Miracle-dz/UniFAR-FTUs huggingface dataset:
Grid side regulation of wireless power charging of plug-in electric vehicles

Conductive charging of plug-in and battery electric vehicles (PEV's) is now well established and becoming more pervasive in the market. Conductive charger regulation of vehicle regenerative energy storage system (RESS), or battery pack charge rate is controlled by the dedicated on-board-charger (OBC) in coordination with the vehicles battery management system (BMS). Wireless Power Transfer (WPT) charging of PEV's is a relatively new and emerging technology that will not benefit from standardization work until 2014 or later. As such, various approaches are currently underway to manage the power flow from the grid-tied high frequency power inverter to the vehicle RESS. WPT regulation approaches can be secondary side only, primary side only or a combination of both. In this paper Oak Ridge National Laboratory (ORNL) envisions a system that is fast charge compatible and that minimizes the vehicle on board complexity by placing the burden of power regulation on the grid side converter. This paper summarizes the ORNL approach and experimental lessons learned at the National Transportation Research Center WPT laboratory1.
Avian sarcoma-leukosis virus pol-endo proteins expressed independently in mammalian cells accumulate in the nucleus but can be directed to other cellular compartments

Eucaryotic expression vectors have been used to study transient expression of the avian sarcoma-leukosis retrovirus pol-endo protein in COS cells. The constructs encode proteins with N termini identical to that of authentic viral pp32 endonuclease with the exception of a single met residue encoded by the initiator AUG. The C termini correspond to unprocessed viral pol protein, authentic processed pp32, or a derivative which includes eight amino acids from the unprocessed portion. All three proteins localize to the nucleus. However, when the pol-endo domain is fused to a secretory signal peptide, the protein is found in medium and appears also to localize in the Golgi bodies and the cell membrane. These and derivative vectors will make it possible to assess the consequence of retroviral pol gene expression in eucaryotic cells.
Reply to: “Polychlorinated biphenyls in prospectively collected serum and Parkinson's disease risk”

We read with great interest the article by Weisskopf et al. addressing the potential role of polychlorinated biphenyls (PCBs) on the risk for Parkinson’s disease (PD). We wish to add own unpublished observations from a population-based study investigating neurological performance in association with long-term, low-dose residential pesticide exposure. Body burden with persistent organochlorine pesticides, PCBs, and several other toxicants (eg Pb, Hg, Cd) was assessed as a potential confounder. Our 213 participants were dichotomized into an “exposed” group and a “non-exposed” group if they had been living within 1 km or more than 2 km away, respectively, from tree nurseries in Europe’s largest continuous area of tree nurseries for at least 25 years. The mean age (6 standard deviation) of participants was 55.5 6 6.6 years, 60% were women, and none carried a diagnosis of PD. Toxicants, including PCBs (congeners 138, 153, and 183) were measured in serum. The in-person examination included hypothesized markers of pre-diagnostic or pre-motor PD. We used the Wechsler Adult Intelligence Scale (WAIS) for cognitive testing, the Auditory Verbal Learning Test (AVLT) for short-term memory, the “learning over trials” (LOT) score for immediate recall, the AVLT5 and AVLT1 to test for differences between trials, and the “total learning score” (TLS) to compare the overall scores on the AVLT1 and the AVLT5, and the Benton test for visuospatial functioning. Upon neurological examination, gait, balance, muscle tone, coordination, reflexes, sensory discrimination, proprioception, and vibration sense were assessed. Fine motor ability was rated using 4 subtests on a conventional apparatus: (1) “aiming” (duration in seconds), (2) “steadiness” (number of errors, duration of errors in seconds), (3) “line pursuit’ (number of errors), and (4) “tapping” (rate). We screened for psychiatric symptoms using depression and personality assessments. Group comparisons revealed comparable test performance, and there was no case of PD in either group. PCB exposure levels were comparable to those in the cohort studied by Weisskopf et al. Median serum concentrations of estimated “total” PCBs (sum of the 3 major PCB congeners [PCB-138 1 PCB-153 1 PCB-180] 3 1.64) were 5.4 ng/mL (95th percentile, 17.9), and the maximum was 29.8 ng/
Plasma Myeloperoxidase and Total Sialic Acid as Prognostic Indicators in Acute Coronary Syndrome.

INTRODUCTION Acute Coronary Syndrome (ACS) is the leading cause of death worldwide. Oxidative stress and inflammation play important role in the destabilization of plaques leading to ACS. Markers which reflect this pathophysiologic mechanism may have prognostic value. Myeloperoxidase (MPO) and Sialic acid are markers of inflammation and oxidative stress. Both these markers are increased in patients with ACS. Their prognostic value in ACS is not well established. AIM To analyse the prognostic value of plasma myeloperoxidase and total sialic acid levels in patients with suspected acute coronary syndrome. MATERIALS AND METHODS A prospective study was conducted on 93 consecutively admitted patients with chest pain from July 2011 to September 2011. Plasma MPO and total sialic acid levels on admission were estimated spectrophotometrically. These were compared with extent of disease, development of complications during the hospital stay, left ventricular ejection fraction and mean duration of stay in hospital. RESULTS Plasma MPO and total sialic acid levels were significantly higher in patients with myocardial infarction than those with unstable and stable angina (p<0.001 and p<0.007 respectively). The levels of plasma MPO and sialic acid levels were significantly higher in patients who developed complications like heart failure, arrhythmias, renal failure during their stay in hospital (p<0.011 and p<0.006 respectively). Ejection fraction was significantly low in patients with high MPO levels (p<0.011). CONCLUSION In patients with ACS, plasma MPO and total sialic acid levels on admission could predict the development of complications during their hospital stay. MPO levels correlated with ejection fraction in patients with ACS.
Ionic Metal–Oxide TFTs for Integrated Switching Applications

Disordered ionic-bonded transition metal oxide thin-film transistors (TFTs) show promise for a variety of dc and RF switching applications, especially those that can leverage their low-temperature, substrate-agnostic process integration potential. In this paper, enhancement-mode zinc-oxide TFTs were fabricated and their switching performance evaluated. These TFTs exhibit the drain-current density of 0.6 A/mm and minimal frequency dispersion, as evidenced by dynamic current-voltage tests. A high-frequency power switch figure of merit RONQG of 359 mQ · nC was experimentally determined for 0.75-μm long-channel devices, and through scaling 45.9 mQ · nC is achievable for 11 V-rated devices (where RON is ON-state drain-source resistance, and QG is gate charge). An RF switch cutoff frequency fc of 25 GHz was measured for the same 0.75-μm TFT, whereas fc exceeding 500 GHz and power handling in the tens of watts are projected with optimization.
Multinomial i-vectors for Phonotactic Language Recognition

Deep neural networks have recently shown great promise for language recognition. In particular, the expected counts of clustered context-dependent phone states (senones) can serve as a simple but effective phonotactic system. This paper introduces multinomial i-vectors applied to senone counts and shows that they work better than current PCA approaches. In addition, we show that a new approach using a standard normal prior and MAP multinomial i-vector estimation further improves performance, particularly for shorter test durations. Finally, we present a reduced-complexity version of Newton’s method to greatly accelerate multinomial i-vector extraction. Experimental results on the NIST LRE11 task show that this approach performs significantly better than top-performing acoustic and phonotactic systems from that evaluation.
Featured Article How Package Design and Packaged-based Marketing Claims Lead to Overeating

Because packaging reaches consumers at the critical moments of purchase and consumption, it has become an important marketing tool for food manufacturers and retailers. In this paper, I first review how the marketing, health and nutrition claims made on packaging create "health halos" that make foods appear healthier than they are, thereby leading to higher consumption yet lower perceived calorie intake. I then show how packaging design (cues, shapes, and sizes) biases people's perception of quantity and increases their preference for supersized packages and portions that appear smaller than they are. Finally, I examine the extent to which mandatory nutrition labels, stricter regulation of package claims, public promotion of mindful eating, and mindless eating nudges could limit the biasing effects of packaging on food perceptions and preferences.
What Should the Physician Do When Creatinine Increases After Starting an Angiotensin‐Converting Enzyme Inhibitor or an Angiotensin Receptor Blocker?

A commonclinical problem arises when these renin-angio-tensin system–blocking drugs are started and theserum creatinine becomes elevated above thepatient’s baseline level. This may cause concernand may lead to stopping the ACE inhibitor orARB. Here, we offer our clinical approach to thisproblem.ACE inhibitors prevent the conversion of angio-tensin I to angiotensin II by inhibiting the ACEinhibitor enzyme complex, while ARBs inhibit thebinding of angiotensin to its AT1 receptor. Angio-tensin II constricts both the afferent and efferentarterioles, but it preferentially increases efferentarteriole resistance. When an ACE inhibitor orARB is used, there is a decrease in resistance at theefferent (postglomerular) arteriole; this lowers intra-glomerular pressure and reduces the glomerular ﬁl-tration rate (GFR).
Early sympathetic hyperactivity in Huntington's disease

To investigate whether Huntington's disease (HD) affects autonomic nervous system (ANS) functioning 33 subjects with positive genetic test results were studied. The subjects were classified according to Shoulson and Fahn (S&F) HD disability scale into three subgroups: subgroup 1 (eight asymptomatic gene carriers), subgroup 2 (13 mildly disabled HD patients) and subgroup 3 (eight moderately and four severely disabled HD patients). A battery of cardiovascular autonomic tests (Valsalva maneuver, deep breathing test, sustained handgrip test, orthostatic test) and the spectral analysis of heart rate variability (HRV) were performed. The results were compared with a group of matched controls. In subgroup 1, there was a higher power of low‐frequency band (LFB) (P < 0.05). In subgroup 2 a higher power of LFB was detected, LFB/high‐frequency band (HFB) coefficient was increased and the blood pressure response to sustained handgrip was elevated (P < 0.05). Subgroup 3 showed significantly lower blood pressure response to sustained handgrip, lower respiratory (P < 0.05) and orthostatic ratio (P < 0.01). Our results suggest that sympathetic hyperfunction is present in asymptomatic gene carriers and mildly disabled HD patients. Contrary to that, ANS hypofunction was found in advanced HD patients.
Advances in Brief T b RI ( 6 A ) Is a Candidate Tumor Susceptibility Allele 1

We have previously described a type I transforming growth factor (TGF)-b receptor (TbR-I) polymorphic allele, TbR-I(6A), that has a deletion of three alanines from a nine-alanine stretch. We observed a higher than expected number ofTbR-I(6A) homozygotes among tumor and nontumor DNA from patients with a diagnosis of cancer. To test the hypothesis that TbR-I(6A) homozygosity is associated with cancer, we performed a case-control study in patients with a diagnosis of cancer and matched healthy individuals with no history of cancer and who were identical in their gender and their geographical and ethnic background to determine the relative germ-line frequencies of this allele. We found nine TbR-I(6A) homozygotes among 851 patients with cancer. In comparison, there were no TbR-I(6A) homozygotes among 735 healthy volunteers (P < 0.01). We also observed an excess of TbR-I(6A) heterozygotes in cancer cases compared to controls (14.6%versus10.6%; P 5 0.02, Fisher’s exact test). A subset analysis revealed that 4 of 112 patients with colorectal cancer wereTbR-I(6A) homozygotes (P< 0.01). Using mink lung epithelial cell lines devoid of TbR-I, we established stably transfected TbR-I and TbR-I(6A) cell lines. We found that, compared to TbR-I, TbR-I(6A) was impaired as a mediator of TGF-b antiproliferative signals. We conclude thatTbR-I(6A) acts as a tumor susceptibility allele that may contribute to the development of cancer, especially colon cancer, by means of reduced TGF-b-mediated growth inhibition.
Ca 2+ sparks and T tubule reorganization in dedifferentiating adult mouse skeletal muscle fibers

Ca + sparks are rare in healthy adult mammalian skeletal muscle but may appear when adult fiber integrity is compromised, and occur in embryonic muscle but decline as the animal develops. Here we used cultured adult mouse flexor digitorum brevis muscle fibers to monitor occurrence of Ca 2+ sparks during maintenance of adult fiber morphology and during eventual fiber morphological dedifferentiation after various times in culture. Fibers cultured for up to 3 days retain normal morphology and striated appearance. Ca 2+ sparks were rare in these fibers. At 5–7 days in culture, many of the original muscle fibers exhibit sprouting and loss of striations, as well as the occurrence of spontaneous Ca 2+ sparks. The average rate of occurrence of Ca 2+ sparks is >10-fold higher after 5–7 days in culture than in days 1–3 . With the use of fibers cultured for 7 days, application of the Ca 2+ channel blockers Co 2+ or nifedipine almost completely suppressed the occurrence of Ca 2+ sparks, as previously shown in embryonic fibers, suggesting that Ca 2+ sparks may be generated by similar mechanisms in dedifferentiating cultured adult fibers and in embryonic fibers before final differentiation. The sarcomeric disruption observed under transmitted light microscopy in dedifferentiating fibers was accompanied by morphological changes in the transverse (T) tubular system, as observed by fluorescence confocal imaging of both an extracellular marker dye and membrane staining dyes. Changes in T tubule morphology coincided with the appearance of Ca 2+ sparks, suggesting that Ca 2+ sparks may either be a signal for, or the result of, disruption of DHPR-ryanodine receptor 1 coupling.
MicroRNA-320 suppresses colorectal cancer by targeting SOX4, FOXM1, and FOXQ1

Colorectal cancer (CRC) is the third most common cancer causing high mortality rates world-wide. Delineating the molecular mechanisms leading to CRC development and progression, including the role of microRNAs (miRNAs), are currently being unravelled at a rapid rate. Here, we report frequent downregulation of the microRNA miR-320 family in primary CRC tissues and cell lines. Lentiviral-mediated re-expression of miR-320c (representative member of the miR-320 family) inhibited HCT116 CRC growth and migration in vitro, sensitized CRC cells to 5-Fluorouracil (5-FU), and inhibited tumor formation in SCID mice. Global gene expression analysis in CRC cells over-expressing miR-320c, combined with in silico prediction identified 84 clinically-relevant potential gene targets for miR-320 in CRC. Using a series of biochemical assays and functional validation, SOX4, FOXM1, and FOXQ1 were validated as novel gene targets for the miR-320 family. Inverse correlation between the expression of miR-320 members with SOX4, FOXM1, and FOXQ1 was observed in primary CRC patients' specimens, suggesting that these genes are likely bona fide targets for the miR-320 family. Interestingly, interrogation of the expression levels of this gene panel (SOX4, FOXM1, and FOXQ1) in The Cancer Genome Atlas (TCGA) colorectal cancer data set (319 patients) revealed significantly poor disease-free survival in patients with elevated expression of this gene panel (P-Value: 0.0058). Collectively, our data revealed a novel role for the miR-320/SOX4/FOXM1/FOXQ1 axes in promoting CRC development and progression and suggest targeting those networks as potential therapeutic strategy for CRC.
MboII endonuclease heat inactivation before agarose gel electrophoresis to prevent artifactual bands in restriction patterns.

MboII restriction enzyme belongs to class-IIS endonucleases group (3–5). Like all of the enzymes belonging to this class, MboII cleaves DNA at a specific distance from its recognition sequence and still binds to its recognition sequence after DNA has been cleaved, because binding and cleaving domains have separate functions (5). In our laboratory, we apply amplified ribosomal DNA restriction analysis (ARDRA) to bacterial identification following the technique of Garcìa-Arata et al. (2). MboII was retained, among other enzymes, because of appropriate frequency of the endonuclease recognition sequence on the amplified ribosomal RNA operon (rrn) of Escherichia coli. Since E. coli K-12 MG1655 strain has now been entirely sequenced (1), we could retrieve from the European Molecular Biology Laboratory (EMBL) database (GenBank Accession No. U00096) the sequences corresponding to the amplified fragment in the seven rrn copies (A, B, C, D, E, G and H). Virtual MboII in silico restrictions could be performed on each of the seven sequences with the Geneman software (DNASTAR, Madison, WI, USA) on a Macintosh (Apple Computer, Cupertino, CA, USA). From the combination of all virtual restriction fragments from the seven operons, an in silico restriction pattern for E. coli K-12 MG1655 strain was obtained and could be compared to experimental patterns. Because the seven rrn operons in the E. coli chromosome differ in length and sequence, some of the fragments are contributed to by only one or a few operons. The amount of DNA contained in a single band will be proportional to the number of operons producing the band. Moreover, because the number of ethidium bromide molecules bound to double-stranded DNA fragments is proportional to fragment length, longer fragments will stain better than smaller ones even if they are produced by the same number of operons. Staining ability (S) of a band was calculated as S = L × N, where L is the fragment length, and N is the number of operons contributing to the band. S values were considered as strong (above 1500), intermediate (600–1499) and weak (below 600). Surprisingly, experimental patterns never entirely corresponded to the in silico one and, moreover, they seemed to vary according to enzyme concentration (Figure 1). MboII endonuclease is heat-sensitive, and enzyme inactivation can be obtained after a 15-min incubation at 50°C (3). To verify enzyme-inactivaBenchmarks
A 9.87 nW 1 kS/s 8.7 ENOB SAR ADC for implantable epileptic seizure detection microsystems

This paper presents an ultra low-power SAR ADC in 0.18 μm CMOS technology for epileptic seizure detection applications. The ADC is powered by a single supply voltage of both analog and digital circuits to avoid using the level-shifters. A latched comparator is used to quickly generate the comparison results while consuming no DC current. Split-cap architecture with an attenuation cap is used to minimize area and to further reduce the power consumption. A smaller-than-unit capacitor is used at the end of the least significant bit array to mitigate the negative impact of the parasitic components on the linearity of the capacitors array. As a result, both DNL/INL and SNDR of the ADC is improved. Our post-layout simulation shows that at 1 V supply, 1 kS/s the proposed SAR archives 8.7 ENOB while consuming only 9.87 nW. This yields an FOM of 23.7 fJ/conversion-step. Its leakage power consumption is 1.46 nW.
Cutting Edge: Identification of E-Cadherin as a Ligand for the Murine Killer Cell Lectin-Like Receptor G11

The killer cell lectin-like receptor G1 (KLRG1) is expressed by NK cells and by T cells. In both humans and mice, KLRG1 identifies Ag-experienced T cells that are impaired in their proliferative capacity but are capable of performing effector functions. In this study, we identified E-cadherin as a ligand for murine KLRG1 by using fluorescently labeled, soluble tetrameric complexes of the extracellular domain of the murine KLRG1 molecule as staining reagents in expression cloning. Ectopic expression of E-cadherin in B16.BL6 target cells did not affect cell-mediated lysis by lymphokine-activated NK cells and by CD8 T cells but inhibited Ag-induced proliferation and induction of cytolytic activity of CD8 T cells. E-cadherin is expressed by normal epithelial cells, Langerhans cells, and keratinocytes and is usually down-regulated on metastatic cancer cells. KLRG1 ligation by E-cadherin in healthy tissue may thus exert an inhibitory effect on primed T cells.
Simulation and fabrication of a new novel 3D injectable biosensor for high throughput genomics and proteomics in a lab-on-a-chip device

Biosensors are used for the detection of biochemical molecules such as proteins and nucleic acids. Traditional techniques, such as enzyme-linked immuno-sorbent assay (ELISA), are sensitive but require several hours to yield a result and usually require the attachment of a fluorophore molecule to the target molecule. Micromachined biosensors that employ electrical detection are now being developed. Here we describe one such device, which is ultrasensitive, real-time, label free and localized. It is called the nanoneedle biosensor and shows promise to overcome some of the current limitations of biosensors. The key element of this device is a 10 nm wide annular gap at the end of the needle, which is the sensitive part of the sensor. The total diameter of the sensor is about 100 nm. Any change in the population of molecules in this gap results in a change of impedance across the gap. Single molecule detection should be possible because the sensory part of the sensor is in the range of bio-molecules of interest. To increase throughput we can flow the solution containing the target molecules over an array of such structures, each with its own integrated read-out circuitry to allow ‘real-time’ detection (i.e. several minutes) of label free molecules without sacrificing sensitivity. To fabricate the arrays we used electron beam lithography together with associated pattern transfer techniques. Preliminary measurements on individual needle structures in water are consistent with the design. Since the proposed sensor has a rigid nano-structure, this technology, once fully developed, could ultimately be used to directly monitor protein quantities within a single living cell, an application that would have significant utility for drug screening and studying various intracellular signaling pathways.