Miracle-dz/UniFAR-FTUs huggingface dataset:
Assessing vibrotactile feedback strategies by controlling a cursor with unstable dynamics

Brain computer interface (BCI) control predominately uses visual feedback. Real arm movements, however, are controlled under a diversity of feedback mechanisms. The lack of additional BCI feedback modalities forces users to maintain visual contact while performing tasks. Such stringent requirements result in poor BCI control during tasks that inherently lack visual feedback, such as grasping, or when visual attention is diverted. Using a modified version of the Critical Tracking Task [1] which we call the Critical Stability Task (CST), we tested the ability of 9 human subjects to control an unstable system using either free arm movements or pinch force. The subjects were provided either visual feedback, `proportional' vibrotactile feedback, or `on-off' vibrotactile feedback about the state of the unstable system. We increased the difficulty of the control task by making the virtual system more unstable. We judged the effectiveness of a particular form of feedback as the maximal instability the system could reach before the subject lost control of it. We found three main results. First, subjects can use solely vibrotactile feedback to control an unstable system, although control was better using visual feedback. Second, `proportional' vibrotactile feedback provided slightly better control than `on-off' vibrotactile feedback. Third, there was large intra-subject variability in terms of the most effective input and feedback methods. This highlights the need to tailor the input and feedback methods to the subject when a high degree of control is desired. Our new task can provide a complement to traditional center-out paradigms to help boost the real-world relevance of BCI research in the lab.
An enhanced area-efficient on-chip compensation technique for power converters

A novel high area-efficient on-chip lag (PI) compensation technique for power converters is proposed in this paper. This technique combined current-mode with voltage-mode capacitor multiplier. The compensation capacitor can be reduced to smaller than 10% of the conventional one. This proposed technique is successfully verified by a boost converter system with current program mode (CPM) control. The system proves to be stable for loading conditions from 100mA to 300mA. While conventional compensation capacitor and resistor are 30pF and 2. 5MΩ, the proposed technique needs only 3pF and 1. 2MΩ consuming 8μA extra current.
Effects of cysteine on the pharmacokinetics of itraconazole in rats with protein‐calorie malnutrition

The effects of cysteine on the pharmacokinetics of itraconazole were investigated after intravenous, 20 mg/kg, and oral, 50 mg/kg, administration of the drug to control rats (fed for 4 weeks on 23% casein diet) and rats with PCM (protein‐calorie malnutrition, fed for 4 weeks on 5% casein diet) and PCMC (PCM with oral cysteine supplementation, 250 mg/kg, twice daily during the fourth week). After intravenous administration of itraconazole to rats with PCM, the area under the plasma concentration–time curve from time zero to time infinity (AUC) of itraconazole was significantly greater (3580 compared with 2670 and 2980 µg min/ml) than those in control rats and rats with PCMC (the values between control rats and rats with PCMC were not significantly different). The above data suggested that metabolism of itraconazole decreased significantly in rats with PCM due to suppression of hepatic microsomal cytochrome P450 (CYP) 3A23 in the rats. The results could be expected since in rats with PCM, the level of CYP3A23 decreased significantly as compared to control. Itraconazole was reported to be metabolized via CYP3A4 to several metabolites, including hydroxyitraconazole, in human subjects. Human CYP3A4 and rat CYP3A1 (CYP3A23) proteins have 73% homology. By cysteine supplementation (rats with PCMC), the AUC of itraconazole was restored fully to control levels. Copyright © 2003 John Wiley & Sons, Ltd.
Genome‐wide search for loss of heterozygosity in Burkitt lymphoma cell lines

The molecular biological characteristics of Burkitt lymphoma (BL), in addition to the presence of the Epstein‐Barr virus (EBV) in some forms, relies on well‐characterized alterations, such as MYC translocations and TP53 inactivations. To ascertain the number and location of other genome alterations, we used 191 polymorphic markers in a genome‐wide search for loss of heterozygosity (LOH) in 31 Burkitt lymphoma cell lines and their normal counterparts. We were able to distinguish two types of altered allelic patterns: a bona fide LOH profile, indicative of deletion (LOH), and a profile indicative of increased dosage (ID). The former type was most frequent at chromosome arm 17p, most likely indicating TP53 gene inactivation. Increased dosage at 1q was found almost exclusively in non‐EBV cell lines (P < 0.00004) and correlated well with karyotypic abnormalities affecting region 1q21‐25. Our results suggest that a gene important for BL pathogenesis is located in region 1q21‐25 and that the activation of this gene mimics the effects of EBV. © 2002 Wiley‐Liss, Inc.
P2Y purinergic receptor regulation of CFTR chloride channels in mouse cardiac myocytes

The intracellular signalling pathways and molecular mechanisms responsible for P2‐purinoceptor‐mediated chloride (Cl−) currents (ICl,ATP) were studied in mouse ventricular myocytes. In standard NaCl‐containing extracellular solutions, extracellular ATP (100 μm) activated two different currents, ICl,ATP with a linear I–V relationship in symmetrical Cl− solutions, and an inwardly rectifying cation conductance (cationic IATP). Cationic IATP was selectively inhibited by Gd3+ and Zn2+, or by replacement of extracellular NaCl by NMDG; ICl,ATP was Cl− selective, and inhibited by replacement of extracellular Cl− by Asp−; both currents were prevented by suramin or DIDS pretreatment. In GTPγS‐loaded cells, ICl,ATP was irreversibly activated by ATP, but cationic IATP was still regulated reversibly. GDPβS prevented activation of the ICl,ATP, even though pertussis toxin pretreatment did not modulate ICl,ATP. These results suggest that activation of ICl,ATP occurs via a G‐protein coupled P2Y purinergic receptor. The ICl,ATP persistently activated by GTPγS, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pharmacological properties of cystic fibrosis transmembrane conductance regulator (CFTR) Cl− channels. In ventricular cells of cftr−/− mice, extracellular ATP activated cationic IATP, but failed to activate any detectable ICl,ATP. These results provide compelling evidence that activation of CFTR Cl− channels in mouse heart are coupled to G‐protein coupled P2Y purinergic receptors.
Chlorogenic acid reduces the plasma glucose peak in the oral glucose tolerance test: effects on hepatic glucose release and glycaemia

The effects of chlorogenic acid (CA) on hepatic glucose output, blood glucose levels and on glucose tolerance were analysed. Hepatic uptake of CA and its effects on hepatic catabolism of L‐alanine and glucose‐6‐phosphatase (G‐6‐Pase) activity were also evaluated. CA (1 mM) inhibited about 40% of G‐6‐Pase activity (p < 0.05) in the microsomal fraction of hepatocytes, but no effect was observed on production of glucose from gluconeogenesis or on L‐alanine catabolism, at various concentrations of CA (0.33, 0.5 and 1 mM), in liver perfusion experiments. Since there were indications of a lack of uptake of CA by the liver, it is possible that this compound did not reach sufficiently high intracellular levels to inhibit the target enzyme. Accordingly, intravenous administration of CA also failed to provoke a reduction in blood glucose levels. However, CA did promote a significant reduction (p < 0.05) in the plasma glucose peak at 10 and 15 min during the oral glucose tolerance test, probably by attenuating intestinal glucose absorption, suggesting a possible role for it as a glycaemic index lowering agent and highlighting it as a compound of interest for reducing the risk of developing type 2 diabetes. Copyright © 2007 John Wiley & Sons, Ltd.
Frizzled‐7 and limb mesenchymal chondrogenesis: Effect of misexpression and involvement of N‐cadherin

Products of the Frizzled family of tissue polarity genes have been identified as putative receptors for the Wnt family of signaling molecules. Wnt‐signaling is implicated in the regulation of limb mesenchymal chondrogenesis, and our recent study indicates that N‐cadherin and related activities are functionally involved in Wnt‐7a‐mediated inhibition of chondrogenesis. By using an in vitro high‐density micromass culture system of chick limb mesenchymal cells, we have analyzed the spatiotemporal expression patterns and the effects on chondrogenesis of RCAS retroviral‐mediated misexpression of Chfz‐1 and Chfz‐7, two Frizzled genes implicated in chondrogenic regulation. Chfz‐1 expression was localized at areas surrounding the cartilaginous nodules at all time points examined, whereas Chfz‐7 expression was limited to cellular aggregates during initial mesenchymal condensation, and subsequently was down‐regulated from the centers toward the periphery of cartilage nodules at the time of chondrogenic differentiation, resembling the pattern of N‐cadherin expression. Chondrogenesis in vitro was inhibited and limited to a smaller area of the culture upon misexpression of Chfz‐7, but not affected by Chfz‐1 misexpression. Analyses of cellular condensation and chondrogenic differentiation showed that the inhibitory action of Chfz‐7 is unlikely to be at the chondrogenic differentiation step, but instead affects the earlier precartilage aggregate formation event. At 24 hr, expression of N‐cadherin, a key component of the cellular condensation phase of chondrogenesis, was delayed/suppressed in Chfz‐7 misexpressing cultures, and was limited to a significantly smaller cellular condensation area within the entire culture at 48 hr, when compared with control cultures. Chfz‐1 misexpressing cultures appeared similar to control cultures at all time points. However, neither Chfz‐1 nor Chfz‐7 misexpression affected mesenchymal cell proliferation in vitro. These results suggest that Chfz‐7 is active in regulating N‐cadherin expression during the process of limb mesenchymal chondrogenesis and that Chfz‐1 and Chfz‐7 are involved in different Wnt‐signaling pathways. © 2002 Wiley‐Liss, Inc.
Nanofiber-reinforced myocardial tissue-construct as ventricular assist device

Objectives This study aimed to create a myocardial tissue construct by tissue engineering to repair, replace, and regenerate damaged cardiac tissue. Methods and results Human cardiac muscles harvested from a homograft heart retrieval system were decellularized followed by coating with electrospun nanofibers to make them amenable to scaffolding. These processed cardiac tissues were nourished in modified media having ischemic cardiac tissue conditioned media in 6 separate experimental variants, and cord blood mononuclear cells were injected into 4 of them. On the 17th day of culture, the nanofiber-coated scaffolds injected with mononuclear cells and/or reinforced by electrical and mechanical forces, started contracting spontaneously at varying rates, while the control remain noncontractile. Histological staining confirmed the pre-culture acellularity as well as post-culture stem cell viability, and revealed expression of troponin I and cardiac myosin. The acellular processed scaffold when implanted into sheep ischemic myocardial apex revealed transformation into sheep myocardium after 4 months of implantation. Conclusion These results provide direct evidence for the re-cellularization of decellularized cardiac tissue grafts reinforced with a polymer nanofiber coating, by human mononuclear cells injection, leading to generation of a tissue-engineered myocardial construct.
A 0.65-V, 500-MHz Integrated Dynamic and Static RAM for Error Tolerant Applications

The diminishing returns provided by voltage scaling have led to a recent paradigm shift toward so-called “approximate computing,” where computation accuracy is traded off for cost in error-tolerant applications. In this paper, a novel approach to achieving the power–performance–area versus data integrity tradeoff is proposed by integrating robust static memory cells and error-prone dynamic cells within a single array. In addition, the resulting integrated dynamic and static random access memory (iD-SRAM) provides the ability to trade off power consumption and accuracy on-the-fly according to the current conditions and operating mode. A 4-kB iD-SRAM array was implemented in a low-power, 65-nm CMOS technology, providing as much as an 80% power reduction and a 20% area reduction as compared with standard approaches, when applied to a video decoder at 500 MHz.
Mortality Among Type 2 Diabetic Individuals and Associated Risk Factors: The Three City Study

The 10 year mortality experience was determined in a population‐based cohort of 540 Type 2 diabetic individuals. The association between potential risk factors and all causes mortality was examined. Diabetes was not mentioned anywhere on the death certificate in 46% of 274 decedents. Diseases of the circulatory system (ICD9‐390–459) accounted for the majority (62%) of deaths in this cohort. Ten‐year survival was poorer than expected for both men and women compared to the age‐ and sex‐matched Minnesota population. Standardized mortality ratios for selected causes of death indicated excess for cardiovascular disease (ICD9‐390–459), coronary heart disease (ICD9 410–414) and cerebrovascular disease. Baseline variables associated with all causes of mortality included age and a history of macrovascular disease. These findings indicate that mortality data significantly underestimate the magnitude of diabetes and that individuals with diabetes have poorer survival than non‐diabetic individuals.
Recombinant human IL‐7 administration in mice affects colony‐forming units‐spleen and lymphoid precursor cell localization and accelerates engraftment of bone marrow transplants

Murine reconstitution assays were used to investigate the effects of recombinant human interleukin‐7 (rhIL‐7) on myeloid and lymphoid precursors and on bone marrow engraftment. Reconstitution with bone marrow from rhIL‐7‐treated mice results in a 3.4‐fold decrease in total colony‐forming unit‐spleen (CFU‐S) activity (day 9) and an 18.1‐ and 11.9‐fold decrease in its ability to generate thymocytes and splenic B lineage cells, respectively. In contrast, after reconstitution with splenocytes from rhIL‐7‐treated mice, CFU‐S activity increased 23.6‐fold (day 9) and the thymocyte and splenic B lineage cell regenerative capacity increased by 4.0‐ and 3.2‐fold, respectively. In addition, CD43low+, B220low+ cells that contain pre‐pro‐B cells and pro‐B cells were expanded two‐ to threefold and Igμ‐, B220+, CD2‐ and Igμ‐, B220+, CD2+ B lineage cells were expanded approximately 10‐fold and 10‐ to 45‐fold (depending on the tissue examined), respectively, after rhIL‐7 treatment Administration of rhIL‐7 to irradiated mice transplanted with bone marrow resulted in accelerated T cell and B cell reconstitution by up to 2–4 weeks. Thus, rhIL‐7 administration affects the distribution of myeloid and lymphoid precursors. Moreover, rhIL‐7 administration accelerates murine bone marrow cell engraftment and therefore may be useful in reducing the engraftment time in bone marrow transplant patients. J. Leukoc. Biol. 58: 151–158; 1995.
The learning curve for laparoscopic cholecystectomy.

The introduction of laparoscopic cholecystectomy (LC) in 1987 has resulted in its wide acceptance by surgeons in the United States. Questions about proper training and learning curve for surgeons wishing to perform laparoscopic procedures have been raised during this period. We retrospectively evaluated 416 consecutive cholecystectomy cases that were performed by eight surgeons in a community teaching hospital. In this report, 374 patients had LC and 42 patients (10%) had an attempted LC, which had to be converted to an open cholecystectomy (CONV). Surgeons A and B performed 40% and 18% of all LC cases, respectively, and were classified as the surgeons with the highest volume of cases. Parameters, including conversion rate, operative time, and complications, were evaluated to define the learning curve. Surgeons A and B experienced 17% and 14% initial conversion rates for the first 35 cases, respectively. These rates dramatically dropped to an acceptable level (4% and 3%) with increased experience. The operative time for surgeon A for the first and last 35 cases improved from 97 +/- 25 min to 74 +/- 32 min (p = 0.01). Although the procedure time for surgeon B improved by 4 min, this difference was not statistically significant. The operative time for all cases was 81 +/- 31 min and 87 +/- 27 min, respectively, for surgeons A and B, which was significantly less than that for other surgeons (p = 0.01). A total of 12 patients experienced complications related to LC. Most of the complications (75%) occurred in the first 30 cases for all surgeons. (ABSTRACT TRUNCATED AT 250 WORDS)
Capabilities and limitations of DGGE for the analysis of hydrocarbonoclastic prokaryotic communities directly in environmental samples

Prokaryotic communities in pristine and oil‐contaminated desert soil, seawater, and hypersaline coastal soil were analyzed using culture‐dependent and culture‐independent approaches. The former technique was the dilution‐plating method. For the latter, total genomic DNA was extracted and the 16S rRNA genes were amplified using a universal bacterial primer pair and primer pairs specific for Actinobacteria, Gammaproteobacteria, and Archaea. The amplicons were resolved using denaturing gradient gel electrophoresis (DGGE) and sequenced, and the sequences were compared to those in GenBank. The plating method offered the advantages of capturing the targeted hydrocarbonoclastic microorganisms, counting them and providing cultures for further study. However, this technique could not capture more than a total of 15 different prokaryotic taxa. Those taxa belonged predominantly to the genera Alcanivorax, Pseudoxanthomonas, Bosea, Halomonas, and Marinobacter. The individual isolates in culture consumed between 19 and 50% of the available crude oil in 10 days. Although the culture‐independent approach revealed much more microbial diversity, it was not problem‐free. The subdivision primers exhibited satisfactory specificity, but they failed to capture all the available taxa. The universal bacterial primer pair ignored Actinobacteria altogether, although the primer pair specific for Actinobacteria captured many of them, for example, the genera Geodermatophilus, Streptomyces, Mycobacterium, Pontimonas, Rhodococcus, Blastococcus, Kocuria, and many others. Because most researchers worldwide use universal primers for PCR, this finding should be considered critically to avoid misleading interpretations.
Transneuronal regulation of tyrosine hydroxylase expression in olfactory bulb of mouse and rat

Peripheral afferent input regulates the expression of dopaminergic properties in a population of local circuit intrinsic neurons of the rodent olfactory bulb. Lesions of the olfactory receptor neurons produced in the mouse by intranasal irrigation with either ZnSO4 or Triton X-100 and in the rat by surgical deafferentation or axotomy are associated with a decrease in the levels of dopamine (DA), the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), the activity of the enzyme tyrosine hydroxylase (TH), bulb weight and an increase in norepinephrine (NE) levels in the olfactory bulb. The anatomical correlates of the biochemical sequelae of deafferentation of olfactory bulb DA neurons were studied using immunohistochemical techniques to localize TH. Within 3 to 4 weeks all lesions produced a dramatic and uniform reduction in TH staining of the juxtaglomerular DA neurons and their processes which was paralleled by a reduction in DA and DOPAC levels and bulb weight. Seven weeks following reversible chemical lesions produced by Triton X-100, DA and DOPAC levels and tissue weight as well as TH staining in the juxtaglomerular neurons returned to control levels. These observations suggested that DA neurons remained present even when not demonstrable with TH antibodies. Additional evidence for the continued presence of the DA neurons was the ability of the olfactory bulbs from both lesioned mouse and rat to synthesize DA from exogenously administered L-3,4-dihydroxyphenylalanine (l-DOPA). These data suggested that the decrease in DA levels and TH staining in the olfactory bulb following lesions of the olfactory receptor neurons were produced by transneuronal mechanisms since there was no direct injury of the bulb. Furthermore, the demonstration that following reinnervation, catecholamine synthetic capacity is restored suggests that the juxtaglomerular dopamine neurons remain in the bulb and that afferent receptor input is required for expression of TH enzyme.
Structure of the trypanosome cyanide-insensitive alternative oxidase

In addition to haem copper oxidases, all higher plants, some algae, yeasts, molds, metazoans, and pathogenic microorganisms such as Trypanosoma brucei contain an additional terminal oxidase, the cyanide-insensitive alternative oxidase (AOX). AOX is a diiron carboxylate protein that catalyzes the four-electron reduction of dioxygen to water by ubiquinol. In T. brucei, a parasite that causes human African sleeping sickness, AOX plays a critical role in the survival of the parasite in its bloodstream form. Because AOX is absent from mammals, this protein represents a unique and promising therapeutic target. Despite its bioenergetic and medical importance, however, structural features of any AOX are yet to be elucidated. Here we report crystal structures of the trypanosomal alternative oxidase in the absence and presence of ascofuranone derivatives. All structures reveal that the oxidase is a homodimer with the nonhaem diiron carboxylate active site buried within a four-helix bundle. Unusually, the active site is ligated solely by four glutamate residues in its oxidized inhibitor-free state; however, inhibitor binding induces the ligation of a histidine residue. A highly conserved Tyr220 is within 4 Å of the active site and is critical for catalytic activity. All structures also reveal that there are two hydrophobic cavities per monomer. Both inhibitors bind to one cavity within 4 Å and 5 Å of the active site and Tyr220, respectively. A second cavity interacts with the inhibitor-binding cavity at the diiron center. We suggest that both cavities bind ubiquinol and along with Tyr220 are required for the catalytic cycle for O2 reduction.