Miracle-dz/UniFAR-FTUs huggingface dataset:
Recruitment of Uterine NK Cells: Induction of CXC Chemokine Ligands 10 and 11 in Human Endometrium by Estradiol and Progesterone1

Uterine NK (uNK) cells express a unique set of markers compared with blood NK cells. However, recent studies suggest that uNK cells may be derived from the recruitment of blood NK cells into the endometrium. In this study, we used an in vitro organ culture system to demonstrate that estradiol induces expression of chemokines CXCL10 and/or CXCL11 within human endometrium in 85% of patient samples tested. The average increase in gene expression after 10−9 M estradiol treatment was 8.5-fold for CXCL10 and 7.7-fold for CXCL11 compared with medium alone. We observed that a specific estrogen receptor antagonist (ICI182780) was able to prevent chemokine gene induction, indicating that the effect of estradiol was receptor mediated. Moreover, our study showed that progesterone induced CXCL10 and CXCL11 expression in 83% of endometrial samples tested. We have also found that uNK cells and blood NK cells express the receptor for CXCL10 and CXCL11, CXCR3, with the highest expression found on uNK cells and CD56bright blood NK cells. These data indicate that sex hormones induce specific chemokines in nonpregnant human endometrium that can activate NK cell migration, and suggest that this mechanism may account for the increased NK cell numbers in endometrium during the menstrual cycle.
Association of fine particulate matter from different sources with daily mortality in six U.S. cities.

Previously we reported that fine particle mass (particulate matter [less than and equal to] 2.5 microm; PM(2.5)), which is primarily from combustion sources, but not coarse particle mass, which is primarily from crustal sources, was associated with daily mortality in six eastern U.S. cities (1). In this study, we used the elemental composition of size-fractionated particles to identify several distinct source-related fractions of fine particles and examined the association of these fractions with daily mortality in each of the six cities. Using specific rotation factor analysis for each city, we identified a silicon factor classified as soil and crustal material, a lead factor classified as motor vehicle exhaust, a selenium factor representing coal combustion, and up to two additional factors. We extracted daily counts of deaths from National Center for Health Statistics records and estimated city-specific associations of mortality with each source factor by Poisson regression, adjusting for time trends, weather, and the other source factors. Combined effect estimates were calculated as the inverse variance weighted mean of the city-specific estimates. In the combined analysis, a 10 microg/m(3) increase in PM(2.5) from mobile sources accounted for a 3.4% increase in daily mortality [95% confidence interval (CI), 1.7-5.2%], and the equivalent increase in fine particles from coal combustion sources accounted for a 1.1% increase [CI, 0.3-2.0%). PM(2.5) crustal particles were not associated with daily mortality. These results indicate that combustion particles in the fine fraction from mobile and coal combustion sources, but not fine crustal particles, are associated with increased mortality.
Short-range Wnt5 signaling initiates specification of sea urchin posterior ectoderm

The border between the posterior ectoderm and the endoderm is a location where two germ layers meet and establish an enduring relationship that also later serves, in deuterostomes, as the anatomical site of the anus. In the sea urchin, a prototypic deuterostome, the ectoderm-endoderm boundary is established before gastrulation, and ectodermal cells at the boundary are thought to provide patterning inputs to the underlying mesenchyme. Here we show that a short-range Wnt5 signal from the endoderm actively patterns the adjacent boundary ectoderm. This signal activates a unique subcircuit of the ectoderm gene regulatory network, including the transcription factors IrxA, Nk1, Pax2/5/8 and Lim1, which are ultimately restricted to subregions of the border ectoderm (BE). Surprisingly, Nodal and BMP2/4, previously shown to be activators of ectodermal specification and the secondary embryonic axis, instead restrict the expression of these genes to subregions of the BE. A detailed examination showed that endodermal Wnt5 functions as a short-range signal that activates only a narrow band of ectodermal cells, even though all ectoderm is competent to receive the signal. Thus, cells in the BE integrate positive and negative signals from both the primary and secondary embryonic axes to correctly locate and specify the border ectoderm.
Enhanced Mortality to Metastatic Bladder Cancer Cell Line MB49 in Vasoactive Intestinal Peptide Gene Knockout Mice

To identify if the absence of the vasoactive intestinal peptide (VIP) gene enhances susceptibility to death from metastatic bladder cancer, two strains of mice were injected with MB49 murine bladder cancer cells. The growth and spread of the cancer was measured over a period of 4 weeks in C57BL/6 mice and 5 weeks in VIP knockout (KO) mice. A Kaplan–Meier plot was constructed to compare control C57BL/6 mice and C57BL/6 mice with MB49 vs. VIP KO controls and VIP KO mice with MB49. The wild-type (WT) strain (C57BL/6) contained the VIP gene, while the other strain, VIP knockout backcrossed to C57BL/6 (VIP KO) did not and was thus unable to endogenously produce VIP. VIP KO mice had increased mortality compared to C57BL/6 mice at 4 weeks. The number of ulcers between both groups was not statistically significant. In vitro studies indicated that the presence VIP in high doses reduced MB49 cell growth, as well as macrophage inhibitory factor (MIF), a growth factor in bladder cancer cells. These findings support the concept that VIP may attenuate susceptibility to death from bladder cancer, and that it exerts its effect via downregulation of MIF.
Bounds on the entropy of patterns of I.I.D. sequences

Bounds on the entropy of patterns of sequences generated by independently identically distributed (i.i.d.) sources are derived. A pattern is a sequence of indices that contains all consecutive integer indices in increasing order of first occurrence. If the alphabet of a source that generated a sequence is unknown, the inevitable cost of coding the unknown alphabet symbols can be exploited to create the pattern of the sequence. This pattern can in turn be compressed by itself. The bounds derived here are functions of the i.i. d. source entropy, alphabet size, and letter probabilities. It is shown that for large alphabets, the pattern entropy must decrease from the i.i. d. one. The decrease is in many cases more significant than the universal coding redundancy bounds derived in prior works. The pattern entropy is confined between two bounds that depend on the arrangement of the letter probabilities in the probability space. For very large alphabets whose size may be greater than the coded pattern length, all low probability letters are packed into one symbol. The pattern entropy is upper and lower bounded in terms of the i.i. d. entropy of the new packed alphabet. Correction terms, which are usually negligible, are provided for both upper and lower bounds.
Effects of attentional load on early visual processing depend on stimulus timing

A growing number of studies suggest that early visual processing is not only affected by low‐level perceptual attributes but also by higher order cognitive factors such as attention or emotion. Using high‐density electroencephalography, we recently demonstrated that attentional load of a task at fixation reduces the response of primary visual cortex to irrelevant peripheral stimuli, as indexed by the C1 component. In the latter study, peripheral stimuli were always presented during intervals without task‐relevant stimuli. Here, we use a similar paradigm but present central task stimuli and irrelevant peripheral stimuli simultaneously while keeping all other stimulus characteristics constant. Results show that rather than to suppress responses to peripheral stimulation, high attentional load elicits higher C1 amplitudes under these conditions. These findings suggest that stimulus timing can profoundly alter the effects of attentional load on the earliest stages of processing in human visual cortex. Hum Brain Mapp, 2012. © 2011 Wiley Periodicals, Inc.
Stress Influence on Fracture Aperture and Permeability of Fragmented Rocks

The influence of far‐field stresses on fracture apertures in a fragmented rock layer is investigated using finite element analysis of a three‐dimensional mechanical model. The model implements realistic boundary conditions, interactions between the fragmented layer and neighboring plastic rock layers, and frictional interfaces between the rock blocks. Stress‐strain analysis is conducted to obtain stress variations within the fragmented rock layer and the block displacements and rotations. The fracture apertures are calculated using the local stress states instead of the far‐field stresses simply being projected on the fractures. It is observed that fracture apertures can vary for the fracture segments over the individual blocks. Ensemble permeability is calculated by running a single‐phase flow analysis considering the obtained fracture apertures for fracture segments. The influence of the rock block displacements, rotations and deformations, difference between the mechanical properties of the rock layers, and the orientation of the horizontal stresses is investigated on the ensemble permeability. It is demonstrated that the compressibility of the neighboring layers and block rotations and deformations have significant influence on the permeability of the fragmented rock layer. These effects, which may be ignored in simpler aperture calculation models, can result in considerable inaccuracies in the estimation of fracture apertures and ensemble permeability. Hence, such methods may only be used as indicative tools.
Manipulation of Neutrophils by Porphyromonas gingivalis in the Development of Periodontitis

The pathogenesis of the chronic periodontal disease is associated with a skewed host inflammatory response to periodontal pathogens, such as Porphyromonas gingivalis, that accounts for the majority of periodontal tissue damage. Neutrophils are the most abundant leukocytes in periodontal pockets and depending on the stage of the disease, also plentiful PMNs are present in the inflamed gingival tissue and the gingival crevice. They are the most efficient phagocytes and eliminate pathogens by a variety of means, which are either oxygen-dependent or -independent. However, these secretory lethal weapons do not strictly discriminate between pathogens and host tissue. Current studies describe conflicting findings about neutrophil involvement in periodontal disease. On one hand literature indicate that hyper-reactive neutrophils are the main immune cell type responsible for this observed tissue damage and disease progression. Deregulation of neutrophil survival and functions, such as chemotaxis, migration, secretion of antimicrobial peptides or enzymes, and production of reactive oxygen species, contribute to observed tissue injury and the clinical signs of periodontal disease. On the other hand neutrophils deficiencies in patients and mice also result in periodontal phenotype. Therefore, P. gingivalis represents a periodontal pathogen that manipulates the immune responses of PMNs, employing several virulence factors, such as gingipains, serine proteases, lipid phosphatases, or fimbriae. This review will sum up studies devoted to understanding different strategies utilized by P. gingivalis to manipulate PMNs survival and functions in order to inhibit killing by a granular content, prolong inflammation, and gain access to nutrient resources.
Gene Expression Profiles Link Respiratory Viral Infection, Platelet Response to Aspirin, and Acute Myocardial Infarction

Background Influenza infection is associated with myocardial infarction (MI), suggesting that respiratory viral infection may induce biologic pathways that contribute to MI. We tested the hypotheses that 1) a validated blood gene expression signature of respiratory viral infection (viral GES) was associated with MI and 2) respiratory viral exposure changes levels of a validated platelet gene expression signature (platelet GES) of platelet function in response to aspirin that is associated with MI. Methods A previously defined viral GES was projected into blood RNA data from 594 patients undergoing elective cardiac catheterization and used to classify patients as having evidence of viral infection or not and tested for association with acute MI using logistic regression. A previously defined platelet GES was projected into blood RNA data from 81 healthy subjects before and after exposure to four respiratory viruses: Respiratory Syncytial Virus (RSV) (n=20), Human Rhinovirus (HRV) (n=20), Influenza A virus subtype H1N1 (H1N1) (n=24), Influenza A Virus subtype H3N2 (H3N2) (n=17). We tested for the change in platelet GES with viral exposure using linear mixed-effects regression and by symptom status. Results In the catheterization cohort, 32 patients had evidence of viral infection based upon the viral GES, of which 25% (8/32) had MI versus 12.2% (69/567) among those without evidence of viral infection (OR 2.3; CI [1.03-5.5], p=0.04). In the infection cohorts, only H1N1 exposure increased platelet GES over time (time course p-value = 1e-04). Conclusions A viral GES of non-specific, respiratory viral infection was associated with acute MI; 18% of the top 49 genes in the viral GES are involved with hemostasis and/or platelet aggregation. Separately, H1N1 exposure, but not exposure to other respiratory viruses, increased a platelet GES previously shown to be associated with MI. Together, these results highlight specific genes and pathways that link viral infection, platelet activation, and MI especially in the case of H1N1 influenza infection.
Web Service Composition with Case-Based Reasoning

To run a smart E-Business or provide efficient Web service, a web services composition model is needed. Web services composition refers to the process of collaborating the heterogeneous web services. This paper presents a model of web services composition by using Case-Based Reasoning (CBR) techniques. CBR is applied in the process of service discovery, which is the crucial composition process. Our service composition model integrates the two behaviours of proactive and reactive service compositions. We will address dynamic composition and collaboration among services. The similarity feature of CBR is used for efficient service discovery.
Reducing the risk of hepatitis B virus transfusion-transmitted infection

Before 1970, approximately 6% of multi-transfused recipients acquired a transfusion-transmitted Hepatitis B virus (HBV) infection. The safety improvements since then have been tremendous. From a level of a few infections per 1000 donations, the risk today, depending on the screening algorithm and additional measurements performed, has decreased to around 1:500,000 to 1:1,000,000, an improvement greater than 1000-fold compared to 50 years ago. This enormous gain in safety has been achieved through many factors, including development of increasingly more sensitive Hepatitis B antigen (HBsAg) assays; the adoption in some countries of hepatitis B core antibody (anti-HBc) screening; an improved donor selection procedure; HBV vaccination programs; and finally the introduction of HBV nucleic acid testing (NAT). Because there is a tendency in transfusion medicine to add one safety measure on top of another to approach the ultimate goal of zero risks, costs become increasingly a matter of debate. It is obvious that any new measure in addition to existing methods or measures will have very poor cost effectiveness. Therefore each country needs to perform its own calculation based on the country’s own epidemiology, resources, political and public awareness of the risks, in order to choose the correct and most cost-efficient measures. Ideally, each country would make decisions regarding implementation of additional blood safety measures in the context of both the perceived benefit and the allocation of overall health care resources.
Large-Scale Bayesian Multi-Label Learning via Topic-Based Label Embeddings

We present a scalable Bayesian multi-label learning model based on learning low-dimensional label embeddings. Our model assumes that each label vector is generated as a weighted combination of a set of topics (each topic being a distribution over labels), where the combination weights (i.e., the embeddings) for each label vector are conditioned on the observed feature vector. This construction, coupled with a Bernoulli-Poisson link function for each label of the binary label vector, leads to a model with a computational cost that scales in the number of positive labels in the label matrix. This makes the model particularly appealing for real-world multi-label learning problems where the label matrix is usually very massive but highly sparse. Using a data-augmentation strategy leads to full local conjugacy in our model, facilitating simple and very efficient Gibbs sampling, as well as an Expectation Maximization algorithm for inference. Also, predicting the label vector at test time does not require doing an inference for the label embeddings and can be done in closed form. We report results on several benchmark data sets, comparing our model with various state-of-the art methods.
An empirical evaluation of bufferbloat in IEEE 802.11n wireless networks

In this paper, we analyze the impact of large, persistently-full buffers (`bufferbloat') on various network dynamics in IEEE 802.11n wireless networks. Bufferbloat has mostly been studied in the context of wired networks. We study the impact of bufferbloat on a variety of wireless network topologies, including wireless LAN (WLAN) and multi-hop wireless networks. Our results show that a single FTP transfer between two Linux wireless hosts can saturate the buffers in the network stack, leading to RTT delays exceeding 4.5 s in multi-hop configurations. We show that well-designed Aggregate MAC Protocol Data Unit (A-MPDU) MAC-layer frame aggregation can reduce RTT delays while simultaneously increasing network throughput. However, additional measures may still be required to meet the constraints of real-time flows (such as VoIP). Our experiments show that large buffers can deteriorate the fairness in rate allocation in parking lot based multi-hop networks.
Molecular screening for a personalized treatment approach in advanced adrenocortical cancer.

CONTEXT Adrenocortical cancer (ACC) is a rare cancer with poor prognosis and scant treatment options. In ACC, no personalized approach has emerged but no extensive molecular screening has been performed to date. OBJECTIVE The objective of the study was to evaluate the presence of a large number of potentially targetable molecular events in a large cohort of advanced ACC. DESIGN, SETTING, AND PARTICIPANTS We used hot spot gene sequencing (Ion Torrent, 40 patients) and comparative genomic hybridization (CGH; 28 patients; a subset of the entire cohort) in adult stage III-IV ACC samples to screen for mutations and copy number abnormalities of potential interest for therapeutic use in 46 and 130 genes, respectively. RESULTS At least one copy number alteration or mutation was found in 19 patients (47.5%). The most frequent mutations were detected on TP53, ATM, and CTNNB1 [6 of 40 (15%), 5 of 40 (12.5%), and 4 of 40 (10%), respectively]. The most frequent copy number alterations identified were: amplification of the CDK4 oncogene (5 of 28; 17.9%) and deletion of the CDKN2A (4 of 28; 14.3%) and CDKN2B (3 of 28; 10.7%) tumor suppressor genes. Amplifications of FGFR1, FGF9, or FRS2 were discovered in three subjects (10.7%). Associated alterations were: deletions of CDKN2A, CDKN2B with ATM mutations, and TP53 mutations with CTNNB1 mutations. CONCLUSIONS No simple targetable molecular event emerged. Drugs targeting the cell cycle could be the most relevant new therapeutic approach for patients with advanced ACC. Inhibitors of the fibroblast growth factor receptor pathway could also be a therapeutic option in a subset of patients, whereas other targeted therapies should be considered on a case-by-case basis.
Different pathways with distinct properties conduct dilations in the microcirculation in vivo.

AIMS Conduction of vasomotor signals along the vessel coordinates the behaviour of vascular cells and is attributed to the spread of hyperpolarizations through gap junctions. Intriguingly, conducted dilations encompass larger distances than can be expected by passive electrotonic spread. Because distances are quite distinct for different dilators, we hypothesized that separate pathways with distinct properties are involved. METHODS AND RESULTS We characterized local and conducted responses elicited by acetylcholine (ACh) and adenosine (Ado) in the murine microcirculation in vivo. Local (and remote) ACh dilations were nearly abrogated by blockade of K(Ca) channels (charybdotoxin), but dilations to Ado were abolished by the K(ATP) blocker glibenclamide. Bupivacaine, a blocker of Na+ and K+ channels, and similarly the blockade of inwardly rectifying K+ channels (barium) revealed different conduction mechanisms, as the remote dilation to Ado, but not ACh, was abrogated. Surprisingly, expression of connexin37 (Cx37) was not detected in Cx40-deficient arterioles, although abundantly expressed in endothelium of wild-type arterioles. In contrast to the wild-type mice, the amplitude of conducted ACh and Ado dilations decreased similarly with distance in Cx40-deficient mice. Recordings of membrane potential in vivo showed endothelial hyperpolarization by approximately 10 mV in response to ACh, whereas Ado did not alter endothelial membrane potential. CONCLUSION Distinct pathways conduct responses along the vessel wall which involve dissimilar K+ channels and connexins in initiation and spreading. Most likely, the endothelium is the preferential conduction pathway activated by ACh, whereas in the case of Ado the smooth muscle serves as the signalling pathway. However, in arterioles nearly devoid of Cx40 and Cx37, ACh responses can likewise be conducted along the smooth muscle.
Experimental Infection of Eurasian Collared-Dove (Streptopelia decaocto) with West Nile virus

ABSTRACT: The Eurasian collared-dove (Streptopelia decaocto) has recently experienced a population explosion in North America. It is frequently infected with West Nile virus (WNV). To test the hypothesis that the Eurasian collared-dove is competent to transmit WNV, we experimentally infected two cohorts of doves with two different strains of WNV, CO08, and NY99, respectively. Both virus strains induced a low-level viremia, capable of infecting a small fraction of vector mosquitoes. We suggest that the Eurasian collared-dove plays a relatively insignificant role as an amplifying host for WNV, but it may be important where it is locally abundant.