Miracle-dz/UniFAR-FTUs huggingface dataset:
Modeling High-Frequency Multiwinding Magnetic Components Using Finite-Element Analysis

This paper presents a magnetic component equivalent circuit as well as a methodology to extract its parameters by using a finite- element analysis tool. The model is valid for any kind of magnetic component-transformers and gapped and nongapped inductors-and takes into account frequency and geometry effects such as skin, proximity, interleaving, gap, and end effects. An additional model for capacitive effects may be coupled with the previous one to obtain a more precise result. The impedances in this model represent not only the self terms, but also all mutual terms shared between the windings. Because the simplification of concentrating impedances in one winding is not invoked, simultaneous conduction of all windings (such as forward-like converters) or in alternate conduction of the windings (such as flyback-like converters) can be accurately simulated. The parameters of these self and mutual impedances are frequency dependent, so the model represents the frequency behavior of windings in detail. This allows simulating components with nonsinusoidal currents like the ones present in switched-mode power supplies, provided there is no saturation of magnetic materials. This is not a serious limitation of the model because this kind of power supply works in linear (no-saturation) mode. When there is saturation, the core model determines the component behavior. Applying the model to several actual components has shown its usefulness and accuracy. Details concerning model parameters extraction are presented here with simulation and measurement results.
The Cyclin-dependent Kinase Inhibitor p27Kip1 Is Stabilized in G0 by Mirk/dyrk1B Kinase*

Elevated levels of the cyclin-dependent kinase (CDK) inhibitor p27 block the cell in G0/G1 until mitogenic signals activate G1 cyclins and initiate proliferation. Post-translational regulation of p27 by different phosphorylation events is critical in allowing cells to proceed through the cell cycle. We now demonstrate that the arginine-directed kinase, Mirk/dyrk1B, is maximally active in G0 in NIH3T3 cells, when it stabilizes p27 by phosphorylating it at Ser-10. The phospho-mimetic mutant p27-S10D was more stable, and the non-phosphorylatable mutant p27-S10A was less stable than wild-type when expressed in G0-arrested cells. Following phosphorylation by Mirk, p27 remains a functional CDK inhibitor, capable of binding to CDK2. Mirk did not induce the translocation of p27 from the nucleus in G0, but instead co-localized with nuclear p27. Depletion of Mirk by RNA interference decreased the phosphorylation of p27 at Ser-10 and the stability of endogenous p27. RNAi to Mirk increased cell entry from G0 into G1 as shown by increased expression of proliferating cell nuclear antigen and decreased expression of p27. These data suggest a model in which Mirk increases the amount of nuclear p27 by stabilizing it during G0 when Mirk is most abundant. Mitogen stimulation then causes cells to enter G1, reduces Mirk levels (Deng, X., Ewton, D., Pawlikowski, B., Maimone, M., and Friedman, E. (2003) J. Biol. Chem. 278, 41347-41354), and initiates the translocation of p27 to the cytoplasm. In addition, depletion of Mirk by RNAi in postmitotic C2C12 myoblasts decreased protein but not mRNA levels of p27, suggesting that stabilization of p27 by Mirk also occurs during differentiation.
Hepatectomy for hepatocellular carcinoma: Patient selection and postoperative outcome

Hepatic resection and liver transplantation are considered the only curative treatments for hepatocellular carcinoma (HCC). Liver transplantation for HCCs ≤ 5 cm in diameter has been shown to produce favorable survival results, but its application is limited by the lack of donors. Hepatic resection remains the treatment of choice for patients who are not transplantation candidates because of large tumor, macroscopic vascular invasion, or advanced age. For small HCCs associated with Child's A cirrhosis, hepatic resection should still be considered the first‐line treatment, but salvage transplantation for intrahepatic recurrence may be a feasible strategy. Recent improvement in surgical techniques and perioperative care has increased the safety and expanded the indication of hepatic resection for HCC to include large tumors that require extended hepatectomy in cirrhotic patients. Selection of appropriate candidates for hepatectomy depends on careful assessment of the tumor status and liver function reserve. Evaluation of the general fitness of patients is also critical because comorbid illness is an important cause of postoperative mortality, even if the patients have good liver function reserve. With careful patient selection and surgical expertise, the current operative mortality of hepatectomy for HCC is about 5% or less in major centers. Improved long‐term survival results after resection of HCC have also been reported recently, with an overall 5‐year survival rate of about 50%. The improved perioperative and long‐term survival results have strengthened the role of hepatectomy as the mainstay of treatment for HCC despite the availability of a number of other treatment options for localized HCC. (Liver Transpl 2004;10:S39–S45.)
Prognostic factors in intracranial ependymomas in children.

OBJECT The occurrence of intracranial ependymomas in children is relatively infrequent, and their prognostic factors are still controversial, especially regarding histological composition. METHODS A retrospective study was conducted of 37 children treated during the last 20 years for intracranial ependymomas at the Hôpital de la Timone. Both univariate and multivariate statistical analyses were performed to assess the prognostic relevance of patient age and sex, extent of tumor removal, location of the tumor (supratentorial compared with infratentorial, median compared with lateral), tumor histological composition, and adjuvant therapies in affecting the 5-year progression-free survival (PFS) rate and overall survival (OS) rate. The following histopathological features, either alone or in combination, were analyzed: endothelial proliferation, necrosis, loss of differentiating structures (present compared with absent), the number of mitotic figures per 10 hpf, and cellularity (number of nuclei/5 hpf). In addition, immunohistochemical detection of Ki-67 antigen was performed and the Ki-67 labeling index (LI) evaluated in all cases. The 5-year OS and PFS rates were 45% and 25%, respectively (median follow up 34 months). Four patients died of disease without remission (median 163 days) and disease in 21 patients relapsed: 18 in situ and three both in situ and distantly. On univariate analysis total surgical resection and median infratentorial location were associated with a better outcome (p < 0.002) for both OS and PFS. Loss of differentiating structures was associated with poor prognosis (p < 0.008) and the combination of necrosis, endothelial proliferation, and mitotic index greater than 5 was also a negative predictive factor for both OS (p < 0.002) and PFS (p = 0.02). The PFS time was shorter in patients younger than 4 years of age and in patients in whom a Ki-67 LI greater than 1 was found (p = 0.03 and 0.006, respectively). Adjuvant radiotherapy and chemotherapy were not relevant to prognosis. Moreover, among the 15 patients in whom total excision was achieved, OS was better in those who did not receive adjuvant therapies. In contrast, adjuvant therapies significantly enhanced PFS time in patients in whom tumor excision was incomplete. CONCLUSIONS This study and analysis of the literature further highlight that total tumor removal is the treatment of choice for ependymomas in children. Postoperative measurement of residual tumor is required, especially because a subgroup of patients might be treated by surgery alone. Median infratentorial ependymomas have to be distinguished from the lateral type. Appropriate and reproducible histological parameters and Ki-67 LI are of interest as predictors of outcome.
Effects of small-sided game and change-of-direction training on reactive agility and change-of-direction speed

Abstract The purpose of this study was to determine the effects of training change-of-direction speed and small-sided games on performance in the Planned-AFL agility test and reactive agility. Twenty-five elite-standard U-18 Australian Rules football players were randomly allocated either to a change-of-direction group or a small-sided games group. Players participated in one or two 15-min sessions per week with 11 sessions conducted over a 7-week period during the season. Tests conducted immediately before and after the training period included the Planned-AFL agility test and a video-based reactive agility test specific to Australian Rules football. The reactive agility test variables were total time, decision time and movement response time. The small-sided games group improved total time (P = 0.008, effect size = 0.93), which was entirely attributable to a very large reduction in decision time (P < 0.001, effect size = 2.32). Small-sided games produced a trivial change in movement response time as well as in the Planned-AFL agility test (P > 0.05). The change-of-direction training produced small to trivial changes in all of the test variables (P > 0.05, effect size = 0–0.2). The results suggest that small-sided games improve agility performance by enhancing the speed of decision-making rather than movement speed. The change-of-direction training was not effective for developing either change-of-direction speed as measured by the Planned-AFL test or reactive agility.
Clinical significance of the circle of Willis in intracranial atherosclerotic stenosis

Introduction The effectiveness of a scoring system based on the circle of Willis for evaluations of collateral circulation was studied in patients with intracranial atherosclerotic stenosis. Methods Eighty-three patients who underwent medical or endovascular treatment for symptomatic and severe intracranial atherosclerotic stenosis were enrolled in the study. Clinical profiles, status of the circle of Willis (poor and good integrity group), and clinical outcomes were analyzed. Primary endpoints were: (1) symptomatic ischemic or hemorrhagic stroke within 30 days; and (2) recurrent transient ischemic attack or ischemic stroke beyond 30 days. Results The estimated rates of the primary endpoint at 1 and 2 years after treatment were 8.5% and 11.4% in the medical group and 7.0% and 9.7% in the endovascular group, respectively. A primary endpoint event after medical treatment was only identified in patients with poor integrity of the circle of Willis (p=0.059). In patients with poor integrity of the circle of Willis, previous antiplatelet medication before initial presentation (p=0.026) and hypertension (p=0.006) were more prevalent. During the follow-up period, complete arterial occlusion was identified in 9 patients. The circle of Willis score of the patients with complete arterial occlusion was 1.33±1.52 in the fatal stroke group (n=3) and 3.20±1.64 in the asymptomatic group (n=6, p=0.099). Conclusions If patients have poor integrity of the circle of Willis, the risk of recurrent stroke may be increased. Such patients appear to be good candidates for endovascular treatment.
Bevacizumab in combination chemotherapy for colorectal and other cancers.

PURPOSE The pharmacology, pharmacokinetics, pharmacodynamics, clinical efficacy, adverse effects, and dosage and administration of bevacizumab in patients with colorectal and other cancers are reviewed. SUMMARY Bevacizumab is a recombinant human monoclonal antibody that inhibits the biological activities of vascular endothelial growth factor (VEGF), a protein involved in the neovascularization of multiple malignant tumors. A single dose of bevacizumab 0.1-10 mg/kg yields a maximum concentration of 2.8-284 microg/mL and shows a dose-response relationship. Pre-clinical and clinical studies have shown that bevacizumab has both cytostatic and cytotoxic effects, resulting in a reduction in tumor growth and increases in median survival time and time to tumor progression. Bevacizumab is available as an intravenous agent and carries FDA-approved labeling for use in the first-line treatment of meta-static colorectal cancer in combination with fluorouracil-based chemotherapy. Bevacizumab 5 mg/kg is infused intravenously over 30-90 minutes every two weeks. No dosage reductions are required for patients with renal or hepatic dysfunction. Bevacizumab has also yielded preliminary evidence of efficacy for breast, non-small-cell lung, pancreatic, prostate, renal, and hepatic cancers, as well as for melanoma and acute myelogenous leukemia. The most frequent adverse effects are nausea, vomiting, headache, epistaxis, anorexia, stomatitis, dyspnea, and constipation. CONCLUSION Bevacizumab combined with fluorouracil-based chemotherapy has become the standard of care for the first-line treatment of metastatic colorectal cancer and may prove useful for other tumors as well.
Alz‐50 and MC‐1, a new monoclonal antibody raised to paired helical filaments, recognize conformational epitopes on recombinant tau

Using a series of recombinant tau and FAC1 mutant proteins, this study demonstrates by Western and dot blot analysis that 1) shared epitopes between tau and FAC1 are responsible for Alz‐50 binding; 2) Alz‐50 reactivity is dependent on two discontinuous portions of the tau molecule; 3) Alz‐50 reactivity is most likely the result of a conformational alteration of tau monomers in Alzheimer's disease; and 4) the epitope for MC‐1, a novel monoclonal antibody, maps to similar regions of tau but does not react with FAC1. These data raise questions regarding previous studies which have suggested that tau lacks a specific conformation and illustrate the utility of the Alz‐50 and MC‐1 antibodies in recognizing a distinct pathological conformation of the tau molecule in Alzheimer's disease. J. Neurosci. Res. 48:128–132, 1997. © 1997 Wiley‐Liss, Inc.
Effects of the SOD mimic nitroxide 3-carbamoyl-PROXYL on oxidative stress markers and endothelial dysfunction in streptozotocin-induced diabetic rats.

OBJECTIVE To evaluate the effects of 3-carbamoyl-PROXYL (CP), a stable superoxide dismutase (SOD) mimic compound, on oxidative stress markers and endothelial dysfunction in diabetic rats. ANIMALS AND METHODS Rats were made diabetic by a single vein injection of streptozotocin (65 mg/kg) and diabetes was verified by the existence of excessive hyperglycemia a week after the treatment. Control and diabetic rats received vehicle or drug for eight weeks, after which the vascular tissue was examined for relaxation and oxidative stress markers. RESULTS Diabetic rats showed increased vascular levels of superoxide that were accompanied by increased tissue levels of the oxidative stress markers malondialdehyde (MDA) and 8-iso-prostaglandin F2alpha (8-ISO). The vasorelaxant as well as the cyclic guanosine 5'-monophosphate (cGMP)-producing effects of acetylcholine (ACh) and nitroglycerine were reduced in diabetic rats. Treatment of diabetic rats with CP (50 mg/kg intraperitoneally, bid) abolished not only the differences in superoxide, MDA and 8-ISO levels, but also the differences in the relaxation and cGMP responses of vascular tissue between control and diabetic rats to both ACh and nitroglycerine. CONCLUSIONS These results support the involvement of reactive oxygen species in mediation of diabetes-induced endothelial dysfunction in vivo, and provide the rationale for the potential use of SOD mimics in the treatment of diabetes.
Graphical Web directory for Web search

This study addresses graphical Web directory, a new way to present hierarchical structure of Web directory. An analysis of the characteristics and problems of current Web directories is presented. The feature graphical Web directory for supporting information processing and decision making in Web directory browsing in Web search is proposed to improve users' performance and satisfaction. An experiment was conducted to test the effectiveness of the proposed feature. The results of the experiment indicated that (a) the enhancement of this feature improved users' initial and overall search performance by 32.6 and 43.4%, respectively, (b) the enhancement of this feature also improved users' satisfaction by 27.7%.
Knowledge curation discussions and activity dynamics in a short lived social Q&A community

Studying the dynamics and lifecycles of online knowledge curation communities is essential to identify and assemble community type specific repertoires of strategies, rules, and actions of community design, governance, content creation and curation. This paper examines the lifecycle of a short lived social Q&A community on Stack Exchange by performing the content analysis of the logs of member discussions and content curation actions.
Expression of Tumor Necrosis Factor Alpha-Induced Protein 3 mRNA in Peripheral Blood Mononuclear Cells Negatively Correlates with Disease Severity in Psoriasis Vulgaris

ABSTRACT Psoriasis vulgaris is considered a chronic inflammatory disease, but its immunopathogenesis has not been well understood. The tumor necrosis factor alpha-induced protein 3 (TNFAIP3) gene functions in negative-feedback regulation of inflammation, and its single nucleotide polymorphism is associated with psoriasis. However, the relationship between the expression level of the TNFAIP3 gene in immune cells and psoriasis is not known so far. In the present study, TNFAIP3 mRNA expression levels in peripheral blood mononuclear cells from 44 patients with psoriasis vulgaris and 30 healthy controls were determined using real-time reverse transcription-PCR analysis. We found that expression of TNFAIP3 mRNA in all patients negatively correlated with the psoriatic area and severity index (PASI) (r = −0.5126; P = 0.0004) as well as with the percentage of body surface area affected by psoriasis (r = −0.5013; P = 0.0005). Patients were divided into mild and severe groups based on the mean PASI score. Expression of TNFAIP3 mRNA in the mild group was higher than that in the severe group (P = 0.0064). Moreover, compared with that in healthy controls, the expression of TNFAIP3 mRNA in the mild group was significantly upregulated (P = 0.0004), but the expression of TNFAIP3 mRNA in the severe group was not. These results suggest that the expression level of TNFAIP3 plays an important role in the pathology of psoriasis vulgaris and that the loss of upregulation of TNFAIP3 expression may contribute to the severity of psoriasis vulgaris.
Mutational analysis of the hsp70-interacting protein Hip

The hsp70-interacting protein Hip participates in the assembly pathway for progesterone receptor complexes. During assembly, Hip appears at early assembly stages in a transient manner that parallels hsp70 interactions. In this study, a cDNA for human Hip was used to develop various mutant Hip forms in the initial mapping of functions to particular Hip structural elements. Hip regions targeted for deletion and/or truncation included the C-terminal region (which has some limited homology with Saccharomyces cerevisiae Sti1 and its vertebrate homolog p60), a glycine-glycine-methionine-proline (GGMP) tandem repeat, and a tetratricopeptide repeat (TPR). Binding of Hip to hsp70's ATPase domain was lost with deletions from the TPR and from an adjoining highly charged region; correspondingly, these Hip mutant forms were not recovered in receptor complexes. Truncation of Hip's Sti1-related C terminus resulted in Hip binding to hsp70 in a manner suggestive of a misfolded peptide substrate; this hsp70 binding was localized to the GGMP tandem repeat. Mutants lacking either the C terminus or the GGMP tandem repeat were still recovered in receptor complexes. Truncations from Hip's N terminus resulted in an apparent loss of Hip homo-oligomerization, but these mutants retained association with hsp70 and were recovered in receptor complexes. This mutational analysis indicates that Hip's TPR is required for binding of Hip with hsp70's ATPase domain. In addition, some data suggest that hsp70's peptide-binding domain may alternately or concomitantly bind to Hip's GGMP repeat in a manner regulated by Sti1-related sequences.
An Efficient Reconfigurable RF-DC Converter With Wide Input Power Range for RF Energy Harvesting

This paper presents a reconfigurable radio frequency to direct current (RF-DC) converter operating at 902 MHz frequency designed to efficiently harvest RF signals and convert into useable DC voltages for RF energy harvesting applications. The proposed scheme employs a dual-path, a series (low-power) path and a parallel (high-power) path, to maintain high power conversion efficiency (PCE) over wide input power range. The dual-path is composed of two identical rectifier blocks utilizing internal threshold voltage cancellation (IVC) technique to efficiently compensate the threshold voltage of the transistors used as rectifying devices. An adaptive control circuit (ACC) consisting of a comparator, an inverter and three switches is used in the proposed scheme. The ACC activates the series path or the parallel path to maximize the harvested power based on the input power range. The proposed scheme is designed and fabricated in a 180 nm complementary metal-oxide semiconductor (CMOS) technology. The measurement results show that PCE of the proposed circuit is above 20% from −18 dBm to −5 dBm, maintaining 13-dB input power range with peak PCE of 33% at −8 dBm for 200 $\text{k}\Omega $ load resistance. The proposed circuit demonstrates −20.2 dBm sensitivity across 1 $\text{M}\Omega $ load resistance while producing 1 V output DC voltage.
Multiple Controls Regulate the Expression of mobE, an HNH Homing Endonuclease Gene Embedded within a Ribonucleotide Reductase Gene of Phage Aeh1

ABSTRACT Mobile genetic elements have the potential to influence the expression of genes surrounding their insertion site upon invasion of a genome. Here, we examine the transcriptional organization of a ribonucleotide reductase operon (nrd) that has been invaded by an HNH family homing endonuclease, mobE. In Aeromonas hydrophila phage Aeh1, mobE has inserted into the large-subunit gene (nrdA) of aerobic ribonucleotide reductase (RNR), splitting it into two smaller genes, nrdA-a and nrdA-b. This gene organization differs from that in phages T4, T6, RB2, RB3, RB15, and LZ7, where mobE is inserted in the nrdA-nrdB intergenic region. We present evidence that the expression of Aeh1 mobE is regulated by transcriptional, posttranscriptional, and translational controls. An Aeh1-specific late promoter drives expression of mobE, but strikingly the mobE transcript is processed internally at an RNase E-like site. We also identified a putative stem-loop structure upstream of mobE that sequesters the mobE ribosome binding site, presumably acting to down regulate MobE translation. Moreover, our transcriptional analyses indicate that the surrounding nrd genes of phage Aeh1 are expressed by a different strategy than are the corresponding phage T4 genes and that transcriptional readthrough is the only mechanism by which the promoterless Aeh1 nrdB gene is expressed. We suggest that the occurrence of multiple layers of control to limit the expression of mobE to late in the Aeh1 infection cycle is an adaptation of Aeh1 to reduce any effects on expression of the surrounding nrd genes early in phage infection when RNR function is critical.