One-Hop Throughput of Wireless Networks with Random Connections

We consider one-hop communication in wireless networks with random connections. In the random connection model, the channel powers between different nodes are drawn from a common distribution in an i.i.d. manner. An scheme achieving the throughput scaling of order $n^{1/3-\delta}$, for any $\delta>0$, is proposed, where $n$ is the number of nodes. Such achievable throughput, along with the order $n^{1/3}$ upper bound derived by Cui et al., characterizes the throughput capacity of one-hop schemes for the class of connection models with finite mean and variance.Comment: Submitted to IEEE Communications Letter

Immune-inflammation gene signatures in endometriosis patients

To determine if the molecular profiles of endometriotic lesions contain informative measures of inflammation and immune dysfunction that may contribute to better understanding of the interplay between immune dysfunction and inflammation and their contribution to endometriosis pathogenesis

Interleukin-33 modulates inflammation in endometriosis

Abstract Endometriosis is a debilitating condition that is categorized by the abnormal growth of endometrial tissue outside the uterus. Although the pathogenesis of this disease remains unknown, it is well established that endometriosis patients exhibit immune dysfunction. Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic inflammation. Although plasma and peritoneal fluid levels of IL-33 have been associated with deep infiltrating endometriosis, its contribution to the disease pathophysiology is unknown. We investigated the role of IL-33 in the pathology of endometriosis using patient samples, cell lines and a syngeneic mouse model. We found that endometriotic lesions produce significantly higher levels of IL-33 compared to the endometrium of healthy, fertile controls. In vitro stimulation of endometrial epithelial, endothelial and endometriotic epithelial cells with IL-33 led to the production of pro-inflammatory and angiogenic cytokines. In a syngeneic mouse model of endometriosis, IL-33 injections caused systemic inflammation, which manifested as an increase in plasma pro-inflammatory cytokines compared to control mice. Furthermore, endometriotic lesions from IL-33 treated mice were highly vascularized and exhibited increased proliferation. Collectively, we provide convincing evidence that IL-33 perpetuates inflammation, angiogenesis and lesion proliferation, which are critical events in the lesion survival and progression of endometriosis

A balancing act: RNA binding protein HuR/TTP axis in endometriosis patients

Endometriosis, a major reproductive pathology affecting 8-10% of women is characterized by chronic inflammation and immune dysfunction. Human antigen R (HuR) and Tristetraprolin (TTP) are RNA binding proteins that competitively bind to cytokines involved in inflammation including: tumor necrosis factor alpha (TNF-α), granulocyte macrophage colony stimulating factor (GM-CSF), interleukin 6 (IL-6) among others, and stabilize and destabilize them, respectively. The aim of this study was to examine RNA binding protein (RNABP) HuR/TTP axis in endometriosis patients compared to menstrual stage matched healthy fertile controls in hopes of better understanding their contribution to the pathogenesis of endometriosis. Additionally, using a targeted in vitro siRNA approach, we examined whether knock-down of TTP can play a functional role on other RNABPs that competitively bind to inflammatory targets of TTP in both endometriotic and endometrial epithelial cell lines. Our results suggest that RNABPs TTP and HuR are dysregulated in endometriotic lesions compared to matched eutopic patient samples as well endometrium from healthy controls. Silencing of TTP in endometriotic and endometrial epithelial cells revealed differential response to inflammatory cytokines and other RNABPs. Our results suggest potential involvement of HuR/TTP RNA binding protein axis in regulation of inflammation in endometriosis

Estrogen mediates inflammatory role of mast cells in endometriosis pathophysiology

Endometriosis is an estrogen dependent, chronic inflammatory disease characterized by the growth of endometrial lining outside of the uterus. Mast cells have emerged as key players in regulating not only allergic responses but also other mechanisms such as angiogenesis, fibrosis, and pain. The influence of estrogen on mast cell function has also been recognized as a potential factor driving disease pathophysiology in number of allergic and chronic inflammatory conditions. However, precise information is lacking on the cross talk between endocrine and immune factors within the endometriotic lesions and whether that contributes to the involvement of mast cells with disease pathophysiology. In this study, we observed a significant increase in mast cell numbers within endometriotic lesions compared to matched eutopic endometrium from the same patients. Compared to eutopic endometrium, endometriotic lesions had significantly higher levels of stem cell factor (SCF), a potent growth factor critical for mast cell expansion, differentiation, and survival for tissue resident mast cells. Targeted mRNA Q-PCR array revealed that the endometriotic lesions harbour microenvironment (upregulation of CPA3, VCAM1, CCL2, CMA1, CCR1, and KITLG) that is conducive to mast cells recruitment and subsequent differentiation. To examine cross-talk of mast cells within the endometriotic lesion microenvironment, endometriotic epithelial cells (12Z) and endometrial stromal cells (hESC) incubated with mast cell-conditioned media showed significantly increased production of pro-inflammatory and chemokinetic cytokines. To further understand the impact of estrogen on mast cells in endometriosis, we induced endometriosis in C57BL/6 mice. Mature mast cells were significantly higher in peritoneal fluid of estrogen-treated mice compared to untreated mice within the sham operated groups. Mouse endometriotic lesion tissue revealed several genes (qRT-PCR) relevant in mast cell biology significantly upregulated in the estrogen treated, endometriosis-induced group compared to control endometrium. The endometriotic lesions from estrogen treated mice also had significantly higher density of Alcian blue stained mast cells compared to untreated lesions or control endometrium. Collectively, these findings suggest that endometriotic lesions provide a microenvironment necessary for recruitment and differentiation of mast cells. In turn, mast cells potentially release pro-inflammatory mediators that contribute to chronic pelvic pain and endometriosis disease progression

Flourishing follicles: Overview of ovarioles

Ovarian follicle development is essential for the propagation of species, and unifies both vertebrates and invertebrates. In Drosophila melanogaster, follicle development occurs through a spectacularly coordinated sequence within the highly polarized ovariole (pictured). A single ovary contains more than a dozen ovarioles that cluster together to form bud-like structures. Gentle mechanical disruption of the ovary allows for the separation and visualization of individual ovarioles and, thus, the progression of follicle development. Here, D. melanogaster ovarioles were isolated and stained with 4´,6-diamidino-2-phenylindole (DAPI) to identify the characteristic stages of follicular maturation. Follicle development occurs in a distinct anterior-to-posterior direction, beginning in the germarium (red) and progressing through a set of egg chambers of increasing numerical stage (green, blue, yellow, and magenta), before terminating an a mature oocyte (cyan). Germ line stem cells, residing within the germarium, are a self-renewing population that divide to form a daughter stem cell, which remains in the germarium, and a cystoblast. The cystoblast traverses through the ovariole, where it undergoes sequential rounds of division to form an egg chamber housing 15 nurse cells that work in tandem to nourish a single developing oocyte. The egg chamber is additionally surrounded by numerous follicular cells. Ultimately, the developmentally competent egg will exit the assembly line seven days later and enter the uterus where it may be fertilized. A fertilized egg activates during its deposition on an exterior surface, allowing and embryonic development to commence externallyFil: Kelleher, Andrew M.. University of Missouri; Estados UnidosFil: Khalaj, Kasra. Queens University; CanadáFil: Martin, Jacinta H.. University of Newcastle; Reino UnidoFil: Scaia, María Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Biodiversidad y Biología Experimental y Aplicada. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Biodiversidad y Biología Experimental y Aplicada; ArgentinaFil: Wilson, Rebecca L.. University of Adelaide; Australi

The microRNAome of pregnancy: deciphering miRNA networks at the maternal-fetal interface.

MicroRNAs (miRNAs) post-transcriptionally regulate a vast network of genes by inhibiting mRNA translation. Aberrant miRNA expression profiles have been implicated in pathologies and physiological processes including pregnancy and angiogenesis. Using our established model of implantation failure and spontaneous fetal loss in pigs (Sus scrofa), 236 miRNAs were profiled and compared between 1) non-pregnant and pregnant endometrium, 2) maternal and fetal tissues, and 3) viable and growth-arrested conceptus attachment sites by microarray and Real-Time PCR. Many significant differences in miRNA expression were observed between each of the aforementioned comparisons, and several were validated by PCR. Results indicated which miRNAs were important during pregnancy, which were elevated on the maternal or fetal side of the maternal-fetal interface, and they implicated the maternal expression of miR-10a, 27a, 29c, 323, 331-5p, 339-3p, 374b-5p, and 935 in the spontaneous loss observed in pigs. Several putative mRNA targets of the miRNAs (elevated in endometrium associated with arresting conceptuses) were assessed by quantitative Real-Time PCR and were depressed, supporting their regulation by miRNAs. Finally, targets were clustered by function to obtain ranked lists of gene networks that indicated which pathways/physiological processes might be important in non-pregnant (extracellular matrix factors) versus pregnant endometrium (nuclear transcription factor regulation), maternal (blood vessel development) versus fetal (neuronal differentiation) tissue, and healthy (extracellular matrix factors) versus arresting (GRAM domain) conceptus attachment sites. Overall, we demonstrate the presence of miRNAs on both sides of the maternal-fetal interface, implicate them in spontaneous fetal loss, and present a unique glimpse into the vast microRNAome of pregnancy

miRNA Expression in Endometrium and Trophoblast.

<p>Expression levels of miRNAs detected by microarray which were significantly different (<i>p</i><0.05) between endometrium (n = 3) and trophoblast (n = 3) from isolated from healthy (A) and arresting conceptus attachment sites (B). Real-Time PCR validation was performed for several miRNAs, and significant fold changes are listed for comparison. A positive fold change indicates that the miRNA was elevated in endometrium. A negative fold change indicates a decrease in the miRNA in endometrium. N/A: not assessed, N.S.: not significant.</p