Ring-theoretic (in)finiteness in reduced products of Banach algebras

We study ring-theoretic (in)finiteness properties -- such as \emph{Dedekind-finiteness} and \emph{proper infiniteness} -- of ultraproducts (and more generally, reduced products) of Banach algebras. Whilst we characterise when an ultraproduct has these ring-theoretic properties in terms of its underlying sequence of algebras, we find that, contrary to the C∗-algebraic setting, it is not true in general that an ultraproduct has a ring-theoretic finiteness property if and only if "ultrafilter many" of the underlying sequence of algebras have the same property. This might appear to violate the continuous model theoretic counterpart of Łoś's Theorem; the reason it does not is that for a general Banach algebra, the ring theoretic properties we consider cannot be verified by considering a bounded subset of the algebra of \emph{fixed} bound. For Banach algebras, we construct counter-examples to show, for example, that each component Banach algebra can fail to be Dedekind-finite while the ultraproduct is Dedekind-finite, and we explain why such a counter-example is not possible for C∗-algebras. Finally the related notion of having \textit{stable rank one} is also studied for ultraproducts

Relative photometry of HAT-P-1b occultations

We present HST STIS observations of two occultations of the transiting exoplanet HAT-P-1b. By measuring the planet to star flux ratio near opposition, we constrain the geometric albedo of the planet, which is strongly linked to its atmospheric temperature gradient. An advantage of HAT-P-1 as a target is its binary companion ADS 16402 A, which provides an excellent photometric reference, simplifying the usual steps in removing instrumental artifacts from HST time-series photometry. We find that without this reference star, we would need to detrend the lightcurve with the time of the exposures as well as the first three powers of HST orbital phase, and this would introduce a strong bias in the results for the albedo. However, with this reference star, we only need to detrend the data with the time of the exposures to achieve the same per-point scatter, therefore we can avoid most of the bias associated with detrending. Our final result is a 2 sigma upper limit of 0.64 for the geometric albedo of HAT-P-1b between 577 and 947 nm.Comment: 8 pages, 2 figures, 3 table

Astrocytes regulate GLP-1 receptor-mediated effects on energy balance

© 2016 the authors. Astrocytes are well established modulators of extracellular glutamate, but their direct influence on energy balance-relevant behaviors is largely understudied. As the anorectic effects of glucagon-like peptide-1 receptor (GLP-1R) agonists are partly mediated by central modulation of glutamatergic signaling, we tested the hypothesis that astrocytic GLP-1R signaling regulates energy balance in rats. Central or peripheral administration of a fluorophore-labeled GLP-1R agonist, exendin-4, localizes within astrocytes and neurons in the nucleus tractus solitarius (NTS), a hindbrain nucleus critical for energy balance control. This effect is mediated by GLP-1R, as the uptake of systemically administered fluorophore-tagged exendin-4 was blocked by central pretreatment with the competitive GLP-1R antagonist exendin-(9–39). Ex vivo analyses show prolonged exendin-4-induced activation (live cell calcium signaling) of NTS astrocytes and neurons; these effects are also attenuated by exendin-(9–39), indicating mediation by the GLP-1R. In vitro analyses show that the application of GLP-1R agonists increases cAMP levels in astrocytes. Immunohistochemical analyses reveal that endogenous GLP-1 axons form close synaptic apposition with NTS astrocytes. Finally, pharmacological inhibition of NTS astrocytes attenuates the anorectic and body weight-suppressive effects of intra-NTS GLP-1R activation. Collectively, data demonstrate a role for NTS astrocytic GLP-1R signaling in energy balance control

Varga et al.: Macrophage PPARγ, a Lipid Activated Transcription Factor Controls the Growth Factor GDF3 and Skeletal Muscle Regeneration Immunity. 2016 Nov 15;45(5):1038-1051. doi: 10.1016/j.immuni.2016.10.016.

Tissue regeneration requires inflammatory and reparatory activity of macrophages. Macrophages detect and eliminate the damaged tissue and subsequently promote regeneration. This dichotomy requires the switch of effector functions of macrophages coordinated with other cell types inside the injured tissue. The gene regulatory events supporting the sensory and effector functions of macrophages involved in tissue repair are not well understood. Here we show that the lipid activated transcription factor, PPARγ, is required for proper skeletal muscle regeneration, acting in repair macrophages. PPARγ controls the expression of the transforming growth factor-β (TGF-β) family member, GDF3, which in turn regulates the restoration of skeletal muscle integrity by promoting muscle progenitor cell fusion. This work establishes PPARγ as a required metabolic sensor and transcriptional regulator of repair macrophages. Moreover, this work also establishes GDF3 as a secreted extrinsic effector protein acting on myoblasts and serving as an exclusively macrophage-derived regeneration factor in tissue repair

The Incidence of Venous Thromboembolism in Children Following Colorectal Resection for Inflammatory Bowel Disease: A Multi-Center Study

Background/Purpose Children with inflammatory bowel disease (IBD) have increased risk for venous thromboembolism (VTE). We sought to determine incidence and risk factors for postoperative VTE in a multicenter cohort of pediatric patients undergoing colorectal resection for IBD. Methods Retrospective review of children ≤18 years who underwent colorectal resection for IBD from 2010 to 2016 was performed at four children's hospitals. Primary outcome was VTE that occurred between surgery and last follow-up. Factors associated with VTE were determined using univariable and multivariable analyses. Results Two hundred seventy-six patients were included with median age 15 years [13,17]. Forty-two children (15%) received perioperative VTE chemoprophylaxis, and 88 (32%) received mechanical prophylaxis. DVT occurred in 12 patients (4.3%) at a median of 14 days postoperatively [8,147]. Most were portomesenteric (n = 9, 75%) with the remaining catheter-associated DVTs in extremities (n = 3, 25%). There was no association with chemoprophylaxis (p > 0.99). On Cox regression, emergent procedure [HR 18.8, 95%CI: 3.18–111], perioperative plasma transfusion [HR 25.1, 95%CI: 2.4–259], and postoperative infectious complication [HR 10.5, 95%CI: 2.63–41.8] remained predictive of DVT. Conclusion Less than 5% of pediatric IBD patients developed postoperative VTE. Chemoprophylaxis was not protective but rarely used. Patients with risk factors identified in this study should be monitored or given prophylaxis for VTE

PPARα and PPARγ activation is associated with pleural mesothelioma invasion but therapeutic inhibition is ineffective

Mesothelioma is a cancer that typically originates in the pleura of the lungs. It rapidly invades the surrounding tissues, causing pain and shortness of breath. We compared cell lines injected either subcutaneously or intrapleurally and found that only the latter resulted in invasive and rapid growth. Pleural tumors displayed a transcriptional signature consistent with increased activity of nuclear receptors PPARα and PPARγ and with an increased abundance of endogenous PPAR-activating ligands. We found that chemical probe GW6471 is a potent, dual PPARα/γ antagonist with anti-invasive and anti-proliferative activity in vitro. However, administration of GW6471 at doses that provided sustained plasma exposure levels sufficient for inhibition of PPARα/γ transcriptional activity did not result in significant anti-mesothelioma activity in mice. Lastly, we demonstrate that the in vitro anti-tumor effect of GW6471 is off-target. We conclude that dual PPARα/γ antagonism alone is not a viable treatment modality for mesothelioma

The SH3 domain of postsynaptic density 95 mediates inflammatory pain through phosphatidylinositol-3-kinase recruitment

Sensitization to inflammatory pain is a pathological form of neuronal plasticity that is poorly understood and treated. Here we examine the role of the SH3 domain of postsynaptic density 95 (PSD95) by using mice that carry a single amino-acid substitution in the polyproline-binding site. Testing multiple forms of plasticity we found sensitization to inflammation was specifically attenuated. The inflammatory response required recruitment of phosphatidylinositol-3-kinase-C2α to the SH3-binding site of PSD95. In wild-type mice, wortmannin or peptide competition attenuated the sensitization. These results show that different types of behavioural plasticity are mediated by specific domains of PSD95 and suggest novel therapeutic avenues for reducing inflammatory pain