Miracle-dz/UniFAR-FTUs huggingface dataset:
Combined transcranial alternating current stimulation and continuous theta burst stimulation: a novel approach for neuroplasticity induction

Non‐invasive brain stimulation can induce functionally relevant plasticity in the human cortex, making it potentially useful as a therapeutic tool. However, the induced changes are highly variable between individuals, potentially limiting research and clinical utility. One factor that might contribute to this variability is the level of cortical inhibition at the time of stimulation. The alpha rhythm (~ 8–13 Hz) recorded with electroencephalography (EEG) is thought to reflect pulsatile cortical inhibition; therefore, targeting non‐invasive brain stimulation to particular phases of the alpha rhythm may provide an approach to enhance plasticity induction. Transcranial alternating current stimulation (tACS) has been shown to entrain cortical oscillations in a frequency‐specific manner. We investigated whether the neuroplastic response to continuous theta burst stimulation (cTBS) was enhanced by timing bursts of stimuli to the peak or the trough of a tACS‐imposed alpha rhythm. While motor evoked potentials (MEPs) were unaffected when cTBS was applied in‐phase with the peak of the tACS‐imposed oscillation, MEP depression was enhanced when cTBS was applied in‐phase with the trough. This enhanced MEP depression was dependent on the individual peak frequency of the endogenous alpha rhythm recorded with EEG prior to stimulation, and was strongest in those participants classified as non‐responders to standard cTBS. These findings suggest that tACS may be used in combination with cTBS to enhance the plasticity response. Furthermore, the peak frequency of endogenous alpha, as measured with EEG, may be used as a simple marker to pre‐select those individuals likely to benefit from this approach.
Nasopharyngeal carcinoma with intracranial spread: CT and MR characteristics.

PURPOSE Nasopharyngeal carcinoma (NPC) frequently spreads intracranially. We compare CT and MRI in identifying intracranial spread and reexamine the route of infiltration. METHOD One hundred fourteen consecutive patients with proven NPC were evaluated prospectively with T1-, T2-weighted, contrast-enhanced MRI and CT. RESULTS MRI showed 35 (31%) patients with middle cranial fossa involvement. Twenty-nine (25%) patients had cavernous sinus infiltration, while six (5%) showed only dural thickening. The most common route of spread is through the foramen ovale (FO) (12/35 patients, 34%), followed by skull base destruction (6/35 patients, 17%), foramen lacerum (FL) (6/35 patients, 17%), sphenoid sinus (6/35 patients, 17%), and combined FO and FL (5/35 patients, 14%). Using MRI as a standard, CT demonstrated the following involvement: cavernous sinus in 26 of 29 (90%) patients, FO in 9 of 12 patients, skull base in 6 of 6 patients, FO and FL in 3 of 5 patients, FL in 6 of 6 patients, sphenoid sinus in 6 of 6 patients and dura in 0 of 18 patients. CONCLUSION It is believed that NPC most commonly spreads intracranially via the FL or by direct erosion. Perineural spread through the FO is an important route, which explains why with CT evidence of cavernous sinus involvement there may be no skull base erosion. These findings are best seen on MRI.
U3, U8 and U13 comprise a new class of mammalian snRNPs localized in the cell nucleolus.

Using anti‐(U3)RNP autoantibodies, we have isolated and characterized two additional small nucleolar RNAs from HeLa cells, which are less abundant than U3 RNA. Both RNAs possess a trimethylguanosine cap as judged by precipitation with anti‐TMG antibody, but are not precipitated by either anti‐Sm or anti‐La antibodies. In addition, both RNAs are not precipitable by anti‐Th serum, which recognizes another nucleolar RNP autoantigen. Sequence analysis revealed that one of these RNAs, 136 nucleotides long, is the human U8 homolog; while the other, 105 nucleotides long, represents a novel species which we designate U13. Both RNAs share with U3 two conserved sequences (boxes C and D). The role of one or both of these boxes in binding the common 34 kd antigenic protein, otherwise known as fibrillarin, is discussed. Fractionation of HeLa cells revealed that U8 and U13, like U3, reside in the nucleolus. In glycerol gradients both RNAs cosediment with larger structures possibly representing ribosomal precursors. We propose that U3, U8 and U13 comprise a new subset of mammalian snRNPs whose roles in ribosome biogenesis are discussed.
Influence of genetic and environmental factors in peripheral arterial disease natural history: Analysis from six years follow up

Background: Peripheral arterial disease (PAD) is a disease affecting million of patients worldwide. Though traditional cardiovascular risk factors have been associated with the development of PAD, the possible existence of an inherited genetic predisposition to PAD has been investigated in few familial aggregation studies. A link between genetics and PAD may open new avenues for the prevention of this morbid and mortal disorder. Aim: The aim of this study is to investigate a possible role of some genetic determinant involving into coagulation and homocysteine metabolism in the progression of PAD. Materials and Methods: We follow one-hundred patients affected by PAD for six years. We evaluated Ankle-Brachial Index (ABI) two times; first at the time of recruitment and then after six years, in order to assess the progression of disease. Genotypes for the genes of Factor V Leiden, Prothrombin or Factor II G20210A, Cystathionine Beta-Synthase 844ins68bp and Methylenetetrahydrofolate Reductase C677T was ascertained after taking blood samples. Chi-square test was performed to determinate the possible correlation of these genes and the most common environmental factors in the progression of PAD. Results: Genetic disorders resulting in high level of homocysteina or thrombophilic phenotype are not so frequent. None among the genetic factors we considered were correlated with PAD. Conclusion: PAD is a chronic disease whose course can be slowed down especially with the control of environmental risk factors. Genetic analyses are not useful to determine the disease progression or its tendency to remain stable.
A study on the economic impact of bariatric surgery.

OBJECTIVE To evaluate the private third-party payer return on investment for bariatric surgery the United States. STUDY DESIGN Morbidly obese patients aged 18 years or older were identified in an employer claims database of more than 5 million beneficiaries (1999-2005) using International Classification of Diseases, Ninth Revision, Clinical Modification code 278.01. Each of 3651 patients who underwent bariatric surgery during this period was matched to a control subject who was morbidly obese and never underwent bariatric surgery. Bariatric surgery patients and controls were matched based on patient demographics, selected comorbidities, and costs. METHODS Total healthcare costs for bariatric surgery patients and their controls were recorded for 6 months before surgery through the end their continuous enrollment. To account for potential differences in patient characteristics, we calculated the cost differential by estimating a Tobit model. A return on investment was estimated from the resulting coefficients. Costs were inflation adjusted to 2005 US dollars using the Consumer Price Index for Medical Care, and the cost savings were discounted by 3.07%, the month Treasury bill rate during the same period. RESULTS The mean bariatric surgery investment ranged from approximately $17,000 to $26,000. After controlling for observable patient characteristics, we estimated all costs to have been recouped within 2 years for laparoscopic surgery patients and within 4 years for open surgery patients. CONCLUSIONS Downstream savings associated with bariatric surgery are estimated to offset the initial costs in 2 to 4 years. Randomized or quasiexperimental studies would be useful to confirm this conclusion, as unobserved characteristics may influence the decision to undergo surgery and cannot be controlled for in this analysis.
Investigation Into the Quality Factor of Piezoelectric-on-Silica Micromachined Resonators

In this paper, we investigate loss mechanisms in piezoelectric-on-silica bulk acoustic wave resonators, including those resulting from thermoelastic damping (TED), surface roughness, and supporting tethers. Alternate resonator designs, piezoelectric materials, and fabrication processes are demonstrated to empirically test these loss mechanisms. Quality factors (Qs) in the order of ~16000 at a center frequency of 5 MHz have been consistently measured for aluminum nitride (AlN)-on-silica coupled-ring resonators. It is shown that neither TED nor surface losses are the dominant sources of loss for AlN-on-silica resonators in the megahertz regime. Instead, it is suggested that charge redistribution loss resulting from nonuniform strain across the piezoelectric layer is the dominant loss mechanism, with a charge redistribution Q of ~38000 at 5 MHz for AlN-on-silica devices. When all loss mechanisms are considered, the total Q is estimated to be 25000, a value comparable to the measured results of the piezoelectric-on-silica resonators of this paper.
Single-Fiber Study of Contractile and Biochemical Properties of Skeletal Muscles in Streptozotocin-Induced Diabetic Rats

Mechanically skinned, single muscle fibers, isometrically activated in pH and Ca2+ (Sr2+) buffered solutions were used to examine the function of the contractile apparatus in slow- and fast-twitch fibers from soleus (SOL, predominantly slow-twitch) and extensor digitorum longus (EDL, predominantly fast-twitch) muscles of streptozotocin (STZ)-induced diabetic rats and age-matched controls. Three and 14 days after STZ administration, the contractile properties of muscle fibers from diabetic rats did not differ significantly from those of controls with respect to several mechanical parameters, such as maximum Ca-activated tension, activation threshold, and sensitivity to Ca2+ and Sr2+. In contrast, 28 days after STZ administration, 37.5% of the fast-twitch EDL fibers developed maximum activated tensions (77.1 ± 10.4 kN/m2), which were significantly lower than those developed by controls (244.0 ± 14.3 kN/m2), and the slow-twitch SOL fibers displayed a significantly higher sensitivity to Ca2+ (and Sr2+) than the controls. All fibers from diabetic rats, including the low-tension EDL fibers and higher Ca sensitivity SOL fibers displayed control-like electrophoretic profiles of the major myofibrillar proteins. Taken together with data from earlier studies on the effects of long-term diabetes on whole skeletal muscle contractility, these results strongly suggest that 1) the decrease in tetanic tension output of EDL muscles induced by diabetes is caused mainly by direct effects of the diabetic condition on the contractile/regulatory system of a subpopulation of fast-twitch fibers, which develop little force, and 2) the diabetes-induced slowing of twitch times of SOL muscles is caused in part by the increased sensitivity to Ca2+ of the contractile apparatus in the slow-twitch fibers.
Multiplex Droplet Digital PCR Quantification of Recurrent Somatic Mutations in Diffuse Large B-Cell and Follicular Lymphoma.

BACKGROUND A plethora of options to detect mutations in tumor-derived DNA currently exist but each suffers limitations in analytical sensitivity, cost, or scalability. Droplet digital PCR (ddPCR) is an appealing technology for detecting the presence of specific mutations based on a priori knowledge and can be applied to tumor biopsies, including formalin-fixed paraffin embedded (FFPE) tissues. More recently, ddPCR has gained popularity in its utility in quantifying circulating tumor DNA. METHODS We have developed a suite of novel ddPCR assays for detecting recurrent mutations that are prevalent in common B-cell non-Hodgkin lymphomas (NHLs), including diffuse large B-cell lymphoma, follicular lymphoma, and lymphoplasmacytic lymphoma. These assays allowed the differentiation and counting of mutant and wild-type molecules using one single hydrolysis probe. We also implemented multiplexing that allowed the simultaneous detection of distinct mutations and an "inverted" ddPCR assay design, based on employing probes matching wild-type alleles, capable of detecting the presence of multiple single nucleotide polymorphisms. RESULTS The assays successfully detected and quantified somatic mutations commonly affecting enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) (Y641) and signal transducer and activator of transcription 6 (STAT6) (D419) hotspots in fresh tumor, FFPE, and liquid biopsies. The "inverted" ddPCR approach effectively reported any single nucleotide variant affecting either of these 2 hotspots as well. Finally, we could effectively multiplex hydrolysis probes targeting 2 additional lymphoma-related hotspots: myeloid differentiation primary response 88 (MYD88; L265P) and cyclin D3 (CCND3; I290R). CONCLUSIONS Our suite of ddPCR assays provides sufficient analytical sensitivity and specificity for either the invasive or noninvasive detection of multiple recurrent somatic mutations in B-cell NHLs.
The design of competitive manufacturing systems

The design of competitive, complex, modern manufacturing systems requires the consistent professional application of systems engineering skills of the highest order and requires changes from traditional organizational approaches to support the process. In the systems engineering approach attention must be paid to all factors, whether human, organizational or technical. A structured and methodical approach to systems engineering is essential to success, and a new breed of systems engineer and manager is needed who can understand and apply the approach in practice. (Based on a paper presented to the 4th International Conference on Systems Engineering, Lanchester Polytechnic, Coventry, UK, 10–12 September 1985.)
The −1541 C>T and +4259 G>T of TIM‐3 polymorphisms are associated with rheumatoid arthritis susceptibility in a Chinese Hui population

The T‐cell immunoglobulin and mucin domain 3 (TIM‐3) has been shown to be associated with susceptibility to rheumatoid arthritis (RA). In this study, we investigated the association of four single‐nucleotide polymorphisms (SNPs) of the TIM‐3 gene with RA susceptibility in Chinese Hui and Han groups. Using restriction fragment length or sequence‐specific primer–polymerase chain reaction (PCR), patients with RA and nonarthritis control individuals from these two ethnicities were analysed for SNPs of −1541 C>T, −882 T>C, −574 T>G and +4259 G>T, in the TIM‐3 gene. Our results demonstrated that the polymorphisms of +4259 G>T SNP of TIM‐3 gene was associated with the RA susceptibility in both the Hui (P < 0.01) and Han populations (P < 0.05). However, the −1541 C>T and −574 T>G SNPs were distinctly associated with RA for the Hui and Han populations, respectively. In addition, haplotype analysis found no statistically differences in the distribution of nine detected haplotype frequency between patients with RA and controls in this study (P > 0.05). These findings suggest that polymorphism of +4259 G>T in TIM‐3 gene may be one of the most important genetic factors associated with the RA susceptibility among different populations, and genetic variations of TIM‐3 gene contribute to RA susceptibility among different populations.
Koordinace v systémech s více roboty

This thesis deals with planning trips for multiple robots moving simultaneously in a common environment. Specifically, in a separate multiphase decoupled algorithm by Mike Paesgood is described and discussed that uses spanning tree to maintain collision-free paths. The first part describes the algorithm and is supplemented by own observations obtained during the study algorithm. The second part describes the implementation of this algorithm in C++, along with suggestions for improving some of its parts. The part of implementation is also the interface for system ROS and algorithm integration into the mechanism for the preparation of robots in the system SyRoTek. The third part presents the results of the proposed optimization and implemented algorithm results. The evaluation also presents a found solution for the illustrative example.
Technology independent degradation of minimum noise figure due to pad parasitics

In order to investigate the influence of pad parasitics on device noise performance, noise parameters on Si CMOS, GaAs MESFET and GaAs p-HEMT transistors were determined. Measurements of devices with various gate widths demonstrate that the parasitic losses of the pads substantially influence the noise performance independent of FET technology. To accurately separate the noise contribution of the pad and the device, a noise parameter de-embedding procedure has been developed. It is shown that for an improvement of minimum noise figure NF/sub min/ of devices on non ideal substrates, pad losses must be minimized. Especially for small input transistors of amplifiers, pad parasitics must be considered during device modeling and design. A mathematical procedure using noise correlation matrices allows the embedding and de-embedding of noise parameters.
Spontaneous intracerebral haemorrhages in Vestfold county.

BACKGROUND Limited information is available on the incidence and progress of spontaneous intracerebral haemorrhages in Norway. The objective of this article is to describe the frequency of and the prognosis for such haemorrhages in a geographically well-defined population. MATERIAL AND METHOD All patients admitted to Vestfold Hospital with a first-time spontaneous intracerebral haemorrhage during the period from 1 September 2010 to 31 May 2014 were included. Age, gender, risk factors, haemorrhaged volume, treatment and mortality were registered. For survivors, the use of nursing and rehabilitation resources was identified, as were neurological function and the ability to cope with daily activities after three months. RESULTS A total of 182 patients (102 men) were included. The incidence of first-time intracerebral haemorrhages amounted to 20.5/100 000/year. Altogether 25.8 % used anticoagulants prior to the haemorrhage, and 38.5 % used a platelet inhibitor. After two days 23.0 % had died, while the 30-day mortality amounted to 39.6 %. Warfarin use was associated with a significantly increased 90-day mortality when compared to no anticoagulation treatment (p = 0.002). Of those patients who were alive 90 days after their intracerebral haemorrhage, 50.0 % functioned very well according to their Barthel score, and 67.6 % had returned to their own homes. INTERPRETATION First-time spontaneous intracerebral haemorrhage is a serious event with high mortality.
Integral membrane proteins in the mitochondrial outer membrane of Saccharomyces cerevisiae

Mitochondria evolved from a bacterial endosymbiont ancestor in which the integral outer membrane proteins would have been β‐barrel structured within the plane of the membrane. Initial proteomics on the outer membrane from yeast mitochondria suggest that while most of the protein components are integral in the membrane, most of these mitochondrial proteins behave as if they have α‐helical transmembrane domains, rather than β‐barrels. These proteins are usually predicted to have a single α‐helical transmembrane segment at either the N‐ or C‐terminus, however, more complex topologies are also seen. We purified the novel outer membrane protein Om14 and show it is encoded in the gene YBR230c. Protein sequencing revealed an intron is spliced from the transcript, and both transcription from the YBR230c gene and steady‐state level of the Om14 protein is dramatically less in cells grown on glucose than in cells grown on nonfermentable carbon sources. Hydropathy predictions together with data from limited protease digestion show three α‐helical transmembrane segments in Om14. The α‐helical outer membrane proteins provide functions derived after the endosymbiotic event, and require the translocase in the outer mitochondrial membrane complex for insertion into the outer membrane.
Recombinant Extracellular Domains of Tetraspanin Proteins Are Potent Inhibitors of the Infection of Macrophages by Human Immunodeficiency Virus Type 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) infection of human macrophages can be inhibited by antibodies which bind to the tetraspanin protein CD63, but not by antibodies that bind to other members of the tetraspanin family. This inhibitory response was limited to CCR5 (R5)-tropic virus and was only observed using macrophages, but not T cells. Here, we show that recombinant soluble forms of the large extracellular domain (EC2) of human tetraspanins CD9, CD63, CD81, and CD151 produced as fusion proteins with glutathione S-transferase (GST) can all potently and completely inhibit R5 HIV-1 infection of macrophages with 50% inhibitory concentration values of 0.11 to 1.2 nM. Infection of peripheral blood mononuclear cells could also be partly inhibited, although higher concentrations of EC2 proteins were required. Inhibition was largely coreceptor independent, as macrophage infections by virions pseudotyped with CXCR4 (X4)-tropic HIV-1 or vesicular stomatitis virus (VSV)-G glycoproteins were also inhibited, but was time dependent, since addition prior to or during, but not after, virus inoculation resulted in potent inhibition. Incubation with tetraspanins did not decrease CD4 or HIV-1 coreceptor expression but did block virion uptake. Colocalization of fluorescently labeled tetraspanin EC2 proteins and HIV-1 virions within, and with CD4 and CXCR4 at the cell surfaces of, macrophages could be detected, and internalized tetraspanin EC2 proteins were directed to vesicular compartments that contained internalized dextran and transferrin. Collectively, the data suggest that the mechanism of inhibition of HIV-1 infection by tetraspanins is at the step of virus entry, perhaps via interference with binding and/or the formation of CD4-coreceptor complexes within microdomains that are required for membrane fusion events.
Live‐cell imaging reveals sustained centromere binding of CENP‐T via CENP‐A and CENP‐B

At the centromere, a network of proteins, the kinetochore, assembles in order to grant correct chromatin segregation. In this study the dynamics and molecular interactions of the inner kinetochore protein CENP‐T were analyzed employing a variety of fluorescence microscopy techniques in living human cells. Acceptor‐bleaching FRET indicates that CENP‐T directly associates with CENP‐A and CENP‐B. CENP‐T exchange into centromeres is restricted to the S‐phase of the cell cycle as revealed by FRAP, suggesting a coreplicational loading mechanism, as we have recently also demonstrated for CENP‐I. These properties make CENP‐T one of the basic inner kinetochore proteins with most further proteins binding downstream, suggesting a fundamental role of CENP‐T in kinetochore function. (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Quantum Simulation of Device Characteristics of Silicon Nanowire FETs

A quantum simulation of silicon nanowire field-effect transistors has been performed in the frame work of the effective mass theory, where the three-dimensional Poisson equation was solved self-consistently with the mode-space nonequilibrium Green's function equations in the ballistic transport regime. The dependence of the device performance on the gate length and width for three types of gate configuration has been studied, focusing on the contribution of the tunneling current to the total current. The effects of gate underlap and the corner rounding of silicon body on the device performance have been also investigated quantitatively, leading to the conclusions that the gate underlap is an important factor in improving the subthreshold characteristics of the device, but the corner rounding of silicon body is not a significant factor, especially for devices with silicon body width of a few nanometers