Certain Integrals Arising from Ramanujan's Notebooks

In his third notebook, Ramanujan claims that $$\int_0^\infty \frac{\cos(nx)}{x^2+1} \log x \,\mathrm{d} x + \frac{\pi}{2} \int_0^\infty \frac{\sin(nx)}{x^2+1} \mathrm{d} x = 0.$$ In a following cryptic line, which only became visible in a recent reproduction of Ramanujan's notebooks, Ramanujan indicates that a similar relation exists if $\log x$ were replaced by $\log^2x$ in the first integral and $\log x$ were inserted in the integrand of the second integral. One of the goals of the present paper is to prove this claim by contour integration. We further establish general theorems similarly relating large classes of infinite integrals and illustrate these by several examples

Mechanisms for Arsenic-Stimulated Sinusoidal Endothelial Cell Capillarization

The vascular effects of arsenic in drinking water are a global public health concern that contribute to disease in millions of people worldwide. However, the cellular and molecular mechanisms for these pathogenic effects of arsenic are not well defined. This thesis examined the hypothesis that arsenic stimulates pathogenic signals through surface receptors on liver sinusoidal endothelial cells (LSECs) to stimulate NADPH oxidase (NOX) activity that is required for arsenic-stimulated LSEC capillarization. In mice and isolated LSECs, we demonstrated that exposure to arsenic promoted capillarization and increased expression of platelet endothelial cell adhesion molecule (PECAM-1) through a time and dose dependent mechanism. Superoxide generating NOX enzyme complexes participate in vascular remodeling and angiogenesis and are central to arsenic stimulated cell signaling. LSEC arsenic exposure increased NOX dependent superoxide generation that was inhibited using gp91ds-tat protein, NSC23766, a Rac1-GTPase inhibitor, or quenched by the intracellular superoxide scavenger, Tempol. These inhibitors also blocked arsenic-stimulated LSEC PECAM-1 expression and defenestration. In vivo arsenic exposures failed to promote LSEC capillarization in p47phox knockout mice. These data demonstrated that arsenic stimulates capillarization through a NOX dependent mechanism. Given that arsenic rapidly activates NOX in vascular cells, we hypothesized that signaling for these responses was receptor mediated. Since arsenic-stimulated LSEC defenestration and capillarization is Rac1 and NOX dependent, we examined whether a g-protein coupled receptor (GPCR) upstream of Rac1 initiated these effects. Pre-treatment LSECs with Pertussis toxin (PTX), an inhibitor of Gi/o, prevented arsenic-stimulated defenestration. Since capillarization is a gain in barrier function, LSEC expression of the sphingosine-1-phosphate type 1 (S1P1) receptor, a major Gi/o linked regulator of endothelial barrier function, and its role in arsenic-stimulated defenestration were investigated. S1P1 was highly expressed in LSECs relative to large vessels. In ex vivo studies, inhibiting LSEC S1P1 with a selective antagonist, VPC23109, blocked arsenic-stimulated superoxide generation, defenestration, and PECAM-1 expression. These data demonstrated that arsenic targets a specific LSEC GPCR to promote vascular remodeling, and the first demonstrating that S1P1 regulates oxidant-dependent LSEC capillarization. Taken together, these data demonstrate that S1P1 activated NOX stimulates LSEC capillarization, which aids in our understanding of mechanisms underlying arsenic-induced liver disease

Biological synthesis of fluorescent nanoparticles by cadmium and tellurite resistant Antarctic bacteria: exploring novel natural nanofactories

Indexación: Web of ScienceBackground: Fluorescent nanoparticles or quantum dots (QDs) have been intensely studied for basic and applied research due to their unique size-dependent properties. There is an increasing interest in developing ecofriendly methods to synthesize these nanoparticles since they improve biocompatibility and avoid the generation of toxic byproducts. The use of biological systems, particularly prokaryotes, has emerged as a promising alternative. Recent studies indicate that QDs biosynthesis is related to factors such as cellular redox status and antioxidant defenses. Based on this, the mixture of extreme conditions of Antarctica would allow the development of natural QDs producing bacteria. Results: In this study we isolated and characterized cadmium and tellurite resistant Antarctic bacteria capable of synthesizing CdS and CdTe QDs when exposed to these oxidizing heavy metals. A time dependent change in fluorescence emission color, moving from green to red, was determined on bacterial cells exposed to metals. Biosynthesis was observed in cells grown at different temperatures and high metal concentrations. Electron microscopy analysis of treated cells revealed nanometric electron-dense elements and structures resembling membrane vesicles mostly associated to periplasmic space. Purified biosynthesized QDs displayed broad absorption and emission spectra characteristic of biogenic Cd nanoparticles. Conclusions: Our work presents a novel and simple biological approach to produce QDs at room temperature by using heavy metal resistant Antarctic bacteria, highlighting the unique properties of these microorganisms as potent natural producers of nano-scale materials and promising candidates for bioremediation purposes.http://microbialcellfactories.biomedcentral.com/articles/10.1186/s12934-016-0477-

Peter Straub: Pictures In The Fire

This record consists of a transcript of an interview with Peter Straub

Peter Straub: Supplementary Material For My Book

This record consists of a transcript of an interview with Peter Straub

Peter Straub: A Magellan of The Interior

This record consists of the transcript of an interview with Peter Straub

Phosphorylation of Vasodilator-Stimulated Phosphoprotein (VASP) dampens hepatic ischemia-reperfusion injury

Recent work has demonstrated that the formation of platelet neutrophil complexes (PNCs) affects inflammatory tissue injury. Vasodilator-stimulated phosphoprotein (VASP) is crucially involved into the control of PNC formation and myocardial reperfusion injury. Given the clinical importance of hepatic IR injury we pursued the role of VASP during hepatic ischemia followed by reperfusion. We report here that VASP−/− animals demonstrate reduced hepatic IR injury compared to wildtype (WT) controls. This correlated with serum levels of lactate dehydrogenase (LDH), aspartate (AST) and alanine (ALT) aminotransferase and the presence of PNCs within ischemic hepatic tissue and could be confirmed using repression of VASP through siRNA. In studies employing bone marrow chimeric mice we identified hematopoietic VASP to be of crucial importance for the extent of hepatic injury. Phosphorylation of VASP on Ser153 through Prostaglandin E1 or on Ser235 through atrial natriuretic peptide resulted in a significant reduction of hepatic IR injury. This was associated with a reduced presence of PNCs in ischemic hepatic tissue. Taken together, these studies identified VASP and VASP phosphorylation as crucial target for future hepatoprotective strategies