Influence of shoot number and crop load on potted Chambourcin grapevines. 2. Whole-vine vs. single-leaf photosynthesis

Two-year-old potted Chambourcin grapevines were trained to one shoot with 0 or 1 cluster (1/0 and 1/1 respectively) or four shoots with 0 or 4 clusters (4/0 and 4/4 respectively) to determine the effects of canopy development rate, canopy morphology, and crop load on whole-vine photosynthesis. Significant differences in canopy development rate, canopy morphology and dry matter partitioning occurred among treatments but whole-vine net photosynthesis (Pn) and dry matter production were not affected. Photosynthetic compensation by leaves of severely pruned vines enabled them to produce quantities of dry matter similar to vines with greater leaf area. Vines bearing crop supported the development of berries by partitioning carbohydrate to fruit at the expense of vegetative tissues so overall vine dry weight was not different among cropped and non-cropped treatments. Whole-vine Pn determinations were linearly related to vine dry mass. By contrast, single leaf measurements used to estimate whole-vine Pn were not related to dry mass. If a similar relationship can be demonstrated in field vines, it may be possible to quantify the influence of biotic and abiotic stresses on vine biomass production and subsequent yields

HIF-1 alpha-independent hypoxia-induced rapid PTK6 stabilization is associated with increased motility and invasion

© 2014 Landes Bioscience. PTK6/Brk is a non-receptor tyrosine kinase overexpressed in cancer. Here we demonstrate that cytosolic PTK6 is rapidly and robustly induced in response to hypoxic conditions in a HIF-1-independent manner. Furthermore, a proportion of hypoxic PTK6 subsequently re-localized to the cell membrane. We observed that the rapid stabilization of PTK6 is associated with a decrease in PTK6 ubiquitylation and we have identified c-Cbl as a putative PTK6 E3 ligase in normoxia. The consequences of hypoxia-induced PTK6 stabilization and subcellular re-localization to the plasma membrane include increased cell motility and invasion, suggesting PTK6 targeting as a therapeutic approach to reduce hypoxia-regulated metastatic potential. This could have particular significance for breast cancer patients with triple negative disease

Reweighting the Sivers function with jet data from STAR

The reweighting procedure that using Bayesian statistics incorporates the information contained in a new data set, without the need of re-fitting, is applied to the quark Sivers function extracted from Semi-Inclusive Deep Inelastic Scattering (SIDIS) data. We exploit the recently published single spin asymmetry data for the inclusive jet production in polarized $pp$ collisions from the STAR Collaboration at RHIC, which cover a much wider $x$ region compared to SIDIS measurements. The reweighting method is extended to the case of asymmetric errors and the results show a remarkable improvement of the knowledge of the quark Sivers function.Comment: 9 pages, 5 figure

Reweighting the Sivers function with jet data from STAR

The reweighting procedure that using Bayesian statistics incorporates the information contained in a new data set, without the need of re-fitting, is applied to the quark Sivers function extracted from Semi-Inclusive Deep Inelastic Scattering (SIDIS) data. We exploit the recently published single spin asymmetry data for the inclusive jet production in polarized pp collisions from the STAR Collaboration at RHIC, which cover a much wider x region compared to SIDIS measurements. The reweighting method is extended to the case of asymmetric errors and the results show a remarkable improvement of the knowledge of the quark Sivers function

B016 Impact of a 14-night intermittent hypoxia (IH) exposure on metabolic and cardiopulmonary adaptations to exercise in healthy subjects

IntroductionModifications in exercise tolerance have been reported in obstructive sleep apnea (OSA) patients. Also specific mechanisms have been speculated related to intermittent hypoxia (IH), hypertension, obesity or metabolic disturbance associated to OSA may play a significant role in exercise limitation. In order to eliminate these confounding factors we aimed to evaluate the effects of IH exposure during 14 nights in healthy subjects on exercise capacity, cardio-respiratory response and substrate oxidation during exercise.Methods12 healthy subjects (BMI: 21.8 0.5kg.m-2) were exposed to repetitive sequences of hypoxia — re-oxygenation during sleep in a hypoxic tent with appropriate cyclic re-oxygenation (rate: 30 desaturations.h-1). Maximal and sub-maximal exercise tests were performed before and after exposure in order to investigate cardiorespiratory variables and substrate oxidation parameters.ResultsIH did not modify maximal exercise parameters (VO2, heart rate, power output) nor ventilatory threshold (VTh). But this was achieved with a significant PETCO2 reduction and a VE/VCO2 increase during both maximal (Pre IH vs Post IH at VTh and Max, p<0.05) and sub-maximal (Pre vs Post at 30 % and 60 % Pmax, p<0.05) exercise tests, indicating hyperventilation. At the 1st min recovery after submaximal exercise test, diastolic arterial blood pressure (DBP) was higher after IH exposure (Pre: 60±3 vs Post: 78±2mmHg) in favour of a delayed DBP recovery following acute exercise. During sub-maximal exercise, subjects reached maximal lipid oxidation at higher power output and presented a decreased blood lactate at the same percentage of relative power after IH exposure.ConclusionExposure to 14 days of nocturnal IH is associated with an increased ventilatory response to subsequent exercise at sea level. Furthermore, delayed DBP recovery after exercise is in favor of early IH-induced cardiovascular modifications. This observation related to muscular exercise adaptations confirms the efficacy of the model in reproducing early cardiovascular alterations occurring in OSAS. Moreover, this model induces metabolic adaptations as soon as 14 nights of exposure

Unravelling subjectivity, embodied experience and (taking) psychotropic medication

This paper explores how distinctions between ‘intended’ and ‘side’ effects are troubled in personal narratives of taking psychotropic medications. Grounded in interviews with 29 participants diagnosed with mental illness in Victoria, Australia between February and December 2014, we consider how people interpret pharmaceutical compounds beyond their desired or intended effects, and how such effects shape and transform subjectivity and their relationship with their bodies. This paper contributes to recent discussions of mental illness and medication effects, informed by feminist science studies. It emphasises the co-constitution of social, affective and material relations in the context of ‘taking’ psychotropic medication. This paper discusses three key themes as important to the phenomenology of the nexus of illness and psychotropic medication: movement, ambivalence, and sociality. Our analysis demonstrates how psychotropic drugs are productive of subjectivity through their promises and potential, their unexpected harms and the institutions from which they are inseparable

'Asexual isn't who I am': the politics of asexuality

Some literature on asexuality has claimed that it is inherently radical and contains the potential for resistance. Unfortunately, this literature has tended to be unempirical, has imagined asexuality as a disembodied entity, and has marginalised the multiple identities held by asexual people. This article, inspired by Plummer’s critical humanist approach, seeks to explore how individuals understand their asexuality to encourage forms of political action in the areas of identity, activism, online spaces, and LGBT politics. What we found was a plurality of experiences and attitudes with most adopting a pragmatic position in response to their social situation which saw large-scale political action as irrelevant. We conclude by reflecting on what these results mean for those who see asexuality as potentially radical

Different Aspects of Classical Pathway Overactivation in Patients With C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis

The rare and heterogeneous kidney disorder C3 glomerulopathy (C3G) is characterized by dysregulation of the alternative pathway (AP) of the complement system. C3G is often associated with autoantibodies stabilizing the AP C3 convertase named C3 nephritic factors (C3NeF). The role of classical pathway (CP) convertase stabilization in C3G and related diseases such as immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) remains largely unknown. Here, we investigated the CP convertase activity in patients with C3G and IC-MPGN. Using a refined two-step hemolytic assay, we measured the stability of CP convertases directly in the serum of 52 patients and 17 healthy controls. In four patients, CP convertase activity was prolonged compared to healthy controls, i.e. the enzymatic complex was stabilized. In three patients (2 C3G, 1 IC-MPGN) the convertase stabilization was caused by immunoglobulins, indicating the presence of autoantibodies named C4 nephritic factors (C4NeFs). Importantly, the assay also enabled detection of non-immunoglobulin-mediated stabilization of the CP convertase in one patient with C3G. Prolonged CP convertase activity coincided with C3NeF activity in all patients and for up to 70 months of observation. Crucially, experiments with C3-depleted serum showed that C4NeFs stabilized the CP C3 convertase (C4bC2a), that does not contain C3NeF epitopes. All patients with prolonged CP convertase activity showed clear signs of complement activation, i.e. lowered C3 and C5 levels and elevated levels of C3d, C3bc, C3bBbP, and C5b-9. In conclusion, this work provides new insights into the diverse aspects and (non-)immunoglobulin nature of factors causing CP convertase overactivity in C3G/IC-MPGN.</p

Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis

Mutations in the retinoblastoma tumor suppressor gene Rb are involved in many forms of human cancer. In this study, we investigated the early consequences of inactivating Rb in the context of cellular reprogramming. We found that Rb inactivation promotes the reprogramming of differentiated cells to a pluripotent state. Unexpectedly, this effect is cell cycle independent, and instead reflects direct binding of Rb to pluripotency genes, including Sox2 and Oct4, which leads to a repressed chromatin state. More broadly, this regulation of pluripotency networks and Sox2 in particular is critical for the initiation of tumors upon loss of Rb in mice. These studies therefore identify Rb as a global transcriptional repressor of pluripotency networks, providing a molecular basis for previous reports about its involvement in cell fate pliability, and implicate misregulation of pluripotency factors such as Sox2 in tumorigenesis related to loss of Rb function