Miracle-dz/UniFAR-FTUs huggingface dataset:
FDTD Methods for 3-D Room Acoustics Simulation With High-Order Accuracy in Space and Time

Time-domain finite difference (FDTD) methods are popular tools for three-dimensional (3-D) room acoustics modeling, but numerical dispersion is an inherent problem that can place limitations on the usable bandwidth of a given scheme. Compact explicit 27-point schemes and “large-star” schemes with high-order spatial differences offer improvements to the simplest scheme, but are ultimately limited by their second-order accuracy in time. In this paper, we use modified equation methods to derive FDTD schemes with high orders of accuracy in both space and time, resulting in significant improvements in numerical dispersion as compared to the aforementioned schemes. In comparison to such schemes, the high-order accurate schemes presented in this paper use significantly less memory and fewer operations when low error tolerances in numerical phase velocities are critical, leading to higher usable bandwidths for auralization purposes. Simulation results are also presented, demonstrating improved approximations to modal frequencies of a shoe-box room and free-space propagation of a bandlimited pulse.
Dynamic compression influences interleukin-1beta-induced nitric oxide and prostaglandin E2 release by articular chondrocytes via alterations in iNOS and COX-2 expression.

Interleukin-1beta (IL-1beta) induces the release of nitric oxide (.NO) and prostaglandin E2 (PGE2) by chondrocytes and this effect can be reversed with the application of dynamic compression. Previous studies have indicated that integrins may play a role. In addition, IL-1beta upregulates the expression of iNOS and COX-2 mRNA via upstream activation of p38 MAPK. The current study examines the involvement of these pathways in mediating . NO and PGE2 release in IL-1beta stimulated bovine chondrocytes subjected to dynamic compression. Bovine chondrocytes were seeded in agarose constructs and cultured with 0 or 10 ng.ml(-1) IL-1beta with or without the application of 15% dynamic compressive strain at 1 Hz. Selected inhibitors were used to interrogate the role of alpha5beta1 integrin signalling and p38 MAPK activation in mediating the release of . NO and PGE2 in response to both IL-1beta and dynamic compression. The relative expression levels of iNOS and COX-2 were assessed using real-time quantitative PCR. Nitrite, a stable end product of . NO, was measured using the Griess assay and PGE2 release was measured using an enzyme immunoassay. IL-1beta enhanced . NO and PGE2 release and this effect was reversed by the application of dynamic compression. Co-incubation with an integrin binding peptide (GRGDSP) abolished the compression-induced effect. Real-time quantitative PCR analysis revealed that IL-1beta enhanced iNOS and COX-2 mRNA levels, with the maximum expression at 6 or 12 hours. Dynamic compression reduced this effect via a p38 MAPK sensitive pathway. These results suggest that dynamic compression acts to abrogate of . NO and PGE2 release by directly influencing the expression levels of iNOS and COX-2.
Uptake of pp65 in in vitro Generated pp65-Positive Polymorphonuclear Cells Mediated by Phagocytosis and Cell Fusion?

Objective: The cytomegalovirus (CMV) antigenemia consists of the detection of CMV pp65 in the nucleus of polymorphonuclear granulocytes (PMN), but it is unclear where and how PMN pick up virus particles or proteins. In an in vitro model for CMV antigenemia we investigated the mechanism of pp65 uptake by PMN that results in its expression in the nucleus. Methods: A series of inhibitors of different mechanisms was used to study the uptake of pp65 by PMN during coculture with CMV-infected endothelial cells and we performed a morphological analysis by light and transmission electron microscopy. Results: Nocodazole and cytochalasin B inhibited uptake of pp65 by PMN with 59.4 ± 14.1 and 73.3 ± 12.7%, respectively. The presence of anti-CMV hyperimmune globulin or lactoferrin during coculture reduced the number of pp65-positive PMN with 45.8 ± 7.0 or 40.6 ± 3.2%. Furthermore, a small number of the pp65-positive PMN obtained after coculture had fused to large cells with multilobed nuclei. PMN were observed that enclosed viral particles as well as free viral particles containing PMN in the cytoplasm. Conclusion: Fusion of viral particles with PMN and phagocytosis are both involved in the uptake of pp65.
Inhibition of polyamine synthesis alters hair follicle function and fiber composition.

The activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, two of the enzymes involved in the synthesis of the polyamines, were found to be high in follicle-rich homogenates of sheep skin, and to be responsive to the nutrition of the animal. Systemic provision of the inhibitor of ornithine decarboxylase, alpha difluoromethylornithine, markedly altered the length, diameter, and composition of the fiber, the last being accompanied by an increase in the proportion of the fiber occupied by paracortical cells and an increase in the level of mRNA encoding a cysteine-rich family of keratin proteins. The growth of wool follicles cultured in media containing alpha-difluoromethylornithine was not inhibited, even at high concentrations. In contrast, low concentrations of methylglyoxal (bis)guanylhydrazone, the inhibitor of S-adenosylmethionine decarboxylase, completely inhibited fiber growth in culture follicles. Addition of spermidine to the media overcame this inhibition but spermine had no effect. Further evidence that spermine is not required for normal follicle function was provided by incubating follicles with the specific inhibitor of spermine synthase, n-butyl-1,3-diaminopropane. This inhibitor, even at high concentrations, had no effect on fiber growth in vitro. Spermidine partially overcame the growth depression that occurred in follicles cultured in methionine-deficient media, suggesting that part of the requirement for methionine is for spermidine synthesis in the follicle. These investigations provide strong evidence that the polyamines in general , and spermidine in particular, play a major role in hair growth.
Small-Fiber Neuropathy Is Associated With Corneal Nerve and Dendritic Cell Alterations: An In Vivo Confocal Microscopy Study

Purpose: In patients with small-fiber neuropathy (SFN), noninvasive diagnostic tests that allow accurate monitoring of disease progression are urgently needed. The aim of this study was to assess corneal trigeminal small sensory nerves and immune cells by in vivo corneal confocal microscopy (CCM) in SFN. Methods: In this prospective single-center study, 14 patients with histologically confirmed SFN were analyzed. CCM parameters [corneal nerve fiber density (NFD); the total number of nerves, main trunks, and branches; nerve tortuosity; and dendritic cell density] were compared with 14 age-matched healthy controls and correlated with clinical symptoms, disease course, and histopathological findings. Results: Corneal NFD (15,489.3 ± 5927.6 &mgr;m/mm2 vs. 22,687.1 ± 4328.7 &mgr;m/mm2; P = 0.001) and the total number of nerves (10.4 ± 4.6/frame vs. 18.5 ± 4.8/frame; P < 0.0001) were significantly reduced in patients with SFN. In contrast, nerve tortuosity was significantly increased (2.2 ± 0.3 vs. 1.7 ± 0.5; P = 0.02). Corneal NFD did not correlate with intraepidermal NFD (&rgr; = −0.158; P = 0.5) or clinical symptoms (cold P = 0.1; prickling P = 0.2; burning P = 0.8; formication P = 0.7; stabbing P = 0.4; rubbing 0.1; pressure P = 0.1). The average dendritic cell density was increased in SFN (33.5 ± 57.5 cells/mm2 vs. 16.1 ± 13.7 cells/mm2) but did not reach significance (P = 0.7). Conclusions: CCM provides parameters that reliably indicate injury to sensory afferents of the trigeminal nerve in patients with SFN. Our data suggest that CCM may serve both as a noninvasive diagnostic test and as a surrogate marker in SFN.
The empirical research of the relationship between product market competition and surplus information

Ensuring the quality of the information disclosure of the company and itself, which could help investors know the real value of the company, is the necessary premise to help protect the interests of them and the securities market of the rational allocation of resources. This study focus on the emerging market and the research object is China's ashare listed companies. This study mainly discusses the influence of product market competition on the quality of the surplus information from the perspective of industrial organization theory. This paper tried to expand the company's financial theory field to the accounting information theory from the subject basis of the industrial organization theory, further deepening the explanation of surplus information quality. Through this paper we found that (1) Concentration degree of the industry is higher, the company's surplus information quality is worse. (2) There is a certain positive relationship between industry homogeneity and company surplus information quality, industry homogeneity is higher, the better the quality of surplus information company. (3) In a given industry concentration degree of cases, industry homogeneity has positive effect on the surplus information quality. Industry homogeneity will help alleviate the industry concentration and have a negative impact on surplus information quality.
Complete focal adhesion kinase deficiency in the mammary gland causes ductal dilation and aberrant branching morphogenesis through defects in Rho kinase‐dependent cell contractility

The adult, virgin mammary gland is a highly organized branched ductal network comprising two major cell types: myoepithelial and luminal epithelial cells. To study the role and mechanism of focal adhesion kinase (FAK)‐mediated signaling in mammary gland development and differentiation, we used a conditional Fak‐knockout mammary epithelial cell (MEC) transplantation model. Conditional Cre recombinase (Cre)‐mediated Fak deletion in primary cultured MECs isolated from FAKlox/lox/Rosa26Cre‐ERT2 donor mice caused loss of FAK in all mammary cells. Transplantation of Fak‐knockout MECs in a cleared mammary fat pad of immunedeficient recipient mice resulted in development of new but dilated virgin ducts with a disrupted myoepithelial and luminal epithelial cell multilayer and aberrant ductal morphogenesis during pregnancy. In the absence of FAK, MECs spread poorly, showed enhanced Rho kinase (ROCK)‐mediated cytoskeletal contractility, and failed to respond to receptor‐mediated cytoskeletal remodeling. Likewise, FAK deficiency fully inhibited branching morphogenesis of mammary gland organoids in a ROCK‐dependent manner. Altogether these data suggest a model in which FAK coordinates contractile forces in MECs to maintain the bilayered cellular organization of myoepithelial and luminal epithelial cells in ducts, thus allowing proper mammary gland development and function. —Van Miltenburg, M. H. A. M. , Lalai, R. , de Bont, H. , van Waaij, E. , Beggs, H. , Danen, E. H. J., van de Water, B. Complete focal adhesion kinase deficiency in the mammary gland causes ductal dilation and aberrant branching morphogenesis through defects in Rho kinase‐dependent cell contractility. FASEB J. 23, 3482–3493 (2009). www.fasebj. org
Enhancement of anti‐tumor immunity by tumor cells transfected with the secondary lymphoid tissue chemokine EBI‐1‐ligand chemokine and stromal cell–derived factor‐1αchemokine genes

Several new lymphocyte‐specific chemokines, which attract naive and memory T cells, B cells, dendritic cells and natural killer cells, have been isolated. We have found evidence of the anti‐tumor effects of 3 major lymphocyte‐specific chemokines, secondary lymphoid tissue chemokine (SLC), EBI‐1‐ligand chemokine (ELC) and stromal cell–derived factor (SDF)‐1α, in murine models (Meth A fibrosarcoma and HM‐1 ovarian tumor). In both naive and immunized mice, tumors expressing SLC, ELC or SDF‐1α showed delayed progression compared with control tumors. In mice immunized with tumor cells expressing 1 of these 3 chemokine genes, challenge with parental tumor cells resulted in slightly slower progression than in control mice, while in mice immunized with tumor cells transfected to co‐express IL‐2 or granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) as well as these chemokines, all tumors regressed. Furthermore, spleen cells from mice immunized with these “double‐transfected” tumor cells exhibited higher proliferative responses and greater cytotoxic activity against parental tumor cells. These anti‐tumor effects were associated with profound alterations in the leukocyte populations within the tumors and regional lymph nodes, and this was due to activation of type I T cell‐dependent responses that produced high levels of IFN‐γ. These findings show that SLC, ELC and SDF‐1α enhance anti‐tumor immunity both systemically and locally and that these chemokines may be clinically useful, especially when combined with IL‐2 and GM‐CSF. © 2001 Wiley‐Liss, Inc.
Disparities in treatment and outcome for renal cell cancer among older black and white patients.

PURPOSE Black patients with renal cell cancer have shorter survival compared with their white counterparts, but the causes for this disparity are unclear. To elucidate reasons for this inequality, we examined differences in treatment and survival between black and white patients. PATIENTS AND METHODS A retrospective cohort study was conducted using data from the linked Surveillance, Epidemiology and End Results (SEER) cancer registry and Medicare databases. Participants included 964 black and 10,482 white patients age >or= 65 years who were enrolled into Medicare and diagnosed with renal cell cancer between 1986 and 1999. Information on surgical treatment was ascertained from both databases, whereas data regarding coexisting illness and survival was obtained from the Medicare database. RESULTS The percentage of black patients receiving nephrectomy treatment was significantly lower compared with whites (61.2% v 70.4%; P < .0001). After adjustment for age, sex, median income, cancer stage, tumor size, and comorbidity index, blacks were less likely to undergo nephrectomy treatment compared with whites (risk ratio = 0.93; 95% CI, 0.90 to 0.96). Overall survival was worse for blacks than whites even after adjustment for demographic and cancer prognostic factors (hazard ratio [HR] = 1.16; 95% CI, 1.07 to 1.25); however, additional adjustment for comorbidity index and nephrectomy treatment reduced the disparity substantially (HR = 1.00; 95% CI, 0.93 to 1.09). CONCLUSION This study indicates that the lower survival rate among blacks compared with whites with renal cell cancer can be explained largely by the increased number of comorbid health conditions and the lower rate of surgical treatment among black patients.
Using gender research in development.

This book is designed for technical personnel and policymakers in national government and international agencies and nongovernmental organizations (NGOs) as well as other development practitioners who face the task of addressing gender issues in development projects and policy. Practitioners may ask why they should address gender issues in development. First and foremost gender equality is a basic human right--with value in and of itself. Second many disparities in development outcomes arise from gender differences. Third the task of addressing gender inequality is made even more urgent by the reality of its significant effects on the efficiency and welfare outcomes of project or policy interventions. Gender issues are central to the attainment of development goals and poverty reduction. They play a prominent role in the United Nations Millennium Development Goals (MDGs) which have been commonly accepted as a framework for measuring development progress. Of the eight goals four are directly related to gender: achieving universal primary education promoting gender equality and the empowerment of women reducing infant and child mortality and improving maternal health. Gender also plays an important role in goals related to reducing poverty and eradicating hunger; combating HIV/AIDS malaria and other diseases; and ensuring environmental sustainability. Given these linkages it is difficult to see how it would be possible to meet the MDGs without addressing gender. (excerpt)
Twitch interpolation of the elbow flexor muscles at high forces

We investigated factors affecting maximal voluntary torque and the assessment of the level of voluntary drive in the elbow flexor muscles. First, the effective compliance of the system was tested by using single, paired, and trains of four stimuli to measure voluntary activation. At high voluntary torques the responses to all these stimuli were identical, suggesting that single stimuli are adequate for estimating voluntary drive. Second, the contribution of torque from synergist elbow flexor muscles was assessed. In attempted maximal voluntary contractions (MVCs), the voluntary activation of brachioradialis (median 91.5%, range 68.9–100%) was lower than for biceps brachii (median 99.1%, range 78.5–100%; P < 0.01). This suggests extra torque may be generated by brachioradialis during elbow flexion, beyond the torque where biceps brachii is maximally activated. Finally, lengthening of the elbow flexors occurred during MVCs, due to slight shoulder movements. This would allow force to increase independently of an increase in voluntary drive. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:318–328, 1998.
Menopause, but not age, is an independent risk factor for fasting plasma glucose levels in nondiabetic women

Objective:Glucose metabolism is influenced by various genetic and environmental factors. In women the prevalence of abnormal glucose metabolism is known to increase around and after age 50. The aim of this study was to determine whether menopause augments fasting plasma glucose (FPG) levels in women. Design:Of 672 Japanese women who underwent health examinations, we studied 505 nondiabetic participants who had no history of hysterectomy and had never used estrogens or progestins. All participants were administered an oral glucose tolerance test, and their blood measurements and information about their menopause status were obtained. Results:Of these 505 women, 208 were premenopausal and 297 were postmenopausal. Age, body mass index, triglycerides level, total cholesterol level, low-density lipoprotein cholesterol level, blood pressure, and homeostasis model assessment insulin sensitivity index rose across quintiles of FPG levels, whereas high-density lipoprotein cholesterol level and homeostasis model assessment pancreatic &bgr;-cell function index did not. The number of premenopausal women declined and the number of postmenopausal women increased across quintiles of FPG levels. Univariate regression analysis demonstrated that age, body mass index, triglycerides level, low-density lipoprotein cholesterol level, and menopause status were associated with FPG level, whereas high-density lipoprotein cholesterol level was not. Stepwise multivariate regression analysis showed that the independent risk factors for elevated FPG levels were body mass index, menopause, and triglycerides level, whereas age and low-density lipoprotein cholesterol level did not contribute to FPG levels. Conclusions:Menopause, but not age, is directly involved in augmented FPG levels in nondiabetic women.
Demonstration of Blind Quantum Computing

Quantum Blindness While quantum computers offer speed advantages over their classical counterparts, the technological challenges facing their eventual realization suggest that they will need to be located in specialized facilities. Thus, interaction would then need to be on a quantum client:quantum server basis. Barz et al. (p. 303; see the Perspective by Vedral) implemented a proof-of-principle protocol that illustrates complete security in such a setup—for both the client and the server. In this blind quantum computing protocol, the client maintains the security of their data and the specifics of the calculation they want to perform, and the server cannot access the data or calculation of the client. A protocol is implemented that can ensure secure client-server interactions on a quantum computer architecture. Quantum computers, besides offering substantial computational speedups, are also expected to preserve the privacy of a computation. We present an experimental demonstration of blind quantum computing in which the input, computation, and output all remain unknown to the computer. We exploit the conceptual framework of measurement-based quantum computation that enables a client to delegate a computation to a quantum server. Various blind delegated computations, including one- and two-qubit gates and the Deutsch and Grover quantum algorithms, are demonstrated. The client only needs to be able to prepare and transmit individual photonic qubits. Our demonstration is crucial for unconditionally secure quantum cloud computing and might become a key ingredient for real-life applications, especially when considering the challenges of making powerful quantum computers widely available.
Use of the Perceived Physical Competence Scale with Adolescents with Disabilities

The construct validity and reliability of the 1987 Perceived Physical Competence Scale of Lintunen were examined to assess the applicability of the instrument for use with adolescents with disabilities. Subjects were 51 girls and 34 boys (M age = 15.1 yr.) from several schools in central Finland. Principal component factor analysis with varimax rotation yielded the same two factors for adolescents with disabilities as reported for nondisabled adolescents in the related literature. Cronbach alphas for the two factors were . 89 and . 56. It was concluded that the scale is an appropriate measure for adolescents with disabilities. Statistical analysis indicated no gender differences for adolescents with disabilities. When compared with nondisabled groups in the related literature, these adolescents had perceived fitness similar to nondisabled peers but significantly lower than that of athletes without disabilities.
Activation of sPLA2‐IIA and PGE2 production by high mobility group protein B1 in vascular smooth muscle cells sensitized by IL‐1β

Lipid mediators such as prostaglandin E2 (PGE2) play a central role during atherogenesis as a consequence of inflammation. PGE2 is produced from phospholipids by a cascade of enzymatic reactions involving phospholipase A2 (PLA2), cyclooxygenase (COX), and prostaglandin E synthase (PGES). It is released by several cell types, including vascular smooth muscle cells (VSMCs). Recent work has shown that the secretory PLA2‐IIA (sPLA2‐IIA), the most abundant isoform of secreted PLA2 in VSMCs, acts as a potent cytokine and activates VSMCs through a positive feedback loop. High mobility group protein 1 (HMGB1), also known as amphoterin, is a ubiquitous protein that plays various roles in the nucleus. HMGB1 is released by necrotic cells and by immune cells in response to various inflammatory mediators and acts as a potent proinflammatory cytokine. The present study investigates the role of HMGB1 in the activation of sPLA2‐IIA expression and PGE2 production in VSMCs. Recombinant HMGB1 slightly activated the sPLA2‐IIA, COX‐2, and mPGES‐1 genes but dramatically stimulated these genes in VSMCs that had been incubated with the proinflammatory cytokine IL‐1β for 24 h. This effect was accompanied by significantly increased PGE2 release. Induction of the three known receptors of HMGB1, namely RAGE, TLR‐2, and TLR‐4, by IL‐1β suggests that proinflammatory cytokines sensitize VSMCs to HMGB1. This provides new insights into the role of HMGB1 in VSMCs, suggesting it may be essential for the progression of atherosclerosis. —Jaulmes, A. , Thierry, S. , Janvier, B. , Raymondjean, M. , Maréchal, V. Activation of sPLA2‐IIA and PGE2 production by high mobility group protein B1 in vascular smooth muscle cells sensitized by interleukin (IL)‐1β. FASEB J. 20, E1086–E1093 (2006)