Embedding theorems of function classes, IV

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Embedding theorems of function classes, II

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The period function of the generalized Lotka-Volterra centers

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Embedding theorems of function classes, I

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A Descriptive and analytic look at Marx's own explanations of the falling rate of profit (second version)

This paper examines, both descriptively and analytically, Marx's arguments for the falling rate of profit from the Hodgskin section of Theories of Surplus Value, The General Law section of the recently published Volume 33 of the Collected Works and Chapter 3 of Volume III of Capital. The conclusions are as follows: First, Marx realised that his main attempt to give an intrinsic explanation of the falling rate of profit, which occurred in the General Law section, had failed; but he still hoped that he would be able to demonstrate it in the future. Second, the Hodgskin and General Law sections contain a number of subsidiary explanations, mostly related to resource scarcity, some of which are correct. Third, Part III of volume III does not contain a demonstration of the falling rate of profit, but a description of the role of the falling rate of profit in capitalist development. Forth, it also contains suppressed references to resource scarcity. And finally, in Chapter 3 of Volume III, Marx says that it is resource scarcity that causes the fall in the rate of profit described in Part III of the same volume. The key to all these conclusions in the careful analysis of the General Law section.

A descriptive and analytic look at Marxs own explanations for the falling rate of profit

Marxs conclusions about the falling rate of profit have been analysed exhaustively. Usually this has been done by building models which broadly conform to Marxs views and then showing that his conclusions are either correct or, more frequently, that they can not be sustained. By contrast, this paper examines, both descriptively and analytically, Marxs arguments from the Hodgskin section of Theories of Surplus Value, the General Law section of the recently published Volume 33 of the Collected Works and Chapter 3 of Volume III of Capital. It also gives a new interpretation of Part III of this last work. The main conclusions are first, that Marx had an intrinsic explanation of the falling rate of profit but was unable to give it a satisfactory demonstration and second, that he had a number of subsidiary explanations of which the most important was resource scarcity. The paper closes with an assessment of the pedigree of various currents of Marxian thought on this issue.

A descriptive and analytic look at Marxs own explanations for the falling rate of profit (Long Version)

Marxs conclusions about the falling rate of profit have been analysed exhaustively. Usually this has been done by building models which broadly conform to Marxs views and then showing that his conclusions are either correct or, more frequently, that they can not be sustained. By contrast, this paper examines, both descriptively and analytically, Marxs arguments from the Hodgskin section of Theories of Surplus Value, the General Law section of the recently published Volume 33 of the Collected Works and Chapter 3 of Volume III of Capital. It also gives a new interpretation of Part III of this last work. The main conclusions are first, that Marx had an intrinsic explanation of the falling rate of profit but was unable to give it a satisfactory demonstration and second, that he had a number of subsidiary explanations of which the most important was resource scarcity. The paper closes with an assessment of the pedigree of various currents of Marxian thought on this issue.

The third order Melnikov function of a quadratic center under quadratic perturbation

We study quadratic perturbations of the integrable system (1+x)dH; where H =(x²+y²)=2: We prove that the first three Melnikov functions associated to the perturbed system give rise at most to three limit cycles.

Multiplicity of limit cycles and analytic m-solutions for planar differential systems

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The bogomolov conjecture for totally degenerate Abelian varieties

We prove the Bogomolov conjecture for a totally degenerate abelian variety A over a function field. We adapt Zhang's proof of the number field case replacing the complex analytic tools by tropical analytic geometry. A key step is the tropical equidistribution theorem for A at the totally degenerate place.

Tropical varieties for non-archimedean analytic spaces

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Effect on renal function of tenofovir co-administered with either efavirenz or boosted lopinavir or boosted atazanavir: the Swiss HIV Cohort Study

Reduced re'nal function has been reported with tenofovir disoproxil fumarate (TDF). It is not clear whether TDF co-administered with a boosted protease inhibitor (PI) leads to a greater decline in renal function than TDF co-administered with a non-nucleoside reverse transcriptase inhibitor (NNRTI).Methods: We selected ail antiretroviral therapy-naive patients in the Swiss HIV Cohort Study (SHCS) with calibrated or corrected serum creatinine measurements starting antiretroviral therapy with TDF and either efavirenz (EFV) or the ritonavir-boosted PIs, lopinavir (LPV/r) or atazanavir (ATV/r). As a measure of renal function, we used the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation to estimate the glomerular filtration rate (eGFR). We calculated the difference in eGFR over time between two therapies using a marginal model for repeated measures. In weighted analyses, observations were weighted by the product of their point of treatment and censoring weights to adjust for differences both in the sort of patients starting each therapy and in the sort of patients remaining on each therapy over time.Results: By March 2011, 940 patients with at least one creatinine measurement on a first therapy with either TDF and EFV (n=484), TDF and LPVlr (n=269) or TDF and ATV/r (n=187) had been followed for a median of 1. 7, 1.2 and 1.3 years, respectively. Table 1 shows the difference in average estimated GFR (eGFR) over time since starting cART for two marginal models. The first model was not adjusted for potential confounders; the second mode! used weights to adjust for confounders. The results suggest a greater decline in renal function during the first 6 months if TDF is used with a PI rather than with an NNRTI, but no further difference between these therapies after the first 6 months. TDF and ATV/r may lead to a greater decline in the first 6 months than TDF and LPVlr.Conclusions: TDF co-administered with a boosted PI leads to a greater de cline in renal function over the first 6 months of therapy than TDF co-administered with an NNRTI; this decline may be worse with ATV/r than with LPV/r.

Altered NKG2D function in NK cells induced by chronic exposure to NKG2D ligand-expressing tumor cells.

NKG2D is an activation receptor that allows natural killer (NK) cells to detect diseased host cells. The engagement of NKG2D with corresponding ligand results in surface modulation of the receptor and reduced function upon subsequent receptor engagement. However, it is not clear whether in addition to modulation the NKG2D receptor complex and/or its signaling capacity is preserved. We show here that the prolonged encounter with tumor cell-bound, but not soluble, ligand can completely uncouple the NKG2D receptor from the intracellular mobilization of calcium and the exertion of cell-mediated cytolysis. However, cytolytic effector function is intact since NKG2D ligand-exposed NK cells can be activated via the Ly49D receptor. While NKG2D-dependent cytotoxicity is impaired, prolonged ligand exposure results in constitutive interferon gamma (IFNgamma) production, suggesting sustained signaling. The functional changes are associated with a reduced presence of the relevant signal transducing adaptors DNAX-activating protein of 10 kDa (DAP-10) and killer cell activating receptor-associated protein/DNAX-activating protein of 12 kDa (KARAP/DAP-12). That is likely the consequence of constitutive NKG2D engagement and signaling, since NKG2D function and adaptor expression is restored to normal when the stimulating tumor cells are removed. Thus, the chronic exposure to tumor cells expressing NKG2D ligand alters NKG2D signaling and may facilitate the evasion of tumor cells from NK cell reactions.

Differential effects of two anti-apo-cytochrome c-specific monoclonal antibodies on the function of apo-cytochrome c-specific murine T cell clones.

A murine monoclonal antibody (SJL 2-4) specific for the antigen apo-cytochrome c was shown to inhibit both antigen-induced proliferation and lymphokine secretion by an apo-cytochrome c-specific BALB/c helper T cell clone. The inhibition was specific because additional apo-cytochrome c-specific T cell clones were not inhibited by the same monoclonal antibody. Time course studies of the inhibition indicated that the initial 8 hr of contact between T cell clones and antigen-presenting cells were critical for activation of the T cell clones. Inhibition of T cell functions by antigen-specific antibodies appeared to correlate with the antibody-antigen binding constant because a second monoclonal antibody (Cyt-1-59), with identical specificity but with a lower affinity constant for apo-cytochrome c, had very little inhibitory effect on the proliferation or lymphokine secretion of apo-cytochrome c-specific T cell clones.