Miracle-dz/UniFAR-FTUs huggingface dataset:
On the reconfigurability of single-hub WDM ring networks

We study the benefit of reconfigurability for wavelength division multiplexed (WDM) ring networks with dynamic single-hubbed traffic. We showthat the ability to reconfigure wavelength add-drop multiplexers helps to reduce the number of expensive line terminating equipment (LTEs) by a factor of W, where W is the number of wavelengths in the network. In addition, we show that for a general class of traffic, optical networks using reconfigurable wavelength add-drop multiplexers guarantee to be almost as bandwidth efficient as full wavelength add-drop networks, that is, opaque networks. For such traffic, we introduce several fast algorithms that achieve or approximate the optimal performance guarantees. The comparison between reconfigurable networks and opaque networks is quantified using a performance metric called capacity ratio, which captures the relative throughput performance of a reconfigurable network compared to the opaque network.
The Influence of Total Plasma Homocysteine and Traditional Atherosclerotic Risk Factors on Degree of Abdominal Aortic Aneurysm Tissue Inflammation

Objective: Modulating effects of genetic and environmental risk factors on severity of human abdominal aortic aneurysm (AAA) tissue inflammation remain unclear. We investigated the influence of total plasma homocysteine (tHcy) and traditional atherosclerotic risk factors (ARF) on degree of AAA tissue inflammation. Methods: Aneurysm specimens were obtained from 89 male patients aged 52 to 83 years, underwent asymptomatic not ruptured AAA (mean diameter 5.5 cm) open repair and graded for degree of histologic inflammation. Multivariate analysis was used to determine the association of tHcy and ARF, with degree of inflammation. Results: Current cigarette smoking, odds ratio (OR) 4.4, 95% confidence interval 1.3 to 15.2, P = . 01 and no other ARF, neither tHcy levels OR 0.9 (0.9-1.02), P = . 2 were associated with high-grade tissue inflammation. Conclusion: These results provide evidence against a major effect of tHcy levels on AAA tissue inflammation, while current cigarette smoking is a significant modulating factor.
Analysis of packet networks having contention-based reservation with application to GPRS

In this paper, we develop a model to quantify the performance of message transmission systems in which users must reserve transmission resources via a contention mechanism prior to transmission. Our work is motivated by a desire to understand the performance characteristics of systems such as the General Packet Radio Service (GPRS), where the single forward link of the wireless access system is organized as a sequence of frames, each of which has first a contention period and then a service period. There are a fixed number of fixed-length contention slots in each contention period. Each contending customer chooses the slot in which he will contend at random, and success is determined by a capture model. A contender who fails waits for the next contention period, then again chooses the slot in which he will contend at random; this process is repeated until the contender is successful. Customers who have contended successfully are served during the service period, which has a prescribed number of fixed-length slots, on a first-come-first-serve (FCFS) basis, with the required number of service units being drawn independently from a general discrete distribution having finite support. We model the system as a Markov renewal process embedded at service departure times. We solve the model and then compute the equilibrium distributions of the number of customers in the system at arbitrary points in time and at customer arrival epochs. Finally, we give a numerical example in which we demonstrate the usefulness of our results in understanding the behavior of GPRS.
Maximum lifetime routing in wireless sensor networks

A routing problem in static wireless ad hoc networks is considered as it arises in a rapidly deployed, sensor based, monitoring system known as the wireless sensor network. Information obtained by the monitoring nodes needs to be routed to a set of designated gateway nodes. In these networks, every node is capable of sensing, data processing, and communication, and operates on its limited amount of battery energy consumed mostly in transmission and reception at its radio transceiver. If we assume that the transmitter power level can be adjusted to use the minimum energy required to reach the intended next hop receiver then the energy consumption rate per unit information transmission depends on the choice of the next hop node, i.e., the routing decision. We formulate the routing problem as a linear programming problem, where the objective is to maximize the network lifetime, which is equivalent to the time until the network partition due to battery outage. Two different models are considered for the information-generation processes. One assumes constant rates and the other assumes an arbitrary process. A shortest cost path routing algorithm is proposed which uses link costs that reflect both the communication energy consumption rates and the residual energy levels at the two end nodes. The algorithm is amenable to distributed implementation. Simulation results with both information-generation process models show that the proposed algorithm can achieve network lifetime that is very close to the optimal network lifetime obtained by solving the linear programming problem.
Proteomic Analysis of Rickettsia parkeri Strain Portsmouth

ABSTRACT Rickettsia parkeri, a recently recognized pathogen of human, is one of several Rickettsia spp. in the United States that causes a spotted fever rickettsiosis. To gain insights into its biology and pathogenesis, we applied the proteomics approach to establish a two-dimensional gel proteome reference map and combined this technique with cell surface biotinylation to identify surface-exposed proteins of a low-passage isolate of R. parkeri obtained from a patient. We identified 91 proteins by matrix-assisted laser desorption ionization-tandem time of flight mass spectrometry. Of these, 28 were characterized as surface proteins, including virulence-related proteins (e.g., outer membrane protein A [OmpA], OmpB, β-peptide, and RickA). Two-dimensional immunoblotting with serum from the R. parkeri-infected index patient was utilized to identify the immunoreactive proteins as potential targets for diagnosis and vaccine development. In addition to the known rickettsial antigens, OmpA and OmpB, we identified translation initiation factor 2, cell division protein FtsZ, and cysteinyl-tRNA synthetase as immunoreactive proteins. The proteome map with corresponding cell surface protein analysis and antigen detection will facilitate a better understanding of the mechanisms of rickettsial pathogenesis.
MyD88-Dependent Signaling Protects against Anthrax Lethal Toxin-Induced Impairment of Intestinal Barrier Function

ABSTRACT MyD88-deficient mice were previously shown to have increased susceptibility to Bacillus anthracis infection relative to wild-type animals. To determine the mechanism by which MyD88 protects against B. anthracis infection, knockout mice were challenged with nonencapsulated, toxigenic B. anthracis or with anthrax toxins. MyD88-deficient mice had increased susceptibility to B. anthracis and anthrax lethal toxin but not to edema toxin. Lethal toxin alone induced marked multifocal intestinal ulcers in the knockout animals, compromising the intestinal epithelial barrier. The resulting enteric bacterial leakage in the knockout animals led to peritonitis and septicemia. Focal ulcers and erosion were also found in MyD88-heterozygous control mice but with far lower incidence and severity. B. anthracis infection also induced a similar enteric bacterial septicemia in MyD88-deficient mice but not in heterozygous controls. We show that lethal toxin and B. anthracis challenge induce bacteremia as a result of intestinal damage in MyD88-deficient mice. These results suggest that loss of the intestinal epithelial barrier and enteric bacterial septicemia may contribute to sensitizing MyD88-deficient mice to B. anthracis and that MyD88 plays a protective role against lethal toxin-induced impairment of intestinal barrier.
Learning-Based Uplink Interference Management in 4G LTE Cellular Systems

LTE's uplink (UL) efficiency critically depends on how the interference across different cells is controlled. The unique characteristics of LTE's modulation and UL resource assignment poses considerable challenges in achieving this goal because most LTE deployments have 1:1 frequency reuse, and the uplink interference can vary considerably across successive time-slots. In this paper, we propose LeAP, a measurement data-driven machine learning paradigm for power control to manage uplink interference in LTE. The data-driven approach has the inherent advantage that the solution adapts based on network traffic, propagation, and network topology, which is increasingly heterogeneous with multiple cell-overlays. LeAP system design consists of the following components: 1) design of user equipment (UE) measurement statistics that are succinct, yet expressive enough to capture the network dynamics, and 2) design of two learning-based algorithms that use the reported measurements to set the power control parameters and optimize the network performance. LeAP is standards-compliant and can be implemented in a centralized self-organized networking (SON) server resource (cloud). We perform extensive evaluations using radio network plans from a real LTE network operational in a major metro area in the US. Our results show that, compared to existing approaches, LeAP provides 4.9× gain in the 20th percentile of user data rate, 3.25× gain in median data rate.
MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

ABSTRACT Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity.
Increased plasma levels of interleukin-6 and interleukin-8 in β-thalassaemia major

Several immunological defects can be found in patients with beta-thalassaemia, among which the impairment of neurophil and macrophage phagocytic and killing functions and the production of some cytokines are the most important. It is known that interleukin-6 (IL-6) and interleukin-8 (IL-8) are important components of the pro-inflammatory response. The plasma levels of these cytokines may be relevant in the pathophysiology of beta-thalassaemia. To assess this hypothesis, the plasma IL-6 and IL-8 concentrations in patients with beta-thalassaemia, were investigated. Fourteen patients with thalassaemia major were studied by evaluating body iron status, iron supply for erythropoiesis, and plasma IL-6 and IL-8 levels, together with 12 age-matched healthy controls. The plasma levels of IL-6 and IL-8 were determined by enzyme-linked immunosorbent assay (ELISA). Patients with beta-thalassaemia were found to have higher IL-8 concentrations than normal controls (p < 0.001) and plasma IL-6 concentrations increased significantly in the beta-thalassaemic patients compared with control subjects (p = 0.01). Serum ferritin levels of beta-thalassaemic patients were significantly higher than those of control groups (p < 0.05). IL-8 levels correlated with ferritin levels (r = 0.694; p < 0.05) and the total number of transfusions (r = 0.64; p < 0.05). Plasma IL-6 levels in beta-thalassaemic patients did not correlate with any clinical, haematological or biochemical parameters. It was also found that plasma IL-8 levels in the patients who had blood transfusions over 100 times were significantly higher than those of under 100 times (p < 0.05), whereas there was no statistical difference for IL-6. Markedly increased plasma IL-6 and IL-8 levels were documented in patients with beta-thalassaemia. Increased production of IL-6 and IL-8 might have contributed to abnormalities in iron metabolism and it is probably due to overstimulation of macrophages. Before a clinical value can be ascribed to these changes in plasma cytokine levels in beta-thalassaemia, the follow-up samples of larger series of patients with 8-thalassaemia should be evaluated.
Learning styles of entry-level physiotherapy students

This research was conducted to identify the learning styles of Australian physiotherapy students. The subject sample consisted of 206 students from the entry-level physiotherapy programs (Bachelor of Science [Physiotherapy] and Master of Physiotherapy) at Curtin University of Technology. Subjects were recruited from the first and fourth year of the Bachelor of Science (BSc) (Physiotherapy) program and first and second year of the Master of Physiotherapy (MPhysio) program. Three subject groups included: (i) first-year BSc students, (ii) fourth-year BSc students, and (iii) MPhysio students. All subjects completed the Honey & Mumford Learning Style Questionnaire (LSQ) and were classified as having one or more learning styles. The most frequently preferred learning styles were Reflector (26%), followed by Reflector/Theorist (17.2%), then Activist (16.7%). There were no differences in the preferred learning style in the three groups, or between genders. Most physiotherapy students in the entry-level programs preferred a learning style in which they combine reviewing and thinking skills, rather than experiencing or planning skills. Based on the findings of this study, educators in entry-level programs need to develop learning experiences that will enhance students’ experiencing and planning skills.
Perfil lipídico aterogénico en niños con hipotiroidismo subclínico

Objetivo Evaluar el perfil lipidico en ninos con hipotiroidismo subclinico. Pacientes y metodos Se estudiaron 46 ninos de ambos sexos, en edades comprendidas entre 2 y 9 anos, 17 con hipotiroidismo subclinico (grupo de estudio) y 23 ninos sanos (grupo control). El hipotiroidismo subclinico se diagnostico cuando los niveles de tirotropina (TSH) fueron mayores de 4,65 μU/ml y los de tiroxina libre (T4L) fueron normales. Los ninos con hipotiroidismo subclinico se observaron por 4 meses sin intervencion alguna y se les tomo nueva muestra para TSH y T4L con el objeto de corroborar el diagnostico. Se les realizo una historia clinica completa y se les tomo muestra de sangre para lipidograma, que incluyo trigliceridos, colesterol total (CT), colesterol unido a las lipoproteinas de alta densidad (c-HDL) y el calculo del colesterol unido a las lipoproteinas de baja densidad (c-LDL); ademas se determinaron los anticuerpos antitiroglobulina (anti-TG) y antiperoxidasa (anti-TPO). Resultados De los 17 ninos que presentaron niveles sericos elevados de TSH al inicio, 7 (41,2 %) los normalizaron a los 4 meses, por lo que fueron excluidos. No se apreciaron diferencias significativas en cuanto a la edad, peso, talla e indice de masa corporal entre el grupo de estudio y el control. Los niveles de anticuerpos anti-TPO y anti-TG no fueron diferentes entre los grupos. El nivel plasmatico promedio de c-HDL fue significativamente mas bajo en los ninos con hipotiroidismo subclinico que en los controles (p Conclusion El hipotiroidismo subclinico puede ser una condicion transitoria en un porcentaje importante de ninos. Los ninos con hipotiroidismo subclinico presentan una disminucion significativa en los niveles de c-HDL, lo cual sugiere un patron lipidico aterogenico en esta entidad.
Crisis Debriefing Groups for Emergency Responders: Reviewing the Evidence

Rescue workers who are exposed to mutilated bodies, mass destruction, multiple casualties, and life threatening situations may become the hidden victims of disaster. In response to concerns about the mental health implications of exposure to work-related trauma in emergency service personnel, the crisis debriefing model has arisen as an early intervention strategy designed to mitigate stress reactions. Recently however, controversy has arisen about the efficacy of the crisis debriefing group model. Initial reports supporting the efficacy of crisis debriefing groups have relied on anecdotal evidence, client satisfaction surveys, and clinical impressions of group leaders. Subsequent research has suggested that the model fails to reduce and may in fact exacerbate symptoms of post-traumatic stress disorder (PTSD). This article reviews the crisis debriefing model as it has been applied to workers in various emergency fields and discusses the conflicting data surrounding efficacy. It concludes that there is some empirical support for the social support and psychoeducational components of the model. However, the component of the model that reviews graphic details of the event may increase intrusion symptoms through a process of vicarious traumatization.
Database Coverage and Impact Factor of Open Access Journals in Pharmacy

Open access (OA) publishing has recently generated considerable interest. One of the markers of success for conventionally published and OA journals is the impact factor (IF). These elements have not been concurrently assessed in pharmacy journals. Database coverage along with gratis OA status and corresponding IF were examined in an assembled list of 72 OA pharmacy journals. EMBASE provided the most coverage of OA pharmacy journals by a substantial margin (62.5%), followed by Science Citation Index Expanded (37.5%), MEDLINE (30.6%), and International Pharmaceutical Abstracts (27.8%). Twenty-seven journals were tracked for IF with varying database combinations necessary to identify them all.
Regulation of inflammation by collagen-binding integrins α1β1 and α2β1 in models of hypersensitivity and arthritis

Adhesive interactions play an important role in inflammation by promoting leukocyte attachment and extravasation from the vasculature into the peripheral tissues. However, the importance of adhesion molecules within the extracellular matrix-rich environment of peripheral tissues, in which cells must migrate and be activated, has not been well explored. We investigated the role of the major collagen-binding integrins, alpha1beta1 and alpha2beta1, in several in vivo models of inflammation. mAb's against murine alpha1 and alpha2 were found to significantly inhibit effector phase inflammatory responses in animal models of delayed-type hypersensitivity (DTH), contact hypersensitivity (CHS), and arthritis. Mice that were alpha1-deficient also showed decreased inflammatory responses in the CHS and arthritis models when compared with wild-type mice. Decreased leukocyte infiltration and edema formation accompanied inhibition of antigen-specific models of inflammation, as nonspecific inflammation induced by croton oil was not inhibited. This study demonstrates the importance in vivo of alpha1beta1 and alpha2beta1, the collagen-binding integrins, in inflammatory diseases. The study also extends the role of integrins in inflammation beyond leukocyte attachment and extravasation at the vascular endothelial interface, revealing the extracellular matrix environment of peripheral tissues as a new point of intervention for adhesion-based therapies.
Protease-Activated Receptor 2 Has Pivotal Roles in Cellular Mechanisms Involved in Experimental Periodontitis

ABSTRACT The tissue destruction seen in chronic periodontitis is commonly accepted to involve extensive upregulation of the host inflammatory response. Protease-activated receptor 2 (PAR-2)-null mice infected with Porphyromonas gingivalis did not display periodontal bone resorption in contrast to wild-type-infected and PAR-1-null-infected mice. Histological examination of tissues confirmed the lowered bone resorption in PAR-2-null mice and identified a substantial decrease in mast cells infiltrating the periodontal tissues of these mice. T cells from P. gingivalis-infected or immunized PAR-2-null mice proliferated less in response to antigen than those from wild-type animals. CD90 (Thy1.2) expression on CD4+ and CD8+ T-cell-receptor β (TCRβ) T cells was significantly (P < 0.001) decreased in antigen-immunized PAR-2-null mice compared to sham-immunized PAR-2-null mice; this was not observed in wild-type controls. T cells from infected or antigen-immunized PAR-2-null mice had a significantly different Th1/inflammatory cytokine profile from wild-type cells: in particular, gamma interferon, interleukins (interleukin-2, -3, and -17), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha demonstrated lower expression than wild-type controls. The absence of PAR-2 therefore appears to substantially decrease T-cell activation and the Th1/inflammatory response. Regulation of such proinflammatory mechanisms in T cells and mast cells by PAR-2 suggests a pivotal role in the pathogenesis of the disease.
Genetic Analysis of Neisseria meningitidis Sequence Type 7 Serogroup X Originating from Serogroup A

ABSTRACT Neisseria meningitidis causes meningococcal disease, often resulting in fulminant meningitis, sepsis, and death. Vaccination programs have been developed to prevent infection of this pathogen, but serogroup replacement is a problem. Capsular switching has been an important survival mechanism for N. meningitidis, allowing the organism to evolve in the present vaccine era. However, related mechanisms have not been completely elucidated. Genetic analysis of capsular switching between diverse serogroups would help further our understanding of this pathogen. In this study, we analyzed the genetic characteristics of the sequence type 7 (ST-7) serogroup X strain that was predicted to arise from ST-7 serogroup A at the genomic level. By comparing the genomic structures and sequences, ST-7 serogroup X was closest to ST-7 serogroup A, whereas eight probable recombination regions, including the capsular gene locus, were identified. This indicated that serogroup X originated from serogroup A by recombination leading to capsular switching. The recombination involved approximately 8,540 bp from the end of the ctrC gene to the middle of the galE gene. There were more recombination regions and strain-specific single-nucleotide polymorphisms in serogroup X than in serogroup A genomes. However, no specific gene was found for each serogroup except those in the capsule gene locus.