Miracle-dz/UniFAR-FTUs huggingface dataset:
Hierarchical Voronoi diagram-based path planning among polygonal obstacles for 3D virtual worlds

Path planning is one of important problems in virtual reality, computational geometry, robotic and GIS. This paper presents two methods of computing walkthrough paths in a polygon with h holes and a total of n vertices, for 3D virtual worlds such as virtual museums and games. For any two points s and t, one method is presented to compute the shortest Voronoi skeleton path SVSP(s,t) in O(k + hlogh + logn) time, where k is the number of the Voronoi edges in SVSP(s,t) and O(k) ≤ O(n). An approximate shortest path from s to t can be computed in O(k + hlogh + logn) time based on SVSP(s,t). The other is to compute the shortest path SP(s,t) in O(m + hlog(n/h) + h2 logh) time, where m is the number of the edges in SP(s,t) and m ≤ n. They are based on a hierarchical Voronoi diagram presented in this paper, which can be constructed in time O(nlogn) with O(n) space in the preprocessing stage. This data structure also can be used to fast solve visibility information, collision detection and other problems in 3D virtual worlds. The methods are simpler and faster than other existed methods, with lower space.
Ultra wide-band slot antenna based on liquid crystal polymer material for millimeter wave application

A millimeter wave ultra-wide band (UWB) tapered slot antenna is presented based on a multilayer liquid crystal polymer (LCP) circuit process. The multilayer circuit board consists of eight copper layers and seven LCP layers. In order to enhancing the bandwidth, two overlapped tapered slots with different flare angle are applied in the 3rd and the 5th copper layers, respectively. A low backward radiation characteristic is achieved due to using the ground-backed structure. A simple design guideline is detected and the dimension is optimized. The designed results indicate that the millimeter wave UWB slot antenna can work in the frequency band of 33GHz-60GHz (a relative bandwidth of 58%). The radiation patterns are calculated at three typical frequencies and the analysis demonstrates that an elliptical polarization performance is obtained within the total operation frequency band. The study also demonstrates that the LCP process is suitable for developing lightweight and high performance millimeter wave antennas.
Early B Cell Progenitors Deficient for GON4L Fail To Differentiate Due to a Block in Mitotic Cell Division

B cell development in Justy mutant mice is blocked due to a precursor mRNA splicing defect that depletes the protein GON4-like (GON4L) in B cell progenitors. Genetic and biochemical studies have suggested that GON4L is a transcriptional regulator that coordinates cell division with differentiation, but its role in B cell development is unknown. To understand the function of GON4L, we characterized B cell differentiation, cell cycle control, and mitotic gene expression in GON4L-deficient B cell progenitors from Justy mice. We found that these cells established key aspects of the transcription factor network that guides B cell development and proliferation and rearranged the IgH gene locus. However, despite intact IL-7 signaling, GON4L-deficient pro-B cell stage precursors failed to undergo a characteristic IL-7–dependent proliferative burst. These cells also failed to upregulate genes required for mitotic division, including those encoding the G1/S cyclin D3 and E2F transcription factors and their targets. Additionally, GON4L-deficient B cell progenitors displayed defects in DNA synthesis and passage through the G1/S transition, contained fragmented DNA, and underwent apoptosis. These phenotypes were not suppressed by transgenic expression of prosurvival factors. However, transgenic expression of cyclin D3 or other regulators of the G1/S transition restored pro-B cell development from Justy progenitor cells, suggesting that GON4L acts at the beginning of the cell cycle. Together, our findings indicate that GON4L is essential for cell cycle progression and division during the early stages of B cell development.
Tyrosine Phosphorylation of c-ErbB-2 Is Regulated by the Cellular Form of Prostatic Acid Phosphatase in Human Prostate Cancer Cells*

Human prostatic acid phosphatase (PAcP) is a prostate epithelium-specific differentiation antigen. In prostate carcinomas, the cellular PAcP is decreased. We investigated its functional role in these cells. Several lines of evidence support the hypothesis that cellular PAcP functions as a neutral protein-tyrosine phosphatase and is involved in regulating prostate cell growth. In this study, we identify its in vivo substrate. Our results demonstrated that, in different human prostate cancer cell lines, the phosphotyrosine (Tyr(P)) level of a 185-kDa phosphoprotein (pp185) inversely correlates with the cellular activity of PAcP. On SDS-PAGE, this pp185 co-migrates with the c-ErbB-2 oncoprotein. Immunodepletion experiments revealed that c-ErbB-2 protein is the major pp185 in cells. Results from subclones of LNCaP cells indicated the lower the cellular PAcP activity, the higher the Tyr(P) levels of c-ErbB-2. This inverse correlation was further observed in PAcP cDNA-transfected cells. In clone 33 LNCaP cells, l-(+)-tartrate suppresses the cellular PAcP activity and causes an elevated Tyr(P) level of c-ErbB-2 protein. Epidermal growth factor stimulates the proliferation of LNCaP cells, which concurs with a decreased cellular PAcP activity as well as an increased Tyr(P) level of c-ErbB-2. Biochemically, PAcP dephosphorylates c-ErbB-2 at pH 7.0. The results thus suggest that cellular PAcP down-regulates prostate cell growth by dephosphorylating Tyr(P) on c-ErbB-2 oncoprotein in those cells.
Plasmin Prevents Dystrophic Calcification After Muscle Injury

Extensive or persistent calcium phosphate deposition within soft tissues after severe traumatic injury or major orthopedic surgery can result in pain and loss of joint function. The pathophysiology of soft tissue calcification, including dystrophic calcification and heterotopic ossification (HO), is poorly understood; consequently, current treatments are suboptimal. Here, we show that plasmin protease activity prevents dystrophic calcification within injured skeletal muscle independent of its canonical fibrinolytic function. After muscle injury, dystrophic calcifications either can be resorbed during the process of tissue healing, persist, or become organized into mature bone (HO). Without sufficient plasmin activity, dystrophic calcifications persist after muscle injury and are sufficient to induce HO. Downregulating the primary inhibitor of plasmin (α2‐antiplasmin) or treating with pyrophosphate analogues prevents dystrophic calcification and subsequent HO in vivo. Because plasmin also supports bone homeostasis and fracture repair, increasing plasmin activity represents the first pharmacologic strategy to prevent soft tissue calcification without adversely affecting systemic bone physiology or concurrent muscle and bone regeneration. © 2016 American Society for Bone and Mineral Research.
Selective Dielectric Metasurfaces Based on Directional Conditions of Silicon Nanopillars

Dielectric metasurfaces based on high refractive index materials have been proposed recently. This type of structure has several advantages over their metallic counterparts. In this work, we demonstrate that dielectric metasurfaces can be theoretically designed satisfying Kerker’s zero-forward condition. This is the first time that a dielectric metasurface based on this principle has been designed. A selective dielectric metasurface of silicon nanopillars is designed to work at 632.8 nm. This structure could work both as a dielectric mirror and a reject band filter. Furthermore, by scaling up the structure, it could be possible to manufacture a terahertz (THz) dielectric mirror.
Insulin resistance, prehypertension, hypertension and blood pressure values in paediatric age

Objective: The aim of the present study was to evaluate whether insulin resistance [as measured by Homeostasis Model Assessment (HOMA) index] has an effect on prehypertension and hypertension risk in children after acknowledging the role of BMI and waist-to-height ratio. Methods: We studied a sample of 377 children 10.5 ± 2.3 years old who had a first diagnosis of hypertension or family history of cardiovascular disease. In this sample all weight classes were represented. The HOMA index was standardized by a linear regression model including BMI, waist-to-height ratio and pubertal status. Results: The role of BMI and waist-to-height ratio on the risk of prehypertension and hypertension was confirmed by univariate logistic regression models, odds ratio of 1.59 [95% confidence interval (CI) = 1.27–2.00] for BMI, and 1.56 (95% CI = 1.06–2.31) for waist-to-height ratio (>50 vs. ⩽50%). When standardized HOMA index was added to BMI or waist-to-height ratio in a multivariate model, it gave a significant independent contribution to explain the risk of prehypertension and hypertension. Odds ratio was 1.23 (95% CI = 1.01–1.51) in the model with BMI, and 1.23 (95% CI = 1.01–1.50) in the model with waist-to-height ratio. The role of HOMA index was confirmed when continuous values of systolic and diastolic blood pressure (standardized by age, sex and height) were analysed, instead of hypertension category. Conclusions: These results strongly support the hypothesis that in children, insulin resistance plays a role on hypertension independently from obesity, fat distribution and puberty across weight classes.
Comparison of utility measures and their relationship with other health status measures in 1041 patients with rheumatoid arthritis

Objectives The aim of this study was to compare three health utility instruments (15D, EQ-5D, SF-6D) and a rating scale for health (EQ-Visual Analogue Scale (VAS)) and to investigate their relationship to clinical parameters in patients with rheumatoid arthritis (RA). Methods Data were collected from 1041 patients with RA. Agreement between the instruments was assessed with Bland–Altman plots. Linear regression models were fitted for the different instruments and Health Assessment Questionnaire (HAQ) scores, age, gender, patient global, disease duration and educational level. Differences in utility scores across levels of global health and disability, were investigated as well as correlations with disease-specific health status measures. Results The score range in the 1041 patients with RA was 0.41–1.0 for 15D, −0.48 to 1.0 for EQ-5D, 0.0–1.0 for EQ-VAS and 0.30–1.0 for SF-6D, with a bimodal distribution for EQ-5D. Bland–Altman plots indicated poor agreement between EQ-5D and SF-6D/15D and moderate agreement between SF-6D and 15D. Utility scores were correlated with disease-specific measures, pain and fatigue (r>0.60). Mean utilities ranged from 0.30 (EQ-5D) to 0.69 (15D) in patients rating their own health as poor. When correcting for a non-linear relationship between HAQ and EQ-5D/SF-6D in linear regression models, the estimated utilities had non-overlying CI for HAQ values >1.4. Conclusions Diverging scores were observed across utility instruments, especially in patients with high HAQ scores. The choice of utility instrument may have an impact on the results of cost-utility analyses, with large hypothetical differences in price per quality-adjusted life year.
DNA Content Is an Independent Prognostic Indicator in Endometrial Adenocarcinoma A Gynecologic Oncology Group Study

SummaryThe identification of prognostic variables is an important aspect of managing and counseling women with endometrial adenocarcinoma. The surgical stage, age, cell type, depth of myometrial invasion, and histologic grade have all been previously demonstrated to be related to prognosis. Several reports have indicated that tumor ploidy as determined by flow cytometry with fresh or fixed cells removed from paraffin blocks of endometrial adenocarcinomas can contribute to the assessment of prognosis. To verify the significance of DNA content in endometrial adenocarcinoma, we conducted an historical cohort study on a subgroup of women from a Gynecologic Oncology Group (GOG) protocol of early clinical stage disease. Flow cytometry was performed at one facility on cells extracted from blocks obtained from several GOG member institutions. Blocks were submitted for 293 of 933 eligible patients. Ninety-two histograms were of good quality, with 55 interpreted as diploid and 37 as aneuploid. One hundred sixty-two histograms were technically suboptimal, of which 137 were considered probably diploid, 13 probably aneuploid, and 12 unacceptable due to high background noise. Of the commonly accepted prognostic variables, only depth of invasion was significantly related to the ploidy status. There was no discernable difference in survival between patients with diploid and patients with probable diploid and probable aneuploid tumor types. Incorporation of the flow cytometry data into a proportional hazards regression model adjusted for age and surgical stage revealed a significant increased risk of disease-related death (relative risk, 4.1; 95% confidence interval, 2.3 to 7.3) for patients with aneuploid tumor type as compared to patients with diploid tumor type. This study confirms the prognostic significance of ploidy determination by flow cytometry and also indicates some of the difficulties of retrospectively applying this technology to cooperative group studies.
The optimum design of a master-slave D-flip flap (M/S-DFF) based on the modified GDI (m-GDI) method using Non-dominated Sorting Genetic Algorithm II (NSGA-II)

Gate diffusion input (GDI) technique provides the possibility of low power logic gates design with lower number of transistors in a simple structure. In this paper, first the modified GDI (m-GDI) cell is presented by employing carbon nano tube field effect transistor (CNTFET). Then a new configuration for master-slave Data-flip flap (M/S-DFF) is proposed based on the m-GDI cell. For optimizing the performance of the proposed M/S-DFF and gaining the minimum power and delay, the transistors size is adjusted with Non-dominated Sorting Genetic Algorithm II (NSGA-II) in MATLAB software. The circuit simulation is done with the help of H-SPICE software in 32nm CNTFET technology. Due to the achieved results of the proposed M/S-DFF simulation, the power consumption and delay decrease about 74.6% and 13.75%, respectively, in compare with similar flip flaps which aren't optimized.
Structural Basis and Targeting of the Interaction between Fibroblast Growth Factor-inducible 14 and Tumor Necrosis Factor-like Weak Inducer of Apoptosis*

Background: Aberrant TNF-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling is observed in inflammation, autoimmune diseases, and cancers. Results: An integrated computational and experimental study identified small molecule inhibitors of TWEAK-Fn14 interaction. Conclusion: The TWEAK-Fn14 interaction is tractable and can be inhibited by small molecules. Significance: This is the first evidence of small molecules targeting TWEAK-Fn14 signaling. Deregulation of the TNF-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling pathway is observed in many diseases, including inflammation, autoimmune diseases, and cancer. Activation of Fn14 signaling by TWEAK binding triggers cell invasion and survival and therefore represents an attractive pathway for therapeutic intervention. Based on structural studies of the TWEAK-binding cysteine-rich domain of Fn14, several homology models of TWEAK were built to investigate plausible modes of TWEAK-Fn14 interaction. Two promising models, centered on different anchoring residues of TWEAK (tyrosine 176 and tryptophan 231), were prioritized using a data-driven strategy. Site-directed mutagenesis of TWEAK at Tyr176, but not Trp231, resulted in the loss of TWEAK binding to Fn14 substantiating Tyr176 as the anchoring residue. Importantly, mutation of TWEAK at Tyr176 did not disrupt TWEAK trimerization but failed to induce Fn14-mediated nuclear factor κ-light chain enhancer of activated B cell (NF-κB) signaling. The validated structural models were utilized in a virtual screen to design a targeted library of small molecules predicted to disrupt the TWEAK-Fn14 interaction. 129 small molecules were screened iteratively, with identification of molecules producing up to 37% inhibition of TWEAK-Fn14 binding. In summary, we present a data-driven in silico study revealing key structural elements of the TWEAK-Fn14 interaction, followed by experimental validation, serving as a guide for the design of small molecule inhibitors of the TWEAK-Fn14 ligand-receptor interaction. Our results validate the TWEAK-Fn14 interaction as a chemically tractable target and provide the foundation for further exploration utilizing chemical biology approaches focusing on validating this system as a therapeutic target in invasive cancers.
Power management game for cooperative localization in asynchronous networks

High-precision positioning techniques have a promising future in various applications. Recent work shows that inter-node cooperation can increase the positioning accuracy. In general, such cooperation consumes additional power, and current power application techniques are limited in synchronous networks. To study the power allocation in asynchronous networks, this paper proposes a power management game for cooperative localization, where each user allocates power that minimizes its square error positioning bound (SPEB) penalized by the power cost. Such game-theoretic power allocation policy not only considers how to allocate power over different cooperative links, but also manages the total power consumed for a better performance and power trade-off. We show that, in two-user networks, the power management game admits a unique cooperating Nash Equilibrium (NE) in high SNR region. In addition, as the power budget goes to infinity, the proposed game-theoretic power allocation policy can achieve SPEB arbitrarily close to that under exhaustive power allocation, but requires much less power.
Modifications of collagen and chromatin in ECM-related disease

Collagens are subjected to extensive posttranslational modifications, such as lysine hydroxylation. Bruck syndrome (BS) is a connective tissue disorder characterized at the molecular level by a loss of telopeptide lysine hydroxylation, resulting in reduced collagen pyridinoline cross-linking. BS results from mutations in the genes coding for lysyl hydroxylase (LH) 2 or peptidyl-prolyl cis-trans isomerase (PPIase) FKBP65. Given that the immunophilin FKBP65 does not exhibit LH activity, it is likely that LH2 activity is somehow dependent on FKPB65. In this report, we provide insights regarding the interplay between LH2 and FKBP65. We found that FKBP65 forms complexes with LH2 splice variants LH2A and LH2B but not with LH1 and LH3. Ablating the catalytic activity of FKBP65 or LH2 did not affect complex formation. Both depletion of FKBP65 and inhibition of FKBP65 PPIase activity reduced the dimeric (active) form of LH2 but did not affect the binding of monomeric (inactive) LH2 to procollagen Iα1. Furthermore, we show that LH2A and LH2B cannot form heterodimers with each other but are able to form heterodimers with LH1 and LH3. Collectively, our results indicate that FKBP65 is linked to pyridinoline cross-linking by specifically mediating the dimerization of LH2. Moreover, FKBP65 does not interact with LH1 and LH3, explaining why in BS triple-helical hydroxylysines are not affected. Our results provide a mechanistic link between FKBP65 and the loss of pyridinolines and may hold the key to future treatments for diseases related to collagen cross-linking anomalies, such as fibrosis and cancer.
The Use of Intraoperative Radiolymphoscintigraphy for Sentinel Node Biopsy in Patients with Malignant Melanoma

background Selective lymphadenectomy or “sentinel node” biopsy Ms been introduced recently by Morton and colleagues (Arch Surg 1992;127:392–9) to stage patients with intermediate and thick malignant melanomas. It has proven to be an effective way to identify nodal basins at risk for metastasis without the morbidity of a complete lymph node dissection. The majority of biopsies can be performed under local anesthesia with small incisions, but technical difficulties occasionally result in unsuccessful explorations. Identification of the sentinel node can be enhanced by a intraoperative radiolymphoscintigraphy, a technique introduced Alex and Krag (Surg Oncol 1993;137–43) tint uses radiolabeled sulfur colloid and a hand‐held gamma probe. objective We used intraoperative radiolymphoscintigraphy in conjunction with 1% lymphazurin blue dye to define the sentinel node(s) in 148 patients with greater than 0.76 mm in thickness or Clark level TV melanomas. Sentinel lymph nodes were isolated, harvested, and examined using conventional histopathology, and immunohistochemistry for S‐100 and HMB‐45 antibodies. results The overall success rate of sentinel lymph node localization was 97% using a combination of the two techniques. Twenty‐one (34%) patients had micrometastasis, and 17 of these subsequently underwent complete lymph node dissection. A total of 220 of 275 (80%) sentinel nodes harvested were radioactive or “hot” compared with 165 of 275 (60%) with the blue dye alone. Four of the patients with micrometastasis had sentinel nodes positive by gamma probe, but negative by blue dye mapping techniques. conclusion Our results suggest that intraoperative radiolymphosintigraphy using a hand‐held gamma detecting probe improves the identification of sentinel lymph nodes during selective lymphadenectomy. This may reduce the number of “unsuccessful explorations” using the vital blue dye technique for lymphatic mapping, and appeal to a greater variety of surgeons, including dermatologic surgeons.
Exercise and green tea extract stimulate fat oxidation and prevent obesity in mice.

INTRODUCTION/PURPOSE The purpose of the present study was to explore the combined effects of dietary supplementation with green tea extract (GTE) and regular exercise on the development of obesity in high fat-fed C57BL/6J mice. METHODS Weight and age-matched male mice were divided into 5 groups of 10 mice each. Groups were treated as follows: a low-fat diet and not exercised (LF), a high-fat diet and not exercised (HF), a high-fat diet supplemented with GTE and not exercised (GTE-HF), a high-fat diet and exercised regularly (EX-HF), or a high-fat diet supplemented with GTE and exercised regularly (GTEEX-HF). The exercise modality was treadmill running. RESULTS After 15 wk, GTE alone and regular exercise alone caused a 47 and 24% reduction in body weight gain induced by the high-fat diet, respectively, and when combined, resulted in an 89% reduction. In visceral fat accumulation, GTE alone, exercise alone, and their combination caused a 58, 37, and 87% reduction, respectively. Indirect calorimetry showed that the GTEEX-HF group had the highest energy expenditure and fat utilization in the sedentary condition after 4 wk. Furthermore, the GTEEX-HF group utilized more fat than the EX-HF group during exercise. GTE supplementation increased hepatic fatty acid oxidation both in the exercised and nonexercised groups. In addition, when combined with regular exercise, GTE supplementation also stimulated skeletal muscle fatty acid oxidation. CONCLUSION In conclusion, dietary GTE and regular exercise, if combined, stimulate fat catabolism not only in the liver but also in skeletal muscle, and attenuate high-fat diet-induced obesity more effectively than each alone in C57BL/6J mice.