch9, and by calorie restriction. Deletion of stress resistance transcription factors Gis1 and Msn2/4, which are positively regulated by Rim15, also caused a major although not complete reversion of the effect of calorie restriction on life span. The deletion of both RAS2 and the Akt and S6 kinase homolog SCH9 in combination with calorie restriction caused a remarkable 10-fold life span extension, which, surprisingly, was only partially reversed by the lack of Rim15. These results indicate that the Ras/cAMP/PKA/Rim15/Msn2/4 and the Tor/Sch9/Rim15/Gis1 pathways are major mediators of the calorie restriction-dependent stress resistance and life span extension, although additional mediators are involved. Notably, the anti-aging effect caused by the inactivation of both pathways is much more potent than that caused by CR

2-Eth­oxy-6-[(methyl­imino)­meth­yl]phenol

In the title compound, C10H13NO2, synthesized by the reaction of 2-hy­droxy-3-eth­oxy­benzaldehyde with methyl­amine, there is an an intra­molecular O—H⋯N hydrogen bond involving the hy­droxy substituent and the amino N atom. In the crystal, mol­ecules form inversion dimers connected by pairs of C—H⋯O hydrogen bonds

Estrogen regulates miRNA expression: implication of estrogen receptor and miR-124/AKT2 in tumor growth and angiogenesis.

It is currently known that estrogen plays an important role in breast cancer (BC) development, but the underlying molecular mechanism remains to be elucidated. Accumulating evidence has revealed important roles of microRNAs in various kinds of human cancers, including BC. In this study, we found that among the microRNAs regulated by estrogen, miR-124 was the most prominent downregulated miRNA. miR-124 was downregulated by estradiol (E2) treatment in estrogen receptor (ER) positive BC cells, miR-124 overexpression suppressed cell proliferation, migration and invasion in BC cells; while the suppression of miR-124 using Anti-miR-124 inhibitor had opposite cellular functions. Under the E2 treatment, miR-124 had stronger effect to inhibit cellular functions in MCF7 cells than that in MDA-MB-231 cells. In addition, we identified that ERα, but not ERβ, was required for E2-induced miR-124 downregulation. Furthermore, AKT2, a known oncogene, was a novel direct target of miR-124. AKT2 expression levels were inversely correlated with miR-124 expression levels in human breast cancer specimens. AKT2 was overexpressed in BC specimens, and its expression levels were much higher in ERα positive cancer tissues than those ERα negative cancer tissues. Consistent with miR-124 suppression, E2 treatment increased AKT2 expression levels in MCF7 cells via ERα. Finally, overexpression of miR-124 in MCF7 cells significantly suppressed tumor growth and angiogenesis by targeting AKT2. Our results provide a mechanistic insight into a functional role of new ERα/miR-124/AKT2 signaling pathway in BC development. miR-124 and AKT2 may be used as biomarkers for ERα positive BC and therapeutic effect in the future

Unemployment: Study of Causes and Possible Solutions

The following measures against unemployment are proposed: In the short term, to promote greater income for the poorest sectors. It is shown that this can be paid with the resulting increased production, without losing income to the other economic agents. In the mid term, the creation of ad-hoc companies for investment in projects profitable but long lasting. And in the long run, the abandonment of the competitive models. As these proposals go against current ideas (liberalisation, labour market flexibility, free market, etc.), the statements are rigorously demonstrated, even at the risk of making the lecture harder. Part 1 explores the problem and uses a simple model and others heuristic arguments to create familiarity with macroeconomic models. Part 2 is a simplified summary of Macroeconomic Theory textbook. It serves as a review to the reader whose knowledge in economy are out of date, or as a first approximation to the topic if he or she does not have them. In the light of the theory, economic policies are evaluated for the Argentine case in the 90's. The work accepts the Keynesian explanation of unemployment (insufficient demand), but we disagree on its solution (public expenditure). Finally, in Part 3 we elaborate and justify the proposals.Comment: T.P.Eggarter (physicist) passed away in August 1997. This work was done during his last months of life and only locally published up to now. Work is in Spanish and could be translated upon request. Please contact E. Alvarez [email protected]