Many-Access Channels: The Gaussian Case with Random User Activities

Classical multiuser information theory studies the fundamental limits of models with a fixed (often small) number of users as the coding blocklength goes to infinity. This work proposes a new paradigm, referred to as many-user information theory, where the number of users is allowed to grow with the blocklength. This paradigm is motivated by emerging systems with a massive number of users in an area, such as machine-to-machine communication systems and sensor networks. The focus of the current paper is the many-access channel model, which consists of a single receiver and many transmitters, whose number increases unboundedly with the blocklength. Moreover, an unknown subset of transmitters may transmit in a given block and need to be identified. A new notion of capacity is introduced and characterized for the Gaussian many-access channel with random user activities. The capacity can be achieved by first detecting the set of active users and then decoding their messages.Comment: 5 pages, 2 figures, to appear in Proceedings of ISIT 201

Versican/collagen Interactions In Tissue Structure And Mechanics

ABSTRACT VERSICAN/COLLAGEN INTERACTIONS IN TISSUE STRUCTURE AND MECHANICSDongning Chen Rebecca G. Wells Type I collagen is the most abundant structural protein in the extracellular matrix (ECM), forming a dynamic 3D fibrous network that is highly regulated by other ECM components including proteoglycans (PGs) and glycosaminoglycans (GAGs). Matrix PGs, especially the small leucine rich PG (SLRP) subgroup, have been well studied as collagen binding proteins and regulators of fibrillogenesis. However, the impact of the hyalectan subgroup of PGs, particularly versican, on collagen behaviors is not well understood. There is a particular need for understanding the role of versican in the collagen network because of its universal distribution in tissues and its altered expression during collagen-related fibrotic disorders. My aim was to study collagen/versican interactions and to investigate the role of versican in modulating collagen structural and mechanical behaviors. I used solid phase binding assays and the Collagen Toolkit to identify binding sites, and I carried out in vitro turbidity assays combined with fibroblast-derived matrices (FDM) to study fibrillogenesis. Collagen fiber organization was visualized using scanning electron microscopy (SEM), and cell-mediated collagen realignments and contractions were assessed by collagen plug and engineered microtissue assays. Shear rheometry was carried out on collagen gels and liver tissues to evaluate the impact of versican on tissue mechanics. I determined that versican and its V3 isoform bind collagen via the versican G3 domain and collagen R-G-Hydrophobic-O motif, independent of versican GAG residues. Compared to SLRPs and the structurally similar hyalectan aggrecan, versican shows unique effects on multiple collagen behaviors: 1) versican upregulates collagen gelation and promotes the deposition of collagen-rich matrix with aligned fibers; 2) the presence of versican improves fibril fusion into large bundles and forms a looser network; 3) versican improves cell-mediated collagen compaction, alignment and microtissue contraction; 4) versican contributes to collagen gel mechanics by decreasing stiffness and attenuating strain stiffening. In tissues, versican and its GAGs also play a role by downregulating compression stiffening. Thus, versican is a unique regulator of various collagen behaviors and therefore has potential therapeutic value in collagen-related fibroproliferative diseases such as inflammation, fibrosis and cancer

Transcription factor Hlx controls a systematic switch from white to brown fat through Prdm16-mediated co-activation

Browning of subcutaneous white fat (iWAT) involves several reprograming events, but the underlying mechanisms are incompletely understood. Here we show that the transcription factor Hlx is selectively expressed in brown adipose tissue (BAT) and iWAT, and is translationally upregulated by beta3-adrenergic signaling-mediated suppression of the translational inhibitor 4E-BP1. Hlx interacts with and is co-activated by Prdm16 to control BAT-selective gene expression and mitochondrial biogenesis. Hlx heterozygous knockout mice have defects in brown-like adipocyte formation in iWAT, and develop glucose intolerance and high fat-induced hepatic steatosis. Conversely, transgenic expression of Hlx at a physiological level drives a full program of thermogenesis and converts iWAT to brown-like fat, which improves glucose homeostasis and prevents obesity and hepatic steatosis. The adipose remodeling phenotypes are recapitulated by fat-specific injection of Hlx knockdown and overexpression viruses, respectively. Our studies establish Hlx as a powerful regulator for systematic white adipose tissue browning and offer molecular insights into the underlying transcriptional mechanism.The transcriptional co-activator Prdm16 regulates browning of white adipose tissue (WAT). Here, the authors show that Prdm16 interacts with the transcription factor Hlx, which is stabilized in response to beta3-adrenergic signaling, to increase thermogenic gene expression and mitochondrial biogenesis in subcutaneous WAT

Association of blood pressure with development of metabolic syndrome components: a five-year retrospective cohort study in Beijing

Background: Raised blood pressure (BP) is associated with the incidence of metabolic syndrome (MetS). It is unknown if subjects with different BP levels may develop certain components of MetS over time. We investigated the incidence of MetS relative to different levels of BP over a 5-year period in a Chinese population in Tongren Hospital, Beijing. Methods: During the period of 2006–2011, we recruited 2,781 participants with no MetS, or self-reported type 2 diabetes, dyslipidemia, hypertension, or cardiovascular disease at baseline. Association rule was used to identify the transitions of MetS components over time. Results: The incidence of MetS at follow-up was 9.74% for men and 3.21% for women in the group with optimal BP; 10.29% and 7.22%, respectively, in the group with normal BP; 10.49% and 10.84%, respectively, in the group with high-normal BP; and 14.48% and 23.21%, respectively in the group with high BP. The most common transition was from healthy to healthy in the groups with optimal or normal BP (17.9–49.3%), whereas in the high-normal BP group, 16.9-22.1% of subjects with raised BP returned to healthy status or stayed unchanged, while 13.8-21.4% of people with high BP tended to develop raised fasting glucose levels. Conclusions: The incidence of MetS increased in parallel with the increase in BP. People with optimal and normal BP levels were less susceptible to developing MetS over time, whereas abnormal BP seemed to be a pre-existing phase of MetS. High-normal BP was a crucial status for MetS prevention

Association between γ-glutamyl transferase and metabolic syndrome: A cross-sectional study of an adult population in Beijing

The relationship between liver enzymes and clustered components of metabolic syndrome (MetS) is explored and the predictive power of γ-glutamyl transferase (GGT) for the diagnosis of MetS in an adult population in Beijing is investigated. A total of 10,553 adults aged 20-65 years who underwent health examinations at Beijing Tongren Hospital in 2012 were enrolled in the study. Multivariate logistic regression analysis is conducted to determine the associations between the levels of various liver enzymes and clustered components of MetS. A receiver operating characteristic analysis is used to determine the optimal cut-off value of GGT for the diagnosis of MetS. A high level of GGT is found to be positively associated with clustered components of MetS in both men and women after adjusting for age, body mass index (BMI), history of alcoholic fatty liver, and the presence of taking anti-hypertensive, anti-dyslipidemic, and anti-diabetic drugs. Among all components of MetS, GGT is more predictive of triglyceride, and BMI. The area-under-the-curve values of GGT for discriminating MetS from normal metabolic status in men and women are 0.73 and 0.80, respectively. The optimal cut-off value of GGT for men is 31.50 U/L, demonstrating a sensitivity of 74.00% and specificity of 62.00%. For women, it is 19.50 U/L (sensitivity 76.00% and specificity 70.00%). GGT is therefore recommended as a useful diagnostic marker for MetS, because the test is inexpensive, highly sensitive, and frequently encountered in clinical practice