Laws of the single logarithm for delayed sums of random fields

We extend a law of the single logarithm for delayed sums by Lai to delayed sums of random fields. A law for subsequences, which also includes the one-dimensional case, is obtained in passing.Comment: Published in at http://dx.doi.org/10.3150/07-BEJ103 the Bernoulli (http://isi.cbs.nl/bernoulli/) by the International Statistical Institute/Bernoulli Society (http://isi.cbs.nl/BS/bshome.htm

Sharing Means Renting?: An Entire-marketplace Analysis of Airbnb

Airbnb, an online marketplace for accommodations, has experienced a staggering growth accompanied by intense debates and scattered regulations around the world. Current discourses, however, are largely focused on opinions rather than empirical evidences. Here, we aim to bridge this gap by presenting the first large-scale measurement study on Airbnb, using a crawled data set containing 2.3 million listings, 1.3 million hosts, and 19.3 million reviews. We measure several key characteristics at the heart of the ongoing debate and the sharing economy. Among others, we find that Airbnb has reached a global yet heterogeneous coverage. The majority of its listings across many countries are entire homes, suggesting that Airbnb is actually more like a rental marketplace rather than a spare-room sharing platform. Analysis on star-ratings reveals that there is a bias toward positive ratings, amplified by a bias toward using positive words in reviews. The extent of such bias is greater than Yelp reviews, which were already shown to exhibit a positive bias. We investigate a key issue---commercial hosts who own multiple listings on Airbnb---repeatedly discussed in the current debate. We find that their existence is prevalent, they are early-movers towards joining Airbnb, and their listings are disproportionately entire homes and located in the US. Our work advances the current understanding of how Airbnb is being used and may serve as an independent and empirical reference to inform the debate.Comment: WebSci '1

Superconductivity in the two-dimensional Hubbard model?

A refined variational wave function for the two-dimensional repulsive Hubbard model is studied numerically, with the aim of approaching the difficult crossover regime of intermediate values of U. The issue of a superconducting ground state with d-wave symmetry is investigated for an average electron density n=0.8125 and for U=8t. Due to finite-size effects a clear-cut answer to this fundamental question has not yet been reached.Comment: 5 pages, 1 figure, Proc. 30th Int. Conf. of Theoretical Physics, Ustron, Poland, 2006, to be published in phys. stat. so

Between the LIL and the LSL

In two earlier papers, two of the present authors (A.G. and U.S.) extended Lai's [Ann. Probab. 2 (1974) 432--440] law of the single logarithm for delayed sums to a multiindex setting in which the edges of the $\mathbf{n}$th window grow like $|\mathbf {n}|^{\alpha}$, or with different $\alpha$'s, where the $\alpha$'s belong to $(0,1)$. In this paper, the edge of the $n$th window typically grows like $n/\log n$, thus at a higher rate than any power less than one, but not quite at the LIL-rate.Comment: Published in at http://dx.doi.org/10.3150/09-BEJ195 the Bernoulli (http://isi.cbs.nl/bernoulli/) by the International Statistical Institute/Bernoulli Society (http://isi.cbs.nl/BS/bshome.htm

The Brain-Gut-Microbiome Axis.

Preclinical and clinical studies have shown bidirectional interactions within the brain-gut-microbiome axis. Gut microbes communicate to the central nervous system through at least 3 parallel and interacting channels involving nervous, endocrine, and immune signaling mechanisms. The brain can affect the community structure and function of the gut microbiota through the autonomic nervous system, by modulating regional gut motility, intestinal transit and secretion, and gut permeability, and potentially through the luminal secretion of hormones that directly modulate microbial gene expression. A systems biological model is proposed that posits circular communication loops amid the brain, gut, and gut microbiome, and in which perturbation at any level can propagate dysregulation throughout the circuit. A series of largely preclinical observations implicates alterations in brain-gut-microbiome communication in the pathogenesis and pathophysiology of irritable bowel syndrome, obesity, and several psychiatric and neurologic disorders. Continued research holds the promise of identifying novel therapeutic targets and developing treatment strategies to address some of the most debilitating, costly, and poorly understood diseases

Vital dye labelling demonstrates a sacral neural crest contribution to the enteric nervous system of chick and mouse embryos

We have used the vital dye, DiI, to analyze the contribution of sacral neural crest cells to the enteric nervous system in chick and mouse embryos. In order to label premigratory sacral neural crest cells selectively, DiI was injected into the lumen of the neural tube at the level of the hindlimb. In chick embryos, DiI injections made prior to stage 19 resulted in labelled cells in the gut, which had emerged from the neural tube adjacent to somites 29–37. In mouse embryos, neural crest cells emigrated from the sacral neural tube between E9 and E9.5. In both chick and mouse embryos, DiI-labelled cells were observed in the rostral half of the somitic sclerotome, around the dorsal aorta, in the mesentery surrounding the gut, as well as within the epithelium of the gut. Mouse embryos, however, contained consistently fewer labelled cells than chick embryos. DiI-labelled cells first were observed in the rostral and dorsal portion of the gut. Paralleling the maturation of the embryo, there was a rostral-to-caudal sequence in which neural crest cells populated the gut at the sacral level. In addition, neural crest cells appeared within the gut in a dorsal-to-ventral sequence, suggesting that the cells entered the gut dorsally and moved progressively ventrally. The present results resolve a long-standing discrepancy in the literature by demonstrating that sacral neural crest cells in both the chick and mouse contribute to the enteric nervous system in the postumbilical gut

The therapeutic management of gut barrier leaking: the emerging role for mucosal barrier protectors

OBJECTIVE: Gut barrier is a functional unit organized as a multi-layer system and its multiple functions are crucial for maintaining gut homeostasis. Numerous scientific evidences showed a significant association between gut barrier leaking and gastro-intestinal/extra-intestinal diseases. MATERIALS AND METHODS: In this review we focus on the relationship between gut barrier leaking and human health. At the same time we speculate on the possible new role of gut barrier protectors in enhancing and restoring gut barrier physiology with the final goal of promoting gut health. RESULTS: The alteration of the equilibrium in gut barrier leads to the passage of the luminal contents to the underlying tissues and thus into the bloodstream, resulting in the activation of the immune response and in the induction of gut inflammation. This permeability alteration is the basis for the pathogenesis of many diseases, including infectious enterocolitis, inflammatory bowel diseases, irritable bowel syndrome, small intestinal bacterial overgrowth, celiac disease, hepatic fibrosis, food intolerances and also atopic manifestations. Many drugs or compounds used in the treatment of gastrointestinal disease are able to alter the permeability of the intestinal barrier. Recent data highlighted and introduced the possibility of using gelatin tannate, a mucosal barrier protector, for an innovative approach in the management of intestinal diseases, allowing an original therapeutic orientation with the aim of enhancing mucus barrier activity and restoring gut barrier. CONCLUSIONS: These results suggest how the mucus layer recovering, beside the gut microbiota modulation, exerted by gut barrier protectors could be a useful weapon to re-establish the physiological intestinal homeostasis after an acute and chronic injury

Divergent Annexin A1 expression in periphery and gut is associated with systemic immune activation and impaired gut immune response during SIV infection.

HIV-1 disease progression is paradoxically characterized by systemic chronic immune activation and gut mucosal immune dysfunction, which is not fully defined. Annexin A1 (ANXA1), an inflammation modulator, is a potential link between systemic inflammation and gut immune dysfunction during the simian immunodeficiency virus (SIV) infection. Gene expression of ANXA1 and cytokines were assessed in therapy-naïve rhesus macaques during early and chronic stages of SIV infection and compared with SIV-negative controls. ANXA1 expression was suppressed in the gut but systemically increased during early infection. Conversely, ANXA1 expression increased in both compartments during chronic infection. ANXA1 expression in peripheral blood was positively correlated with HLA-DR+CD4+ and CD8+ T-cell frequencies, and negatively associated with the expression of pro-inflammatory cytokines and CCR5. In contrast, the gut mucosa presented an anergic cytokine profile in relation to ANXA1 expression. In vitro stimulations with ANXA1 peptide resulted in decreased inflammatory response in PBMC but increased activation of gut lymphocytes. Our findings suggest that ANXA1 signaling is dysfunctional in SIV infection, and may contribute to chronic inflammation in periphery and with immune dysfunction in the gut mucosa. Thus, ANXA1 signaling may be a novel therapeutic target for the resolution of immune dysfunction in HIV infection