Arrieta et al. (Reports, 17 April 2015, p. 331) propose that low concentrations of labile dissolved organic carbon (DOC) preclude prokaryotic consumption of a substantial fraction of DOC in the deep ocean and that this dilution acts as an alternative mechanism to recalcitrance for long-term DOC storage. Here, we show that the authors' data do not support their claims.T he mechanisms controlling the reactivity/ recalcitrance continuum of dissolved organic carbon (DOC) in the nutrient-rich deep ocean remain a "recalcitrant" problem due to the complexity of the underlying biogeochemical interactions and the limitations of current methods (1). The experimental study by Arrieta et al. Arrieta et al. (2) tested experimentally the null hypothesis that "no significant increase in prokaryotic growth should be detectable when increasing DOC concentrations." Their enrichment experiments showed increased prokaryotic growth, consistent with the dilution hypothesis. However, if low concentrations did limit prokaryotic growth in Arrieta et al.'s (2) incubations, then the corollary of their hypothesis should also hold-i.e., the prokaryotic consumption of DOC should be related to the DOC concentration. We therefore reanalyzed the data of Arrieta et al. (2) to test the null hypothesis that no significant increase in DOC consumption by prokaryotes should be detectable when increasing DOC concentrations. Plotting the authors' incubation measurements from Stations K, L, and N (data from Station M were anomalous due to a second phase of intense growth) shows, first, that the relative fraction of DOC consumed by prokaryotes is below 6% in each of the assays and, second, that this fraction is independent of the DOC enrichment (2×, 5×, or 10×) (Fig. 1). The lack of rejection of our null hypothesis indicates the inconsistency of Arrieta et al.'s data with the dilution hypothesis.Arrieta et al. (2) also based their conclusion that dilute labile DOC is a substantial fraction of DOC in the deep ocean on the results of specific growth rate experiments, in which they used population growth kinetics to estimate the minimum concentration of DOC required for growth of deepwater prokaryotic communities [figure 2, figure S3, and table S2 in (2)]. However, the minimum concentration of bulk DOC required for growth of a prokaryotic community cannot be equated with the threshold values of availability of single DOC compounds. Instead, the dilution hypothesis as formulated by Arrieta et al.(i.e., most organic substrates in the deep ocean are labile but cannot be used by prokaryotes at concentrations below the levels matching the energetic investment required for their uptake and degradation) suggests that at steady state, and neglecting abiotic processes that could transform DOC, the supply of individual dilute labile DOC compounds is balanced by prokaryotic uptake to just below their respective uptake thresholds. This is illustrated in Fig. 2, which shows that, if low concentrations of individual labile DOC compounds had indeed prevented prokaryotic ...
Background/Aims: Microvascular insufficiency takes a critical role in the development of diabetic cardiomyopathy (DCM). So this study was designed to investigate the effects of Neuregulin-1 (NRG-1) treatment on myocardial angiogenesis and the changes of VEGF/Flk1 and Ang-1/Tie-2 signaling in the rat model of DCM. Methods: Diabetic rats were induced by a single intraperitoneal injection of Streptozotocin. 12 weeks after the diabetes induction, the rats with NRG-1 treatment were treated with tail vein injection of NRG-1 at the dose of 10µg/kg/d for consecutive 10 days. Cardiac function was assessed using catheter MPA cardiac function analysis system. Myocardial blood flow (MBF) was assessed with stable-isotope labeled microspheres. Capillary density was measured by CD31 immunohistochemistry. The protein expression and receptors phosphorylation were assessed using western blot. Results: Left ventricular function, capillary density and MBF were significantly reduced in DCM group when compared with those in the control group (P< 0.01, P< 0.01 and P< 0.05 respectively). Left ventricular function and capillary density were significantly increased in NRG-1 treatment group when compared with those in the DCM group (P< 0.05 and P< 0.05 respectively). The expression of VEGF and Ang-1 and the phosphorylation of Flk1 and Tie-1 were significantly decreased in DCM group as compared with those in the control group. However, those in the NRG-1 treatment group were significantly increased as compared with those in the DCM group. In vitro, NRG-1 treatment increased significantly the expression of VEGF and Ang-1 in human coronary artery smooth muscle cells. Conclusions: NRG-1 can increase the myocardial angiogenesis of DCM, probably via the direct effects of NRG-1 and via the increasing expression of VEGF and Ang-1. These findings may contribute to developing a novel approach to reverse the impaired angiogenic responses in diabetes or coronary artery disease.
SummaryWhether the effect of diabetes on patients with unprotected left main coronary artery (ULMCA) disease differs according to different strategies of revascularization was unknown. This study was conducted to evaluate the impact of diabetes on patients with ULMCA disease treated with either percutaneous coronary intervention (PCI) or coronary-artery bypass grafting (CABG).A total of 922 patients with ULMCA disease who received drug-eluting stent (DES) (n = 465) implantation or underwent CABG (n = 457) were retrospectively analyzed. We compared the effects of these 2 treatments on clinical outcomes (death, myocardial infarction, stroke, repeat revascularization, and the composite of death, myocardial infarction, or stroke), according to diabetic status.During the median follow-up of 7.1 years (interquartile range, 5.3 to 8.2 years), no difference was found between PCI and CABG in the adjusted occurrence of death (P = 0.112) and the composite endpoints of death, myocardial infarction, and stroke (P = 0.235). Significantly higher incidence of repeat revascularization (P < 0.001) was observed in the DES group, whereas the CABG group had a significantly higher rate of stroke (P = 0.001). These trends were consistent in both diabetic and nondiabetic patients. We did not observe significant interactions between treatment outcomes and the presence or absence of diabetes after adjustment for covariates (P interaction = 0.580 for the composite of death, MI and stroke, P interaction = 0.685 for death, P interaction = 0.416 for MI, P interaction = 0.470 for stroke, and P interaction = 0.502 for repeat revascularization).Presence of diabetes was not important for decision-making between CABG and PCI in patients with ULMCA disease. (Int Heart J 2015; 56: 43-48)
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