Miracle-dz/UniFAR-FTUs huggingface dataset:
Methanol oxidation genes in the marine methanotroph Methylomonas sp. strain A4

Methanol dehydrogenase has been purified from the type I marine methanotroph Methylomonas sp. strain A4 and found to be similar to other methanol dehydrogenase enzymes in subunit composition, molecular mass, and N-terminal sequence of the two subunits. A heterologous gene probe and a homologous oligonucleotide have been used to identify a DNA fragment from Methylomonas sp. strain A4 which contains moxF, the gene encoding the large subunit of methanol dehydrogenase. Protein expression experiments with Escherichia coli, immunoblotting of expression extracts, and partial DNA sequence determination have confirmed the presence of moxF on this DNA fragment. In addition, expression and immunoblot experiments have shown the presence of the genes for the small subunit of methanol dehydrogenase (moxI) and for the methanol dehydrogenase-specific cytochrome c (moxG). The moxG gene product has been shown to be cytochrome c552. The expression experiments have also shown that two other genes are present on this DNA fragment, and our evidence suggests that these are the homologs of moxJ and moxR, whose functions are unknown. Our data suggest that the order of these genes in Methylomonas sp. strain A4 is moxFJGIR, the same as in the facultative methylotrophs. The transcriptional start site for moxF was mapped. The sequence 5' to the transcriptional start does not resemble other promoter sequences, including the putative moxF promoter sequence of facultative methylotrophs. These results suggest that although the order of these genes and the N-terminal amino acid sequence of MoxF and MoxI are conserved between distantly related methylotrophs, the promoters for this gene cluster differ substantially.
Transitive Trust to Executables Generated During Runtime

Transitive trust is critical in trust computing technology. Transitive trust transits the system control to a second group of executable code based on its trustworthiness description, so as to build a trustworthy computing environment. The acquirement of trustworthy description of executable code is easy for static executables, but is almost impossible for dynamically generated codes (DGC) which software vendors do not carry any trustworthiness proof with the executables, and what's more unfortunately, this is the status in quo. The paper tries to present an associated input based determination framework (AIBDF) in which the trustworthiness can be identified and determined by its associated intermediate codes. AIBDF is designed for present-day applications, though it might cause false positives, the change cost is low and it is more feasible and realistic compared to proof carrying code technologies.
The evolution of pulsed modulators from the Marx generator to the Solid State Marx modulator and beyond

The pulsed modulator has evolved from the early spark gap Mark Generators thru many different design forms to the present in which the Marx design returns using Solid State switches. The paper will chronicle the different types of pulsed modulators, including hard tube/switched modulators, pulse forming network modulators, induction/fractional turn modulators and Marx type modulators. The use of the various types of modulators for short and long pulse operation is reviewed. The advantages and disadvantages of the different types of modulators are evaluated and their possible use in present requirements and future applications is discussed. In addition, the paper speculates on the possible evolutional direction in which modulators might change or develop in the future.
A wavelet-based technique for discrimination between faults and magnetising inrush currents in transformers

Summary form only given, as follows. This paper presents the development of a wavelet-based scheme, for distinguishing between transformer inrush currents and power system fault currents, which proved to provide a reliable, fast and computationally efficient tool. The operating time of the scheme is less than half power frequency cycle (based on 5 kHz sampling rate). In this work, a wavelet transform concept is presented. Feature extraction and method of discrimination between transformer inrush and fault currents is derived. A 132/11 kV, transformer connected to a 132 kV power system were simulated using EMTP. The generated data were used by the MATLAB to test the performance of the technique as to its speed of response, computational burden and reliability. The proposed scheme proved to be reliable, accurate and fast.
ARL 17477, a Potent and Selective Neuronal NOS Inhibitor Decreases Infarct Volume after Transient Middle Cerebral Artery Occlusion in Rats

We tested the effects of administration of a selective neuronal nitric oxide synthase (nNOS) inhibitor, ARL 17477, on ischemic cell damage and regional cerebral blood flow (rCBF), in rats subjected to transient (2 h) middle cerebral artery (MCA) occlusion and 166 h of reperfusion (n = 48) and in rats without MCA occlusion (n = 25), respectively. Animals were administered ARL 17477 (i.v.): 10 mg/kg; 3 mg/kg; 1 mg/kg; N-nitro-L-arginine (L-NA) 10 mg/kg L-NA 1 mg/kg; and Vehicle. Administration of ARL 17477 1 mg/kg, 3 mg/kg and 10 mg/kg reduced ischemic infarct volume by 53 (p < 0.05), 23, and 6.5%, respectively. L-NA 1 mg/kg and 10 mg/kg increased infarct volume by 2 and 15%, respectively (p > 0.05). Administration of ARL 17477 (10 mg/kg) significantly (p < 0.05) decreased rCBF by 27 ± 5.3 and 24 ± 14.08% and cortical NOS activity by 86 ± 14.9 and 91 ± 8.9% at 10 min or 3 h, respectively, and did not alter mean arterial blood pressure (MABP). L-NA (10 mg/kg) significantly reduced rCBF by 23 ± 9.8% and NOS activity by 81 ± 7% and significantly (p < 0.05) increased MABP. Treatment with 3 mg/kg and 1 mg/kg ARL 17477 reduced rCBF by only 2.4 ± 4.5 and 0%, respectively, even when NOS activity was reduced by 63 ± 13.4 and 45 ± 15.7% at 3 h, respectively, (p < 0.05). The data demonstrate that ARL 17477 inhibits nNOS in the rat brain and causes a dose-dependent reduction in infarct volume after transient MCA occlusion.
Digesting all the options: Laboratory testing for celiac disease

Abstract Celiac disease is a complex immune-mediated disorder that is triggered by ingestion of gluten and related proteins in genetically susceptible individuals. Under conditions of increased intestinal permeability, gluten-derived peptides can travel across the intestinal epithelium and undergo deamidation catalyzed by the tissue transglutaminase (TTG) enzyme. This renders them immunogenic in individuals expressing specific human leukocyte antigen (HLA) DQ heterodimers. The resulting immune response is characterized by the production of antibodies against both deamidated gliadin peptides (DGP) and TTG, generation of pro-inflammatory cytokines and activation of cytotoxic T cells. This response damages the intestinal epithelium resulting in the wide range of gastrointestinal and systemic symptoms observed in those with celiac disease. Celiac disease diagnosis has traditionally been based on biopsy and histological examination of the small intestine. While this approach is still considered the gold standard, it is invasive and susceptible to both false-positive and false-negative results. Several laboratory tests have become available to aid in the diagnosis and monitoring of celiac disease, and are the focus of this review. These include serological tests for celiac disease-specific antibodies such as anti-endomysial antibodies, anti-TTG antibodies and anti-DGP antibodies of both the immunoglobulin A (IgA) and immunoglobulin G (IgG) class, genetic tests to elucidate HLA DQ status and ancillary tests such as total IgA. While some have suggested that laboratory tests may replace intestinal biopsy in specific circumstances, others maintain that this procedure remains a critical component of celiac disease diagnosis. We review the analytical methodology, strengths, weaknesses, diagnostic performance and clinical utility of the various laboratory tests for celiac disease. Potential future markers and tests that are now considered obsolete are also discussed. Current clinical practice guidelines for the diagnosis and management of celiac disease from the European Society for Pediatric Gastroenterology, Hepatology and Nutrition, the American College of Gastroenterology and the World Gastroenterology Organisation are summarized, and important differences between these guidelines are highlighted.
Clinical and laboratory measures of postural balance in an elderly population.

The objective of this cross-sectional study was to compare scores on the Balance Scale with laboratory measures of postural sway and other clinical measures of balance and mobility. Thirty-one elderly subjects were assessed on the clinical measures and the laboratory tests of postural sway while standing still and in response to pseudorandom movements of the platform. The average correlation between the Balance Scale and the spontaneous sway measures was -. 55. It was slightly lower (r = -.38) for the same parameters measured during the pseudorandom tests. There were high correlations between the Balance Scale and the Balance Sub-Scale developed by Tinetti (r = .91), Barthel Mobility sub-scale (r = .67), and timed "Up and Go" (r = -.76). The Balance Scale was the most efficient measure (effect size > 1) to statistically discriminate between subjects according to their use of each type of mobility aide (walker, cane, no aids). These data contribute to existing information on the performance of the Balance Scale and supports the validity of the Balance Scale in this geriatric population.
Effects of saddle height, pedaling cadence, and workload on joint kinetics and kinematics during cycling.

CONTEXT It is not clear how noncyclists control joint power and kinematics in different mechanical setups (saddle height, workload, and pedaling cadence). Joint mechanical work contribution and kinematics analysis could improve our comprehension of the coordinative pattern of noncyclists and provide evidence for bicycle setup to prevent injury. OBJECTIVE To compare joint mechanical work distribution and kinematics at different saddle heights, workloads, and pedaling cadences. DESIGN Quantitative experimental research based on repeated measures. SETTING Research laboratory. PATIENTS 9 healthy male participants 22 to 36 years old without competitive cycling experience. INTERVENTION Cycling on an ergometer in the following setups: 3 saddle heights (reference, 100% of trochanteric height; high, +3 cm; and low, -3 cm), 2 pedaling cadences (40 and 70 rpm), and 3 workloads (0, 5, and 10 N of braking force). MAIN OUTCOME MEASURES Joint kinematics, joint mechanical work, and mechanical work contribution of the joints. RESULTS There was an increased contribution of the ankle joint (P=.04) to the total mechanical work with increasing saddle height (from low to high) and pedaling cadence (from 40 to 70 rpm, P<.01). Knee work contribution increased when saddle height was changed from high to low (P<.01). Ankle-, knee-, and hip-joint kinematics were affected by saddle height changes (P<.01). CONCLUSIONS At the high saddle position it could be inferred that the ankle joint compensated for the reduced knee-joint work contribution, which was probably effective for minimizing soft-tissue damage in the knee joint (eg, anterior cruciate ligament and patellofemoral cartilage). The increase in ankle work contribution and changes in joint kinematics associated with changes in pedaling cadence have been suggested to indicate poor pedaling-movement skill.
Induction of Protein Kinase PKR-dependent Activation of Interferon Regulatory Factor 3 by Vaccinia Virus Occurs through Adapter IPS-1 Signaling*

Interferon regulatory factor 3 (IRF-3) undergoes phosphorylation-induced activation in virus-infected cells and plays an important role in the antiviral innate immune response. The E3L protein encoded by vaccinia virus is known to impair phosphorylation and activation of IRF-3. Kinases in addition to IκB kinase-related kinases are implicated in the IRF-3-dependent antiviral response. To test in human cells the role of the protein kinase regulated by RNA (PKR) in IRF-3 activation, HeLa cells made stably deficient in PKR using an RNA interference strategy were compared with PKR-sufficient cells. Rapid phosphorylation and nuclear accumulation of IRF-3 were detected in PKR-sufficient cells following infection with E3L deletion mutant (ΔE3L) virus. By contrast, the full IRF-3 activation response was largely abolished in PKR-deficient cells. The ΔE3L virus-induced IRF-3 activation seen in PKR-sufficient cells was diminished by treatment with cytosine β-d-arabinofuranoside. Furthermore, the vaccinia mutant ts23, which displays increased viral double-stranded RNA production at 39 °C, induced PKR-dependent IRF-3 phosphorylation at 39 °C but not at 31 °C. Both IRF-3 phosphorylation and cell apoptosis induced by infection with ΔE3L virus were dependent upon RIG-I-like receptor signal transduction components, including the adapter IPS-1. These data suggest that PKR facilitates the host innate immune response and apoptosis in virus-infected cells by mediating IRF-3 activation through the mitochondrial IPS-1 signal transduction pathway.
A case of intravascular large B‐cell lymphoma mimicking erythema nodosum: the importance of multiple skin biopsies

Background: Intravascular lymphoma is a rare disease characterized by the proliferation of neoplastic monuclear cells within the lumens of small blood vessels. The neoplastic cells are usually of B‐cell origin, and rarely of T‐cell or histiocytic origin. Although this clinicopathological entity of lymphoma has not been listed in general pathological classifications such as REAL classification or the Working Formulation, it is recently in the WHO classification scheme, which is essentially an updated REAL scheme, and the EORTC classification scheme.
HOX gene network is involved in the transcriptional regulation of in vivo human adipogenesis

Adipogenesis is regulated by the sequential activation of a series of transcription factors: the C/EBP proteins of type β and δ trigger the process while PPARγ and C/EBPα induce the differentiation from pre‐adipocyte to adipocyte, followed by adipo‐specific gene expression. A number of observations suggest the involvement of genes controlling embryonal development in adipogenesis. In human thyroid follicular carcinoma, it has been recently identified an oncogenetic fusion protein resulting from the interaction between the isoform PPARγ1 of PPARγ and the homeoprotein encoded by the PAX‐8 gene. Recent observations have pointed out that gene expression associated with adipocyte differentiation in vivo and in vitro, although partially overlapping, is actually different. HOX genes make up a network of transcription factors (homeoproteins) controlling embryonal development as well as crucial functions of adult eukaryotic cells. The molecular organization of this network of 39 genes appears to be unique in the genome and probably acts regulating phenotypic cell identity. In the present study we have analyzed the expression of the complete HOX gene network, in vivo, in different deposits of human white adipose tissue and in embryonal brown adipose tissues. Most of the genes in the HOX network are active in white as well as brown adipose tissue. Furthermore HOX genes display a deposit‐specific expression in white adipose tissue. Moreover, expression of the paralogous group 4 genes (HOX A4, HOX B4, HOX C4, and HOX D4), together with that of isolated genes in the network, appears to discriminate between white and brown adipose tissue. This data allows us to postulate the involvement of the HOX network in transcriptional regulation of human adipogenesis and to hypothesize on the molecular mechanisms that could be implicated. © 2002 Wiley‐Liss, Inc.
Simultaneous T2* and diffusion measurements with 3He

It has recently been demonstrated that magnetic resonance (MR) imaging of human lungs and airways is possible with hyperpolarized gases such as 3He. Because the influence of the apparent transversal relaxation (T2* decay) and diffusion in 3He imaging have not been quantified, an imaging pulse sequence was developed to measure these two parameters simultaneously. The imaging pulse sequence generates two series of multiply recalled gradient echo images with both different echo‐spacings and diffusion‐sensitizing gradients. From differences in exponential signal decay between the two series, T2* and diffusion coefficients, D, of both hyperpolarized and unpolarized 3He samples could be measured on a standard clinical imager using a home‐built Helmholtz coil. In a hyperpolarized sample of pure 3He values of D = (1.8 ± 0.2) ± 10−4 m2/s and T2* = 36 ± 13 ms were measured, while D = (0.3 ± 0.1) · 10−4 m2/s and T2* = 136 ± 66 ms were found in a Boltzmann‐polarized 3He/O2 mixture.
Instruments to Identify Commercially Sexually Exploited Children: Feasibility of Use in an Emergency Department Setting

Objective This review examines the screening instruments that are in existence today to identify commercially sexually exploited children. The instruments are compared and evaluated for their feasibility of use in an emergency department setting. Methods Four electronic databases were searched to identify screening instruments that assessed solely for commercial sexual exploitation. Search terms included “commercially sexually exploited children,” “CSEC,” “domestic minor sex trafficking,” “DMST,” “juvenile sex trafficking,” and “JST. ” Those terms were then searched in combination with each of the following: “tools,” “instruments,” “screening,” “policies,” “procedures,” “data collection,” “evidence,” and “validity. ” Results Six screening instruments were found to meet the inclusion criteria. Variation among instruments included number of questions, ease of administration, information sources, scoring methods, and training information provided. Two instruments were determined to be highly feasible for use in the emergency department setting, those being the Asian Health Services and Banteay Srei's CSEC Screening Protocol and Greenbaum et al's CSEC/child sex trafficking 6-item screening tool. Conclusions A current dearth of screening instruments was confirmed. It is recommended that additional screening instruments be created to include developmentally appropriate instruments for preadolescent children. Numerous positive features were identified within the instruments in this review and are suggested for use in future screening instruments, including succinctness, a simple format, easy administration, training materials, sample questions, multiple information sources, designation of questions requiring mandatory reporting, a straightforward scoring system, and an algorithm format.
Secular changes in aerobic fitness test performance of Australasian children and adolescents.

INTRODUCTION There have been an increasing number of reports in recent years which have highlighted that the aerobic fitness test performances of Australian and New Zealand children and adolescents are declining. Some researchers have previously commented on secular changes in performance, but have used data dating back only to 1985. Using a metaanalytical approach, this study aimed to quantify the secular changes in the aerobic fitness test performances of Australasian (Australian and New Zealand) children and adolescents over the past half a century. METHODS Forty-six studies reporting on the aerobic fitness test performances of healthy Australasian children and adolescents were included in the analysis. Corrections for methodological variation were made where possible, and data for each aerobic fitness test were expressed in a common metric. Raw data were merged with pseudo data generated from reported means and standard deviations using Monte Carlo simulation. Changes in aerobic test performance were calculated at the country x age x sex x test level using least squares linear regression. RESULTS Secular changes were calculated for 161,419 6-17-year-old tested on five different maximal field-running tests of aerobic fitness between 1961 and 2002. Overall, the aerobic performance of young Australasians declined at an average rate of -0.24% per annum (95% confidence interval -0.22 to -0.26% per annum). The pattern of change, however, was not consistent over time. Early in the 1960s, changes in performance shifted from improvements to declines, with the rate of decline accelerating until about 1990, and slowing thereafter. Secular changes were reasonably similar for boys and girls, but quite different for children and adolescents. DISCUSSION/CONCLUSION There has been a marked decline in aerobic fitness test performances of Australasian children and adolescents in recent decades. It is likely that this secular decline is caused by a network of social, behavioral, physical, psychosocial and physiological factors.
The full-length Tat protein is required for TAR-independent, posttranscriptional trans activation of human immunodeficiency virus type 1 env gene expression

Tat is a protein that dramatically increases the expression of all genes expressed from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat through interaction with a cis-acting target sequence referred to as TAR (for trans-acting responsive region). The tat gene is divided into two coding exons which, when translated, result in the synthesis of an 86-amino-acid protein. However, the 72-amino-acid segment encoded by the first coding exon of tat is sufficient to encode a fully active Tat protein in known assays. We examined expression of the env gene from an LTR that lacks TAR (designated dTAR-env). Surprisingly, only the full-length Tat peptide trans activated expression of the env gene from dTAR-env. Comparison of RNA and protein expression of the env gene in the presence of Tat indicated that the mechanism of trans activation is posttranscriptional rather than transcriptional. To test whether the TAR-independent Tat function is specific to the HIV-1 env gene, we analyzed expression of heterologous genes from the long terminal repeat lacking TAR. These heterologous genes were not trans activated by Tat in the absence of a TAR element, which suggests that the second-exon peptide of Tat has a sequence-specific role in TAR-independent trans activation of the HIV-1 env gene. Analysis of a mutant in the 5' end of the env gene was used to identify a cis-acting sequence required for Tat responsiveness.
Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control) received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively). After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO). After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05), and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.