Implementation of a herd management system with wireless sensor networks

This paper investigates an adaptation of Wireless Sensor Networks (WSNs) to cattle monitoring applications. The proposed solution facilitates the requirement for continuously assessing the condition of individual animals, aggregating and reporting this data to the farm manager. There are several existing approaches to achieving animal monitoring, ranging from using a store and forward mechanism to employing GSM-based techniques; these approaches only provide sporadic information and introduce a considerable cost in staffing and physical hardware. The core of this study is to overcome the aforementioned drawbacks by using alternative cheap, low power consumption sensor nodes capable of providing real-time communication at a reasonable hardware cost. In this paper, both the hardware and software has been designed to provide a solution which can obtain real-time data from dairy cattle whilst conforming to the limitations associated with WSNs implementations

Interstellar Turbulence Driving by Galactic Spiral Shocks

Spiral shocks are potentially a major source of turbulence in the interstellar medium. To address this problem quantitatively, we use numerical simulations to investigate gas flow across spiral arms in vertically stratified, self-gravitating, magnetized models of galactic disks. Our models are isothermal, quasi-axisymmetric, and local in the quasi-radial direction while global in the vertical direction. We find that a stellar spiral potential perturbation promptly induces a spiral shock in the gas flow. For vertically stratified gas disks, the shock front in the radial-vertical plane is in general curved, and never achieves a steady state. This behavior is in sharp contrast to spiral shocks in two-dimensional (thin) disks, which are generally stationary. The non-steady motions in our models include large-amplitude quasi-radial flapping of the shock front. This flapping feeds random gas motions on the scale of the vertical disk thickness, which then cascades to smaller scales. The induced gas velocity dispersion in quasi-steady state exceeds the sonic value for a range of shock strengths, suggesting that spiral shocks are indeed an important generator of turbulence in disk galaxies.Comment: 4 pages, 3 figures, Accepted for publication in ApJ

Galactic Spiral Shocks with Thermal Instability

Using one-dimensional hydrodynamic simulations including interstellar heating, cooling, and thermal conduction, we investigate nonlinear evolution of gas flow across galactic spiral arms. We model the gas as a non-self-gravitating, unmagnetized fluid, and follow its interaction with a stellar spiral potential in a local frame comoving with the stellar pattern. Initially uniform gas rapidly separates into warm and cold phases as a result of thermal instability (TI), and also forms a quasi-steady shock that prompts phase transitions. After saturation, the flow follows a recurring cycle: warm and cold phases in the interarm region are shocked and immediately cool to become a denser cold medium in the arm; post-shock expansion reduces the mean density to the unstable regime in the transition zone and TI subsequently mediates evolution back into warm and cold interarm phases. For our standard model with n_0 = 2 cm^-3, the gas resides in the dense arm, thermally-unstable transition zone, and interarm region for 14%, 22%, 64% of the arm-to-arm crossing time. These regions occupy 1%, 16%, and 83% of the arm-to-arm distance, respectively. Gas at intermediate temperatures represents ~25-30% of the total mass, similar to the fractions estimated from HI observations. Despite transient features and multiphase structure, the time-averaged shock profiles can be matched to that of a diffusive isothermal medium with temperature 1,000 K and "particle" mean free path of l_0 = 100 pc. Finally, we quantify numerical conductivity associated with translational motion of phase-separated gas on the grid, and show that convergence of numerical results requires the numerical conductivity to be comparable to or smaller than the physical conductivity. (Abridged)Comment: 41 pages, 13 figures, 1 table. Accepted for publication in Astrophysical Journal. PDF version with higher resolution figures is available at http://astro.snu.ac.kr/~kimcg/AST/GSS_TI.pd

Mechanisms of CFTR Functional Variants That Impair Regulated Bicarbonate Permeation and Increase Risk for Pancreatitis but Not for Cystic Fibrosis

CFTR is a dynamically regulated anion channel. Intracellular WNK1-SPAK activation causes CFTR to change permeability and conductance characteristics from a chloride-preferring to bicarbonate-preferring channel through unknown mechanisms. Two severe CFTR mutations (CFTRsev) cause complete loss of CFTR function and result in cystic fibrosis (CF), a severe genetic disorder affecting sweat glands, nasal sinuses, lungs, pancreas, liver, intestines, and male reproductive system. We hypothesize that those CFTR mutations that disrupt the WNK1-SPAK activation mechanisms cause a selective, bicarbonate defect in channel function (CFTRBD) affecting organs that utilize CFTR for bicarbonate secretion (e.g. the pancreas, nasal sinus, vas deferens) but do not cause typical CF. To understand the structural and functional requirements of the CFTR bicarbonate-preferring channel, we (a) screened 984 well-phenotyped pancreatitis cases for candidate CFTRBD mutations from among 81 previously described CFTR variants; (b) conducted electrophysiology studies on clones of variants found in pancreatitis but not CF; (c) computationally constructed a new, complete structural model of CFTR for molecular dynamics simulation of wild-type and mutant variants; and (d) tested the newly defined CFTRBD variants for disease in non-pancreas organs utilizing CFTR for bicarbonate secretion. Nine variants (CFTR R74Q, R75Q, R117H, R170H, L967S, L997F, D1152H, S1235R, and D1270N) not associated with typical CF were associated with pancreatitis (OR 1.5, p = 0.002). Clones expressed in HEK 293T cells had normal chloride but not bicarbonate permeability and conductance with WNK1-SPAK activation. Molecular dynamics simulations suggest physical restriction of the CFTR channel and altered dynamic channel regulation. Comparing pancreatitis patients and controls, CFTRBD increased risk for rhinosinusitis (OR 2.3, p<0.005) and male infertility (OR 395, p<<0.0001). WNK1-SPAK pathway-activated increases in CFTR bicarbonate permeability are altered by CFTRBD variants through multiple mechanisms. CFTRBD variants are associated with clinically significant disorders of the pancreas, sinuses, and male reproductive system.Fil: LaRusch, Jessica. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Jung, Jinsei. Yonsei University College of Medicine; Corea del SurFil: General, Ignacio. University of Pittsburgh; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Lewis, Michele D.. Mayo Clinic. Division of Gastroenterology and Hepatology; Estados UnidosFil: Park, Hyun Woo. Yonsei University College of Medicine; Corea del SurFil: Brand, Randall E.. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Gelrud, Andres. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Anderson, Michelle A.. University of Michigan; Estados UnidosFil: Banks, Peter A.. Brigham and Women’s Hospital. Division of Gastroenterology; Estados UnidosFil: Conwell, Darwin. Brigham and Women’s Hospital. Division of Gastroenterology; Estados UnidosFil: Lawrence, Christopher. Medical University of South Carolina; Estados UnidosFil: Romagnuolo, Joseph. Medical University of South Carolina; Estados UnidosFil: Baillie, John. University of Duke; Estados UnidosFil: Alkaade, Samer. St. Louis University. School of Medicine; Estados UnidosFil: Cote, Gregory. Indiana University; Estados UnidosFil: Gardner, Timothy B.. Dartmouth-Hitchcock Medical Center; Estados UnidosFil: Amann, Stephen T.. North Mississippi Medical Center; Estados UnidosFil: Slivka, Adam. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Sandhu, Bimaljit. Virginia Commonwealth University Medical Center; Estados UnidosFil: Aloe, Amy. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Kienholz, Michelle L.. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Yadav, Dhiraj. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Barmada, M. Michael. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Bahar, Ivet. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: Lee, Min Goo. Yonsei University College of Medicine; Corea del SurFil: Whitcomb, David C.. Univeristy of Pittsburgh. School of Medicine; Estados UnidosFil: North American Pancreatitis Study Group. No especifica

Contribution of common and rare variants to bipolar disorder susceptibility in extended pedigrees from population isolates.

Current evidence from case/control studies indicates that genetic risk for psychiatric disorders derives primarily from numerous common variants, each with a small phenotypic impact. The literature describing apparent segregation of bipolar disorder (BP) in numerous multigenerational pedigrees suggests that, in such families, large-effect inherited variants might play a greater role. To identify roles of rare and common variants on BP, we conducted genetic analyses in 26 Colombia and Costa Rica pedigrees ascertained for bipolar disorder 1 (BP1), the most severe and heritable form of BP. In these pedigrees, we performed microarray SNP genotyping of 838 individuals and high-coverage whole-genome sequencing of 449 individuals. We compared polygenic risk scores (PRS), estimated using the latest BP1 genome-wide association study (GWAS) summary statistics, between BP1 individuals and related controls. We also evaluated whether BP1 individuals had a higher burden of rare deleterious single-nucleotide variants (SNVs) and rare copy number variants (CNVs) in a set of genes related to BP1. We found that compared with unaffected relatives, BP1 individuals had higher PRS estimated from BP1 GWAS statistics (P = 0.001 ~ 0.007) and displayed modest increase in burdens of rare deleterious SNVs (P = 0.047) and rare CNVs (P = 0.002 ~ 0.033) in genes related to BP1. We did not observe rare variants segregating in the pedigrees. These results suggest that small-to-moderate effect rare and common variants are more likely to contribute to BP1 risk in these extended pedigrees than a few large-effect rare variants

Characterizing mass, momentum, energy and metal outflow rates of multi-phase galactic winds in the FIRE-2 cosmological simulations

We characterize mass, momentum, energy and metal outflow rates of multi-phase galactic winds in a suite of FIRE-2 cosmological "zoom-in" simulations from the Feedback in Realistic Environments (FIRE) project. We analyze simulations of low-mass dwarfs, intermediate-mass dwarfs, Milky Way-mass halos, and high-redshift massive halos. Consistent with previous work, we find that dwarfs eject about 100 times more gas from their interstellar medium (ISM) than they form in stars, while this mass "loading factor" drops below one in massive galaxies. Most of the mass is carried by the hot phase ($>10^5$ K) in massive halos and the warm phase ($10^3-10^5$ K) in dwarfs; cold outflows ($<10^3$ K) are negligible except in high-redshift dwarfs. Energy, momentum and metal loading factors from the ISM are of order unity in dwarfs and significantly lower in more massive halos. Hot outflows have $2-5\times$ higher specific energy than needed to escape from the gravitational potential of dwarf halos; indeed, in dwarfs, the mass, momentum, and metal outflow rates increase with radius whereas energy is roughly conserved, indicating swept up halo gas. Burst-averaged mass loading factors tend to be larger during more powerful star formation episodes and when the inner halo is not virialized, but we see effectively no trend with the dense ISM gas fraction. We discuss how our results can guide future controlled numerical experiments that aim to elucidate the key parameters governing galactic winds and the resulting associated preventative feedback.Comment: Accepted to MNRAS with minor revisions, main body is 25 pages with 14 figure

IL-4/IL-13 Stimulated Macrophages Enhance Breast Cancer Invasion Via Rho-GTPase Regulation of Synergistic VEGF/CCL-18 Signaling

Tumor associated macrophages (TAMs) are increasingly recognized as major contributors to the metastatic progression of breast cancer and enriched levels of TAMs often correlate with poor prognosis. Despite our current advances it remains unclear which subset of M2-like macrophages have the highest capacity to enhance the metastatic program and which mechanisms regulate this process. Effective targeting of macrophages that aid cancer progression requires knowledge of the specific mechanisms underlying their pro-metastatic actions, as to avoid the anticipated toxicities from generalized targeting of macrophages. To this end, we set out to understand the relationship between the regulation of tumor secretions by Rho-GTPases, which were previously demonstrated to affect them, macrophage differentiation, and the converse influence of macrophages on cancer cell phenotype. Our data show that IL-4/IL-13 in vitro differentiated M2a macrophages significantly increase migratory and invasive potential of breast cancer cells at a greater rate than M2b or M2c macrophages. Our previous work demonstrated that the Rho-GTPases are potent regulators of macrophage-induced migratory responses; therefore, we examined M2a-mediated responses in RhoA or RhoC knockout breast cancer cell models. We find that both RhoA and RhoC regulate migration and invasion in MDA-MB-231 and SUM-149 cells following stimulation with M2a conditioned media. Secretome analysis of M2a conditioned media reveals high levels of vascular endothelial growth factor (VEGF) and chemokine (C-C motif) ligand 18 (CCL-18). Results from our functional assays reveal that M2a TAMs synergistically utilize VEGF and CCL-18 to promote migratory and invasive responses. Lastly, we show that pretreatment with ROCK inhibitors Y-276332 or GSK42986A attenuated VEGF/CCL-18 and M2a-induced migration and invasion. These results support Rho-GTPase signaling regulates downstream responses induced by TAMs, offering a novel approach for the prevention of breast cancer metastasis by anti-RhoA/C therapies