76 research outputs found

    "The Real Wage And The Marginal Product of Labor"

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    As I see it, the errors in Keynes's analysis in Chapter Two of the General Theorv were his acceptance of diminishing returns in the short-period relation between output and labor employed and of perfect competition in the product market. These "errors," however, are easily corrected and do not alter Keynes's basic and correct ideas--that employment is determined by aggregate demand, that real wages are determined by aggregate demand given the degree of competition and the level of capital utilization and other determinants of the productivity of labor, and that the supply of labor, at least below full employment, has no effect on either employment or real wages. I would like to reiterate that the formulation we have established here is "Ricardian" rather than neoclassical. Basically all we have said is that the mark-up represents a deduction from the product of labor and that since the mark-up is certainly not procyclical and productivity probably is procyclical, as the "margin" of production is extended, real wages rise. Sraffa (1960, pp. v-vi) has argued that such a use of the term "marginal" is spurious, since the true application of the term "requires attention to be focused on change," while this use of the term, as in Ricardo's discussion of the margin of cultivation, need only be a matter of differences in quality among existing productive facilities rather than changes in scale or in input proportions. We have come a long way from the neoclassical idea of a marginal product of labor, but this should not make either us or Keynes embarrassed about Chapter Two of the General Theory, one of the most interesting and important chapters in the book. Lawlor, Darity, and Horn (1987) noted that Sraffa (1926) had pointed out that the determination of prices and quantities by the interaction of supply and demand necessitates an independence between supply and demand which does not obtain except under very restrictive conditions. Sraffa (1960) extends this argument by showing that scarcity, as in scarce factors of production, is not necessary to determine value and in fact cannot determine value independently of income distribution. Keynes's and Kalecki's work shows that when we take effective demand into account, output is determined solely by demand and distribution by the conditions of competition. Kalecki's and Keynes's work can thus be taken as an Hegelian "supersession" of classical and neoclassical economics when we realize that workers cannot bargain in terms of a real wage and that output not saleable will soon no longer be produced.

    "The Structure of Class Conflict in a Kaleckian-Keynesian Model"

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    This paper seeks to explore this issue of the existence and nature of class conflict within a picture of the economy that could be called Kaleckian-Keynesian. Though the particular model we will use owes somewhat more to Kalecki than Keynes, it hopefully does not violate the spirit of Keynes very much, and in fact it relies rather heavily on Keynes's appreciation of the rentier aspect of capitalism, a matter not discussed much by Kalecki. In addition, combining the ideas of Kalecki and Keynes we will find leads us to insights beyond what each saw by himself.

    "Profitability and the Time-Varying Liquidity Premium in the Term Structure of Interest Rates"

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    There have been numerous empirical studies of the term structure. Broadly, the evidence may be said to be consistent with some influence from expectations plus the existence of a liquidity premium. Long rates or the spread between long and short rates have seemed to be systematically related to expectations of future rates, though the expectations embodied in long rates or the spread are biased upwards as the liquidity preference theory would predict. The degree of influence of expectations and the behavior of the liquidity premium, however, have remained matters of controversy. In several recent studies (e.g., Robert Shillert 1979; Shiller, John Campbell, and Kermit Schoenholtz, 1983; David Jones and Vance Roley, 1983; Mankiw and Summers, 1984; and Mankiw, 1986) the expectations theory has performed poorly, even allowing for the existence of a constant liquidity premium, in attempts to test the joint hypothesis of rational expectations and the expectations theory. Shiller, Campbell, and Schoenholtz and Mankiw and Summers, among others, have suggested renewing the search for the determinants of a time-varying liquidity premium as a possibility for explaining what is going on but have had little success themselves in finding such.

    A Recursive Partitioning Analysis Demonstrating Risk Subsets for 8-Year Biochemical Relapse After Margin-Positive Radical Prostatectomy Without Adjuvant Hormone or Radiation Therapy.

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    PURPOSE: The cohort of patients with locally advanced prostate cancer (PC) and positive surgical margin(s) at radical prostatectomy (RP) who would benefit from salvage or adjuvant treatment is unclear. This study examines the risk of prostate-specific antigen (PSA) relapse in a large population of men with PC after margin-positive RP. METHODS AND MATERIALS: Using a multi-institutional database, patients with clinically localized PC who underwent RP between 2002 and 2010 with recorded follow-up PSA were retrospectively selected. Patients were excluded for pathologic seminal vesicle or lymph node involvement, metastatic disease, pre-RP PSA ≥ 30, or adjuvant (nonsalvage) radiation therapy or hormone therapy. The primary endpoint was biochemical relapse free survival (bRFS), where PSA failure was defined as PSA > 0.10 ng/mL and rising, or at salvage intervention. The Kaplan-Meier method was employed for bRFS estimates; recursive partitioning analysis using cumulative or single maximal margin extent (ME) and Gleason grade (GG) at RP was applied to identify variables associated with bRFS. RESULTS: At median follow-up of 105 months, 210 patients with positive margins at RP were eligible for analysis, and 89 had experienced PSA relapse. Median age was 61 years (range, 43-76), and median pre-RP PSA 5.8 ng/mL (1.6-26.0). Recursive partitioning analysis yielded 5 discrete risk groups, with the lowest risk group (GG1, ≤ 2 mm ME) demonstrating a bRFS of 92% at 8 years compared with the highest risk group (GG3-5, ≥ 3 mm ME) of 11%. CONCLUSIONS: This retrospective study suggests that it may be possible to risk-stratify patients undergoing margin-positive RP using commonly acquired clinical and pathologic variables. Patients with low-grade tumors and minimally involved margins have a very low recurrence risk and may be able to forego postprostatectomy radiation. Meanwhile, those with higher grade and greater involvement could benefit from adjuvant or early salvage radiation therapy

    Reductions in mesophyll and guard cell photosynthesis impact on the control of stomatal responses to light and CO2

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    Transgenic antisense tobacco plants with a range of reductions in sedoheptulose-1,7-bisphosphatase (SBPase) activity were used to investigate the role of photosynthesis in stomatal opening responses. High resolution chlorophyll a fluorescence imaging showed that the quantum efficiency of photosystem II electron transport (Fq′/Fm′) was decreased similarly in both guard and mesophyll cells of the SBPase antisense plants compared to the wild-type plants. This demonstrated for the first time that photosynthetic operating efficiency in the guard cells responds to changes in the regeneration capacity of the Calvin cycle. The rate of stomatal opening in response to a 30 min, 10-fold step increase in red photon flux density in the leaves from the SBPase antisense plants was significantly greater than wild-type plants. Final stomatal conductance under red and mixed blue/red irradiance was greater in the antisense plants than in the wild-type control plants despite lower CO2 assimilation rates and higher internal CO2 concentrations. Increasing CO2 concentration resulted in a similar stomatal closing response in wild-type and antisense plants when measured in red light. However, in the antisense plants with small reductions in SBPase activity greater stomatal conductances were observed at all Ci levels. Together, these data suggest that the primary light-induced opening or CO2-dependent closing response of stomata is not dependent upon guard or mesophyll cell photosynthetic capacity, but that photosynthetic electron transport, or its end-products, regulate the control of stomatal responses to light and CO2. © 2008 The Author(s)

    Bioluminescent Imaging Reveals Divergent Viral Pathogenesis in Two Strains of Stat1-Deficient Mice, and in αßγ Interferon Receptor-Deficient Mice

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    Pivotal components of the IFN response to virus infection include the IFN receptors (IFNR), and the downstream factor signal transducer and activator of transcription 1 (Stat1). Mice deficient for Stat1 and IFNR (Stat1−/− and IFNαßγR−/− mice) lack responsiveness to IFN and exhibit high sensitivity to various pathogens. Here we examined herpes simplex virus type 1 (HSV-1) pathogenesis in Stat1−/− mice and in IFNαßγR−/− mice following corneal infection and bioluminescent imaging. Two divergent and paradoxical patterns of infection were observed. Mice with an N-terminal deletion in Stat1 (129Stat1−/− (N-term)) had transient infection of the liver and spleen, but succumbed to encephalitis by day 10 post-infection. In stark contrast, infection of IFNαßγR−/− mice was rapidly fatal, with associated viremia and fulminant infection of the liver and spleen, with infected infiltrating cells being primarily of the monocyte/macrophage lineage. To resolve the surprising difference between Stat1−/− and IFNαßγR−/− mice, we infected an additional Stat1−/− strain deleted in the DNA-binding domain (129Stat1−/− (DBD)). These 129Stat1−/− (DBD) mice recapitulated the lethal pattern of liver and spleen infection seen following infection of IFNαßγR−/− mice. This lethal pattern was also observed when 129Stat1−/− (N-term) mice were infected and treated with a Type I IFN-blocking antibody, and immune cells derived from 129Stat1−/− (N-term) mice were shown to be responsive to Type I IFN. These data therefore show significant differences in viral pathogenesis between two commonly-used Stat1−/− mouse strains. The data are consistent with the hypothesis that Stat1−/− (N-term) mice have residual Type I IFN receptor-dependent IFN responses. Complete loss of IFN signaling pathways allows viremia and rapid viral spread with a fatal infection of the liver. This study underscores the importance of careful comparisons between knockout mouse strains in viral pathogenesis, and may also be relevant to the causation of HSV hepatitis in humans, a rare but frequently fatal infection

    Racial Exclusion and the Political Economy of the Subprime Crisis

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    Abstract Th is paper develops a political economic explanation of the 2007-9 US subprime crisis which focuses on one of its central causes: the transformation of racial exclusion in US mortgagemarkets. Until the early 1990s, racial minorities were systematically excluded from mortgagefi nance due to bank-redlining and discrimination. But, then, racial exclusion in credit-markets was transformed: racial minorities were increasingly given access to housing-credit under terms far more adverse than were off ered to non-minority borrowers. Th is paper shows that the emergence of the subprime loan is linked, in turn, to the strategic transformation of banking in the 1980s, and to the unique global circumstances of the US macro-economy. Th us, subprime lending emerged from a combination of the long US history of racial exclusion in credit-markets, the crisis of US banking, and the position of the US within the global economy. From the viewpoint of the capitalist accumulation-process, these loans increased the depth of the fi nancial expropriation of the working class by fi nancial capital. Th e crisis in subprime lending then emerged when subprime loans with exploitative terms became more widespread and were made increasingly on an under-collateralised basis -that is, when housing-loans became not just extortionary but speculative

    Measuring the dynamic photosynthome

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    Background: Photosynthesis underpins plant productivity and yet is notoriously sensitive to small changes inenvironmental conditions, meaning that quantitation in nature across different time scales is not straightforward. The ‘dynamic’ changes in photosynthesis (i.e. the kinetics of the various reactions of photosynthesis in response to environmental shifts) are now known to be important in driving crop yield. Scope: It is known that photosynthesis does not respond in a timely manner, and even a small temporal “mismatch” between a change in the environment and the appropriate response of photosynthesis toward optimality can result in a fall in productivity. Yet the most commonly measured parameters are still made at steady state or a temporary steady state (including those for crop breeding purposes), meaning that new photosynthetic traits remain undiscovered. Conclusions: There is a great need to understand photosynthesis dynamics from a mechanistic and biological viewpoint especially when applied to the field of ‘phenomics’ which typically uses large genetically diverse populations of plants. Despite huge advances in measurement technology in recent years, it is still unclear whether we possess the capability of capturing and describing the physiologically relevant dynamic features of field photosynthesis in sufficient detail. Such traits are highly complex, hence we dub this the ‘photosynthome’. This review sets out the state of play and describes some approaches that could be made to address this challenge with reference to the relevant biological processes involved
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