Miracle-dz/UniFAR-FTUs huggingface dataset:
Parallel rectilinear shortest paths with rectangular obstacles

Given a redilinear convex polygon P having O(n) vertices and which conlains n pairwise disjoint. rectangular rectilinear obstacles, we compute, in parallel, a data structure that supports queries about shortest rectilinear obstacle-avoiding paths in P. That is, a query specifies a Bource and a destination, and the data structure enables effi~ dent processing of the query. We construct the data structure in O(log2 n) time, with O(n2jlog2 n) prace6S0rs in the CREW-PRAM model if all queries are such that the source and the destination are on the boundary of P, with O(n2 jlogn) processors if the source is an obstacle vertex and the destination is on the boundary of P, and with 0(n) processors if both the source and destination are arbitrary points in the plane. The data strucLure we compute enables one processor to obtain the path length for any pair of query vertices (of obsLacles or of P) in constant time, or O( p:/ log n1) processors to retrieve the shortest path itself in logarithmic time, where k is the number of segments of that path. If the two query points are arbitrary rather than vertices, then one processor takes O(log n) time (instead of constant time) for finding the path length, while the complexity bounds for reporting an actuailihortest path remain unchanged. A number of other related shortest paths problems are solved. The techniques we use involve a fast computation of staircase separators, and a scheme for partitioning the obstacles' boundaries in a way that ensures that the resulting path length matrices have a monotonicity property that is apparently absent before applying our partitioning scheme. Sequentially, the data structure can be built in O(n2) time.
Translational Relevance and Recent Advances of Animal Models of Abdominal Aortic Aneurysm.

Human abdominal aortic aneurysm (AAA) pathophysiology is not yet completely understood. In conductance arteries, the insoluble extracellular matrix, synthesized by vascular smooth muscle cells, assumes the function of withstanding the intraluminal arterial blood pressure. Progressive loss of this function through extracellular matrix proteolysis is a main feature of AAAs. As most patients are now treated via endovascular approaches, surgical AAA specimens have become rare. Animal models provide valuable complementary insights into AAA pathophysiology. Current experimental AAA models involve induction of intraluminal dilation (nondissecting AAAs) or a contained intramural rupture (dissecting models). Although the ideal model should reproduce the histological characteristics and natural history of the human disease, none of the currently available animal models perfectly do so. Experimental models try to represent the main pathophysiological determinants of AAAs: genetic or acquired defects in extracellular matrix, loss of vascular smooth muscle cells, and innate or adaptive immune response. Nevertheless, most models are characterized by aneurysmal stabilization and healing after a few weeks because of cessation of the initial stimulus. Recent studies have focused on ways to optimize existing models to allow continuous aneurysmal growth. This review aims to discuss the relevance and recent advances of current animal AAA models. VISUAL OVERVIEW An online visual overview is available for this article.
Joint Beamforming and Power Control for CDMA Uplink Throughput Maximization

We consider joint beamforming and power control as a means to maximize throughput in a CDMA wireless uplink, where a base station equipped with multiple antennas receives from single - antenna wireless users. Throughput maximization gives rise to an optimization problem with objective function that is in general non-concave in the power and beam- forming vectors. We introduce two iterative algorithms searching for the optimal solution; both of these alternate between a power control step, and a beamforming step. Simulation results illustrate the convergence of the proposed algorithms to a locally optimal pair of power vector and beamforming array.
Nowhere‐Zero Flows on Signed Complete and Complete Bipartite Graphs

Bouchet's conjecture asserts that each signed graph which admits a nowhere‐zero flow has a nowhere‐zero 6‐flow. We verify this conjecture for two basic classes of signed graphs—signed complete and signed complete bipartite graphs by proving that each such flow‐admissible graph admits a nowhere‐zero 4‐flow and we characterise those which have a nowhere‐zero 2‐flow and a nowhere‐zero 3‐flow.
Human RNA Polymerase II-Association Factor 1 (hPaf1/PD2) Regulates Histone Methylation and Chromatin Remodeling in Pancreatic Cancer

Change in gene expression associated with pancreatic cancer could be attributed to the variation in histone posttranslational modifications leading to subsequent remodeling of the chromatin template during transcription. However, the interconnected network of molecules involved in regulating such processes remains elusive. hPaf1/PD2, a subunit of the human PAF-complex, involved in the regulation of transcriptional elongation has oncogenic potential. Our study explores the possibility that regulation of histone methylation by hPaf1 can contribute towards alteration in gene expression by nucleosomal rearrangement. Here, we show that knockdown of hPaf1/PD2 leads to decreased di- and tri-methylation at histone H3 lysine 4 residues in pancreatic cancer cells. Interestingly, hPaf1/PD2 colocalizes with MLL1 (Mixed Lineage Leukemia 1), a histone methyltransferase that methylates H3K4 residues. Also, a reduction in hPaf1 level resulted in reduced MLL1 expression and a corresponding decrease in the level of CHD1 (Chromohelicase DNA-binding protein 1), an ATPase dependent chromatin remodeling enzyme that specifically binds to H3K4 di and trimethyl marks. hPaf1/PD2 was also found to interact and colocalize with CHD1 in both cytoplasmic and nuclear extracts of pancreatic cancer cells. Further, reduced level of CHD1 localization in the nucleus in hPaf1/PD2 Knockdown cells could be rescued by ectopic expression of hPaf1/PD2. Micrococcal nuclease digestion showed an altered chromatin structure in hPaf1/PD2-KD cells. Overall, our results suggest that hPaf1/PD2 in association with MLL1 regulates methylation of H3K4 residues, as well as interacts and regulates nuclear shuttling of chromatin remodeling protein CHD1, facilitating its function in pancreatic cancer cells.
A Mathematical Model for the Determination of Steady-State Cardiolipin Remodeling Mechanisms Using Lipidomic Data

Technical advances in lipidomic analysis have generated tremendous amounts of quantitative lipid molecular species data, whose value has not been fully explored. We describe a novel computational method to infer mechanisms of de novo lipid synthesis and remodeling from lipidomic data. We focus on the mitochondrial-specific lipid cardiolipin (CL), a polyglycerol phospholipid with four acyl chains. The lengths and degree of unsaturation of these acyl chains vary across CL molecules, and regulation of these differences is important for mitochondrial energy metabolism. We developed a novel mathematical approach to determine mechanisms controlling the steady-state distribution of acyl chain combinations in CL . We analyzed mitochondrial lipids from 18 types of steady-state samples, each with at least 3 replicates, from mouse brain, heart, lung, liver, tumor cells, and tumors grown in vitro. Using a mathematical model for the CL remodeling mechanisms and a maximum likelihood approach to infer parameters, we found that for most samples the four chain positions have an independent and identical distribution, indicating they are remodeled by the same processes. Furthermore, for most brain samples and liver, the distribution of acyl chains is well-fit by a simple linear combination of the pools of acyl chains in phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylglycerol (PG). This suggests that headgroup chemistry is the key determinant of acyl donation into CL, with chain length/saturation less important. This canonical remodeling behavior appears damaged in some tumor samples, which display a consistent excess of CL molecules having particular masses. For heart and lung, the “proportional incorporation” assumption is not adequate to explain the CL distribution, suggesting additional acyl CoA-dependent remodeling that is chain-type specific. Our findings indicate that CL remodeling processes can be described by a small set of quantitative relationships, and that bioinformatic approaches can help determine these processes from high-throughput lipidomic data.
Charge Contrast Imaging of Gibbsite Using the Variable Pressure SEM

The variable pressure scanning electron microscope (VP-SEM) allows imaging of insulators without the need for a conductive coating, due to charge neutralization at the surface from recombination of positive ions and surface electrons. Varying certain parameters such as pressure, bias, and working distance creates incomplete neutralization, and localized charging develops called charge contrast. Although the exact mechanism creating charge contrast imaging (CCI) is unknown, it is agreed that it is related to an optimum charge compensation. The behavior of the CCI is still vague, which presents a problem for determining the mechanisms. This article provides user-friendly methods of finding the optimum levels of charge contrast in the VP-SEM. We show that the CCI is obtained at optimum operating conditions where the specimen current is between 2.5 nA and 3.5 nA. The specimen current is a function of secondary electrons (SE) emission and ionization potential, producing an ion flux. Therefore an optimum specimen current represents the balanced conditions of SE emission and ion flux. Controlling the pressure, working distance, bias, scan rate, and beam current allows the microscopist to set the specimen current at this optimum level for charge contrast imaging. All the work was performed on gibbsite using the S3000N VP-SEM from Hitachi.
In vitro and In vivo Selective Antitumor Activity of Edelfosine against Mantle Cell Lymphoma and Chronic Lymphocytic Leukemia Involving Lipid Rafts

Purpose: Mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) remain B-cell malignancies with limited therapeutic options. The present study investigates the in vitro and in vivo effect of the phospholipid ether edelfosine (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine) in MCL and CLL. Experimental Design: Several cell lines, patient-derived tumor cells, and xenografts in severe combined immunodeficient mice were used to examine the anti-MCL and anti-CLL activity of edelfosine. Furthermore, we analyzed the mechanism of action and drug biodistribution of edelfosine in MCL and CLL tumor-bearing severe combined immunodeficient mice. Results: Here, we have found that the phospholipid ether edelfosine was the most potent alkyl-lysophospholipid analogue in killing MCL and CLL cells, including patient-derived primary cells, while sparing normal resting lymphocytes. Alkyl-lysophospholipid analogues ranked edelfosine > perifosine ≫ erucylphosphocholine ≥ miltefosine in their capacity to elicit apoptosis in MCL and CLL cells. Edelfosine induced coclustering of Fas/CD95 death receptor and rafts in MCL and CLL cells. Edelfosine was taken up by malignant cells, whereas normal resting lymphocytes hardly incorporated the drug. Raft disruption by cholesterol depletion inhibited drug uptake, Fas/CD95 clustering, and edelfosine-induced apoptosis. Edelfosine oral administration showed a potent in vivo anticancer activity in MCL and CLL xenograft mouse models, and the drug accumulated dramatically and preferentially in the tumor. Conclusions: Our data indicate that edelfosine accumulates and kills MCL and CLL cells in a rather selective way, and set coclustering of Fas/CD95 and lipid rafts as a new framework in MCL and CLL therapy. Our data support a selective antitumor action of edelfosine. Clin Cancer Res; 16(7); 2046–54. ©2010 AACR.
Effect of Mycobacterium tuberculosis-Specific 10-Kilodalton Antigen on Macrophage Release of Tumor Necrosis Factor Alpha and Nitric Oxide

ABSTRACT Secreted proteins of Mycobacterium tuberculosis are major targets of the specific immunity in tuberculosis and constitute promising candidates for the development of more efficient vaccines and diagnostic tests. We show here that M. tuberculosis-specific antigen 10 (MTSA-10, originally designated CFP-10) can bind to the surface of mouse J774 macrophage-like cells and stimulate the secretion of the proinflammatory cytokine tumor necrosis factor alpha (TNF-α). MTSA-10 also synergized with gamma interferon (IFN-γ) for the induction of the microbicidal free radical nitric oxide (NO) in J774 cells, as well as in bone marrow-derived and peritoneal macrophages. On the other hand, pretreatment of J774 cells with MTSA-10 markedly reduced NO but not TNF-α or interleukin 10 (IL-10) release upon subsequent stimulation with lipopolysaccharide or the cell lysate of M. tuberculosis. The presence of IFN-γ during stimulation with M. tuberculosis lysate antagonized the desensitizing effect of MTSA-10 pretreatment on macrophage NO production. The activation of protein tyrosine kinases (PTK) and the serine/threonine kinases p38 MAPK and ERK was apparently required for MTSA-10 induction of TNF-α and NO release, as revealed by specific kinase inhibitors. However, only p38 MAPK activity, not PTK or ERK activity, was partly responsible for MTSA-10-mediated macrophage desensitization. The modulation of macrophage function by MTSA-10 suggests a novel mechanism for its involvement in immunopathogenesis of tuberculosis and might have implications for the prevention, diagnosis, and therapy of this disease.
The inquiry paradox: why doing science doesn't necessarily change ideas about science

A long standing goal of science education in the United States has been that students develop an understanding of the nature of science, of what scientific knowledge is like and how it is constructed. Despite this interest, students continue to leave secondary schools with naïve views of the nature of science. Current science education reforms advocate inquiry as a way for students to learn about the nature of science as well as scientific concepts. Inquiry engages students in their own efforts to construct scientific knowledge, and several efforts to use technology to support inquiry have been effective at helping students understand important scientific concepts and develop certain skills of scientific reasoning. Still, there is no evidence that doing inquiry in school develops students’ understanding of the nature of science. The reason for this is twofold. First, assessments of students’ ideas of the nature of science universally target professional science, rather than students’ own efforts to do science. Students’ views on the nature of their own inquiry may be “scientific,” but not be related to their views of professional science. Second, helping students to draw such relationships may depend upon an explicitly epistemic discourse in the classroom, centered on what students know and how they know it, and that connects their work to professional science. Technology can support such a discourse by helping students to generate artifacts from their inquiry structured to highlight epistemic issues. These epistemic tools should represent important epistemic forms of scientific knowledge that link to practices for making them. Most importantly, research on epistemological development must link students’ practices of inquiry to their expressed beliefs about professional science.
Response of global upper ocean temperature to changing solar irradiance

By focusing on time sequences of basin-average and global-average upper ocean temperature (i.e., from 40oS to 60oN) we find temperatures responding to changing solar irradiance in three separate frequency bands with periods of >100 years, 18-25 years, and 9-13 years. Moreover, we find them in two different data sets, that is, surface marine weather observations from 1990 to 1991 and bathythermograph (BT) upper ocean temperature profiles from 1955 to 1994. Band-passing basin-average temperature records find each frequency component in phase across the Indian, Pacific, and Atlantic Oceans, yielding global-average records with maximum amplitudes of 0.04 o _+ 0.01oK and 0.07 o _+ 0.01oK on decadal and interdecadal scales, respectively. These achieve maximum correlation with solar irradiance records (i.e., with maximum amplitude 0.5 W m -2 at the top of the atmosphere) at phase lags ranging from 30 o to 50 o. From the BT data set, solar signals in global-average temperature penetrate to 80-160 m, confined to the upper layer above the main pycnocline. Operating a global-average heat budget for the upper ocean yields sea surface temperature responses of 0.01o-0.03oK and 0.02o-0.05oK on decadal and interdecadal scales, respectively, from the 0.1 W m -2 penetration of solar irradiance to the sea surface. Since this is of the same order as that observed (i.e., 0.04o-0.07oK), we can infer that anomalous heat from changing solar irradiance is stored in the upper layer of the ocean.
Effective Binaural Multi-Channel Processing Algorithm for Improved Environmental Presence

Binaural noise-reduction algorithms based on multi-channel Wiener filter (MWF) are promising techniques to be used in binaural assistive listening devices. The real-time implementation of the existing binaural MWF methods, however, involves challenges to increase the amount of noise reduction without imposing speech distortion, and at the same time preserving the binaural cues of both speech and noise components. Although significant efforts have been made in the literature, most developed methods so far have focused only on either the former or latter problem. This paper proposes an alternative binaural MWF algorithm that incorporates the non-stationarity of the signal components into the framework. The main objective is to design an algorithm that would be able to select the sources that are present in the environment. To achieve this, a modified speech presence probability (SPP) and a single-channel speech enhancement algorithm are utilized in the formulation. The resulting optimal filter also avoids the poor estimation of the second-order clean speech statistics, which is normally done by simple subtraction. Theoretical analysis and performance evaluation using realistic recorded data shows the advantage of the proposed method over the reference MWF solution in terms of the binaural cues preservation, as well as the noise reduction and speech distortion.
PEG Induces High Expression of the Cell Cycle Checkpoint Gene WEE1 in Embryogenic Callus of Medicago truncatula: Potential Link between Cell Cycle Checkpoint Regulation and Osmotic Stress

Polyethylene glycol (PEG) can be used to mimic osmotic stress in plant tissue cultures to study mechanisms of tolerance. The aim of this experiment was to investigate the effects of PEG (M.W. 6000) on embryogenic callus of Medicago truncatula. Leaf explants were cultured on MS medium with 2 mg L-1 NAA and 0.5 mg L-1 BAP for 5 months. Then, calli were transferred to the same medium further supplemented with 10% (w/v) 6000 PEG for 6 months in order to study physiological and putative molecular markers of water stress. There were no significant differences in growth rate of callus or mitotic index ± PEG although embryogenic potential of PEG treated callus was morphologically enhanced. Cells were rounder on PEG medium and cell size, nuclear size and endoreduplication increased in response to the PEG treatment. Significant increases in soluble sugar and proline accumulation occurred under PEG treatment compared with the control. Significantly, high MtWEE1 and MtCCS52 expression resulted from 6 months of PEG treatment with no significant differences in MtSERK1 or MtP5CS expression but down regulation of MtSOS expression. The results are consistent in showing elevated expression of a cell cycle checkpoint gene, WEE1. It is likely that the cell cycle checkpoint surveillance machinery, that would include WEE1 expression, is ameliorating the effects of the stress imposed by PEG.
Chemoprevention of colon carcinogenesis by dietary curcumin, a naturally occurring plant phenolic compound.

Human epidemiological and laboratory animal model studies have suggested that nonsteroidal antiinflammatory drugs reduce the risk of development of colon cancer and that the inhibition of colon carcinogenesis is mediated through the alteration in cyclooxygenase metabolism of arachidonic acid. Curcumin, which is a naturally occurring compound, is present in turmeric, possesses both antiinflammatory and antioxidant properties, and has been tested for its chemopreventive properties in skin and forestomach carcinogenesis. The present study was designed to investigate the chemopreventive action of dietary curcumin on azoxymethane-induced colon carcinogenesis and also the modulating effect of this agent on the colonic mucosal and tumor phospholipase A2, phospholipase C gamma 1, lipoxygenase, and cyclooxygenase activities in male F344 rats. At 5 weeks of age, groups of animals were fed the control (modified AIN-76A) diet or a diet containing 2000 ppm of curcumin. At 7 weeks of age, all animals, except those in the vehicle (normal saline)-treated groups, were given two weekly s.c. injections of azoxymethane at a dose rate of 15 mg/kg body weight. All groups were continued on their respective dietary regimen until the termination of the experiment at 52 weeks after the carcinogen treatment. Colonic tumors were evaluated histopathologically. Colonic mucosa and tumors were analyzed for phospholipase A2, phospholipase C gamma 1, ex vivo prostaglandin (PG) E2, cyclooxygenase, and lipoxygenase activities. The results indicate that dietary administration of curcumin significantly inhibited incidence of colon adenocarcinomas (P < 0.004) and the multiplicity of invasive (P < 0.015), noninvasive (P < 0.01), and total (invasive plus noninvasive) adenocarcinomas (P < 0.001). Dietary curcumin also significantly suppressed the colon tumor volume by > 57% compared to the control diet. Animals fed the curcumin diet showed decreased activities of colonic mucosal and tumor phospholipase A2 (50%) and phospholipase C gamma 1 (40%) and levels of PGE2 (> 38%). The formation of prostaglandins such as PGE2, PGF2 alpha, PGD2, 6-keto PGF1 alpha, and thromboxane B2 through the cyclooxygenase system and production of 5(S)-, 8(S)-, 12(S)-, and 15(S)-hydroxyeicosatetraenoic acids via the lipoxygenase pathway from arachidonic acid were reduced in colonic mucosa and tumors of animals fed the curcumin diet as compared to control diet. Although the precise mechanism by which curcumin inhibits colon tumorigenesis remains to be elucidated, it is likely that the chemopreventive action, at least in part, may be related to the modulation of arachidonic acid metabolism.
Increased carbon dioxide absorption during retroperitoneal laparoscopy.

BACKGROUND Retroperitoneoscopy for renal surgery is now a common procedure. We compared carbon dioxide absorption in patients undergoing retroperitoneoscopy for adrenal or renal surgery with that of patients undergoing laparoscopic cholecystectomy. METHODS We measured carbon dioxide elimination with a metabolic monitor in 30 anaesthetized patients with controlled ventilation, undergoing retroperitoneoscopy (n=10), laparoscopy (n=10) or orthopaedic surgery (n=10). RESULTS Carbon dioxide production increased by 38, 46 and 63% at 30, 60 and 90 min after insufflation (P<0.01) in patients having retroperitoneoscopy. Carbon dioxide production (mean (SD)) increased from 92 (21) to 150 (43) ml x min(-1) m(-2) 60-90 min after insufflation and remained increased after the end of insufflation. During laparoscopy, V(.)(CO(2)) increased less (by 15%) (P<0.05 compared with retroperitoneoscopy) and remained steady throughout the procedure. CONCLUSION Retroperitoneal carbon dioxide insufflation causes more carbon dioxide absorption than intraperitoneal insufflation, and controlled ventilation should be increased if hypercapnia should be avoided.