Miracle-dz/UniFAR-FTUs huggingface dataset:
Actions of a carbocyanine dye on calcium‐dependent potassium transport in human red cell ghosts.

1. 3,3'‐Diethylthiadicarbocyanine iodide (diS‐C2‐(5)), a fluorescent dye widely used to estimate membrane potentials, inhibits the Ca‐dependent K transport system of human red cells and ghosts. It does not affect non‐specific cation leaks, net chloride movements or the Ca‐activated ATPase. 2. The nature of the inhibitory effect depends upon the conditions under which the dye is applied. When Ca‐containing ghosts with 100 mM internal K are suspended in a choline medium at 37 degrees C, 0.3 microM‐diS‐C2‐(5) causes virtually complete inhibition of K transport within 1 min (haematocrit 0.3%). Inhibition cannot be reversed by washing the ghosts to remove bound dye, although partial recovery occurs on subsequent incubation at 37 degrees C. 3. Inhibition is less marked when ghosts are suspended in solutions containing 100 mM‐K, and is largely reversed by washing. The degree of inhibition varies with the dye concentration: 50% inhibition occurs with a free diS‐C2‐(5) concentration of 0.7 microM, and about 5 x 10(6) dye molecules are bound per ghost. 4. Changes in internal and external K concentrations, keeping internal Ca constant, have no effect on the dye concentration required for 50% inhibition of K efflux. 5. When internal Ca is varied, keeping internal and external K constant, the dye concentration needed for 50% inhibition of K efflux varies inversely with the K efflux in the absence of dye. That is, diS‐C2‐(5) is most effective as an inhibitor when K efflux is at a maximum. This suggests that the dye reacts preferentially with the transport system in the Ca‐activated state. 6. The effects of several related molecules were examined, using Rb influx as a measure of K permeability. Inhibition is obtained in some cases, but is not directly related to the ability of the ghosts to bind the dyes. An anionic dye, diS‐C3SO3‐‐(5) inhibits Rb influx only when present inside the ghosts. 7. The implications of these findings are discussed.
Protein kinase C activation potently down‐regulates the expression of its major substrate, 80K, in Swiss 3T3 cells.

The amino acid sequence of 80K, the major acidic protein kinase C (PKC) substrate of Swiss 3T3 fibroblasts, was deduced from a cDNA nucleotide sequence. Overall, 25% of the predicted amino acid sequence is supported by direct protein sequence data. Southern blot analysis suggests that the mouse genome contains a single copy of this gene. Two 80K mRNA species, a major band of 2.25 kb and a minor band of 3.9 kb, were detected by Northern blot analysis. Stimulation of PKC by biologically active phorbol esters, including phorbol‐12, 13‐dibutyrate (PDB), reduced the steady state level of 80K mRNA to 8.8% of control within 5–7 h. This effect was dose‐dependent, and was abolished by prior depletion of PKC. The PDB‐induced down‐regulation of 80K mRNA levels was transient, and recovery coincided with the disappearance of PKC activity. A similar transient decrease in 80K mRNA levels was also demonstrated in tertiary cultures of mouse embryo fibroblasts. The down‐regulation of 80K mRNA levels was completely abolished by actinomycin D, cycloheximide or anisomycin if added up to 30 min after PDB addition. Since the rate of transcription of the 80K gene was unaltered by PDB treatment, we concluded that the PKC‐induced down‐regulation of 80K mRNA is mediated by a post‐transcriptional mechanism. In addition, PDB transiently decreased the level of 80K protein within 14–18 h, thus reflecting the effects of this phorbol ester on mRNA expression.
Incremental Prognostic Value of Quantified Vulnerable Plaque by Cardiac Computed Tomography: A Pilot Study

Background: Coronary computed tomography (CT) angiography (CCTA) has the ability to detect, characterize, and quantify atherosclerotic plaques. The aim of our study was to evaluate the prognostic power of CCTA-quantified plaque subtypes. Materials and Methods: A total of 36 patients with adverse events and 36 Morise score–matched patients who remained event free on follow-up were identified. Using CCTA images, plaque subtype volumes in the major epicardial arteries were analyzed using predetermined attenuation ranges in Hounsfield units (HU): 1 to 30 HU (low attenuating), 31 to 70 HU (intermediate attenuating), 71 to 150 HU (high attenuating), and mean coronary lumen+2 SD to 1000 HU (calcified). Each epicardial artery was divided into proximal, mid, and distal segments, and plaque volumes were normalized for arterial segment length. Results: The baseline characteristics of the 2 cohorts were similar. Low-attenuation and intermediate-attenuation plaque volumes were greater in the proximal segments as well as in the entire length in the adverse event compared with the event-free group. High-attenuation plaque volume was increased only in the proximal segments in the adverse event group. There was no difference in the volume of calcified plaque between the 2 groups. The log rank test using a cutoff of 3.99 mm3/mm for combined intermediate and low plaque volume showed more adverse events in patients with a plaque volume of ≥3.99 mm3/mm. Conclusions: Adverse events appear to be associated with greater volumes of low-attenuation and intermediate-attenuation plaques that reflect lipid and fibrous atherosclerosis. The difference between the 2 groups is most apparent in the proximal epicardial arteries.
Real Time Compressive Sensing Video Reconstruction in Hardware

Compressive sensing has allowed for reconstruction of missing pixels in incomplete images with higher accuracy than was previously possible. Moreover, video data or sequences of images contain even more correlation, leading to a much sparser representation as demonstrated repeatedly in numerous digital video formats and international standards. Compressive sensing has inspired the design of a number of imagers which take advantage of the need to only subsample a scene, which reduces power consumption by requiring acquisition and transmission of fewer samples. In this paper, we show how missing pixels in a video sequence can be estimated using compressive sensing techniques. We present a real time implementation of our algorithm and show its application to an asynchronous time-based image sensor (ATIS) from the Austrian Institute of Technology. The ATIS only provides pixel intensity data when and where a change in pixel intensity is detected, however, noise randomly causes intensity changes to be falsely detected, thereby providing random samples of static regions of the scene. Unlike other compressive sensing imagers, which typically have pseudo-random sampling designed in at extra effort, the ATIS used here provides random samples as a side effect of circuit noise. Here, we describe and analyze a field-programmable gate array implementation of a matching pursuit (MP) algorithm for compressive sensing reconstruction capable of reconstructing over 1.9 million 8 × 8 pixel regions per second with a sparsity of 11 using a basis dictionary containing 64 elements. In our application to ATIS we achieve throughput of 28 frames per second at a resolution of 304 × 240 pixels with reconstruction accuracy comparable to that of state of the art algorithms evaluated offline.
Activation of PPARβ/δ inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release

The infiltration of PMNs into tissues is a prominent feature in inflammation. The mechanism underlying PMN recruitment depends on the release of chemotactic mediators and CAM expression on endothelial cells. The nuclear receptor PPARβ/δ is widely expressed in many tissues, including the vascular endothelium; however, its role in acute inflammation remains unclear. Using intravital microscopy in the mouse cremasteric microcirculation, we have shown that activation of PPARβ/δ by its selective ligand GW501516 inhibits TNF‐α‐induced leukocyte rolling flux, adhesion, and emigration in a dose‐dependant manner. Moreover, GW501516 reduced the expression of adhesion molecules such as ICAM‐1, VCAM‐1, and E‐selectin in the cremasteric postcapillary venules. Similarly, rolling and adhesion of hPMNs under physiological flow on TNF‐α‐activated HUVECs were also inhibited markedly by GW501516. These inhibitory responses of GW501516 on activated endothelium were accompanied by a reduction in TNF‐α‐induced endothelial GRO‐α release and VCAM‐1, E‐selectin, and ICAM‐1 mRNA expression. Taken together, our results show that PPARβ/δ modulates acute inflammation in vivo and in vitro under flow by targeting the neutrophil‐endothelial cell interaction.
Cloning and expression of genes encoding Haemophilus somnus antigens

A genomic library of Haemophilus somnus 2336, a virulent isolate from a calf with pneumonia (later used to reproduce H. somnus experimental pneumonia), was constructed in the cosmid vector pHC79. The gene bank in Escherichia coli DH1 was screened by filter immunoassay with convalescent-phase serum, which reacted with several outer membrane antigens of H. somnus. On Western blotting (immunoblotting) of immunoreactive colonies, five clones were found to express proteins which comigrated with H. somnus surface antigens. Three clones (DH1 pHS1, pHS3, and pHS4) expressed both a 120-kilodalton (kDa) antigen and a 76-kDa antigen, one clone (DH1 pHS2) expressed only the 76-kDa antigen, and the fifth clone (DH1 pHS5) expressed a 60-kDa antigen. The 120-kDa and 76-kDa antigens were found internally, whereas the 60-kDa protein was detected in the DH1 pHS5 culture supernatant as membrane blebs or insoluble protein. Both the H. somnus 120-kDa antigen and the recombinant 120-kDa antigen had immunoglobulin Fc-binding activity. Restriction endonuclease mapping demonstrated that the genomic DNA inserts of clones expressing the 76-kDa antigen shared a common 28.4-kilobase-pair region, and the three clones also expressing the 120-kDa antigen shared an additional 7.0-kilobase-pair region. The restriction endonuclease map of pHS5, which expressed the 60-kDa antigen, was not similar to the maps of the other four plasmids. Since these three H. somnus antigens reacted with protective convalescent-phase serum, the recombinants which express these proteins should be useful in further studies of protective immunity in bovine H. somnus disease.
Regulation of CO2 assimilation in Ralstonia eutropha: premature transcription termination within the cbb operon

In the facultatively chemoautotrophic bacterium Ralstonia eutropha (formerly Alcaligenes eutrophus), most genes required for CO2 assimilation via the Calvin cycle are organized within two highly homologous cbb operons located on the chromosome and on megaplasmid pHG1, respectively, of strain H16. These operons are subject to tight control exerted by a promoter upstream of the 5'-terminal cbbL gene that is regulated by the activator CbbR. The existence of subpromoters within the operons was now excluded, as determined with lacZ operon fusions to suitable cbb gene fragments in the promoter-probe vector pBK. Nevertheless, marked differential expression of the promoter-proximal ribulose-1,5-bisphosphate carboxylase-oxygenase genes cbbLS and the remaining distal genes occurs within the operons. Computer analysis revealed a potential stem-loop structure immediately downstream of cbbS that was suspected to be involved in the differential gene expression. Nuclease S1 mapping identified a major 3' end and a minor 3' end of the relatively stable cbbLS partial transcript just downstream of this structure. Moreover, operon fusions containing progressively deleted stem-loop structures showed that the structure primarily caused transcriptional termination downstream of cbbS rather than increased the segmental stability of the cbbLS transcript. Premature transcription termination thus represents an important mechanism leading to differential gene expression within the cbb operons.
Compact physical model of a-IGZO TFTs for circuit simulation

Amorphous InGaZnO (a-IGZO) is a candidate material for thin-film transistors (TFTs) owing to its large electron mobility. The development of high functionality circuits requires accurate and efficient circuit simulation that, in turn, is based on compact physical a-IGZO TFTs models. Here we propose a compact physical-based and analytical model of the drain current of a-IGZO TFTs. The model accounts for both trapped and free charges by means of an effective density of states that accurately approximate the actual a-IGZO density of states in the energy range relevant for the TFT operation. The model is implemented in a circuit simulator and it is validated with the measurements of both coplanar and staggered a-IGZO TFTs fabricated on flexible substrates.
Robust nonlinear control for spacecraft rendezvous and docking with disturbance observer

This paper presents a robust nonlinear control strategy for a cooperative spacecraft rendezvous and docking maneuver with coupled attitude and position dynamics. The nonlinear and coupled models of relative attitude and relative position motions are expressed in the pursuer body-fixed frame, respectively. Both parametric uncertainties and disturbances are estimated together by a second-order nonlinear disturbance observer. A robust control strategy based on feedback linearization is developed. It is proved that the states of the closed loop systems are uniformly ultimately bounded in presence of parametric uncertainties and disturbances by using Lyapunov theory. Theoretical conclusions are demonstrated by numerical simulations.
The use of neo adjuvant single-agent vinblastine for tumour shrinkage in a highly vascular paediatric low-grade glioma

Abstract Vinblastine has shown activity as second line treatment in Low Grade Glioma (LGG) in children as well as anti-angiogenic activity in vitro. A 5 year old girl presented with 6 week history of headaches. MRI demonstrated a right temporo-parietal mass with abnormal pathological vasculature including aneurysmal vessels. Biopsy showed a pilocytic astrocytoma. Due to increased risk from surgery, first line treatment with vinblastine was given. Over 10 months, progressive reduction of tumour vascularity was demonstrated. The tumour was then surgically removed after 14 months of therapy. To our knowledge, this is the first report in which vinblastine has been successfully used in LGG to obtain tumour shrinkage prior to total tumor resection in a high vascularized LGG.
Association study and mutational screening of SYNGR1 as a candidate susceptibility gene for schizophrenia

Objective Synaptogyrin 1 (SYNGR1) is a transmembrane protein of neurotransmitter-containing vesicle. Recently, suggestive association between SYNGR1 intragenic polymorphisms and schizophrenia has been reported in the Indian population. Furthermore, some rare nucleotide changes with a potential pathogenic effect have been found in Indian and Chinese schizophrenia patients. In this study, we have performed an association study and a resequencing analysis in an Italian sample. Methods Eight polymorphisms of the SYNGR1 gene were typed in a case–control sample consisting of 274 patients and 335 controls. In parallel, a mutational screening covering all SYNGR1 exons was conducted. Results Evidence of association has been found for rs715505 (P = 0.028), a marker already reported to be associated with the disease. Resequencing analysis revealed two novel polymorphisms and several rare variants (13 of 16 as new variants), some of which might have relevance for gene expression and function. Conclusion The results of our association study support a contribution of SYNGR1 to schizophrenia susceptibility. In addition, the resequencing analysis evidenced mutations with a potential functional role at the mRNA and/or protein level. Of particular interest is the p.isoc:S26G missense mutation identified in six patients (0.011) and three controls (0.004) which might be involved in the elimination of a potential protein kinase C phosphorylation site.
Apoptosis of Oligodendrocytes via Fas and TNF-R1 Is a Key Event in the Induction of Experimental Autoimmune Encephalomyelitis1

In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, immunization with myelin Ags leads to demyelination and paralysis. To investigate which molecules are crucial for the pathogenesis of EAE, we specifically assessed the roles of the death receptors Fas and TNF-R1. Mice lacking Fas expression in oligodendrocytes (ODCs) were generated and crossed to TNF-R1-deficient mice. To achieve specific deletion of a loxP-flanked fas allele in ODCs, we generated a new insertion transgene, expressing the Cre recombinase specifically in ODCs. Fas inactivation alone as well as the complete absence of TNF-R1 protected mice partially from EAE induced by the immunization with myelin ODC glycoprotein. The double-deficient mice, however, showed almost no clinical signs of EAE after immunization. Histological analysis revealed that demyelination was suppressed in CNS tissue and that lymphocyte infiltration was notably reduced. We conclude that the death receptors Fas and TNF-R1 are major initiators of ODC apoptosis in EAE. Although only moderate reduction of lymphocyte infiltration into CNS tissue was observed, the absence of these receptors appears to confer protection from demyelination and development of clinical disease.
Chimeric prion protein expression in cultured cells and transgenic mice

The efficient expression of exogenous prion protein (PrP) molecules in mouse neuroblastoma cells that are chronically infected with murine scrapie prions (ScN2a cells; Butler, D.A., et al., 1988, J. Virol. 62, 1558–1564) and in transgenic mice is described. This technology allows investigation of the PrP molecule for structural regions involved in determining species specificity, as well as ablation experiments designed to address the functionality of particular regions of the PrP molecule. Previous reports demonstrated that the PrP gene specifies the host range for susceptibility of transgenic animals to prions (Scott, M., et al., 1989, Cell 59, 847–857; Prusiner, S.B., et al., 1990, Cell 63, 673–686). Consistent with these results, we showed that Syrian hamster (SHa) PrP is ineligible for efficient conversion to PrPSc in ScN2a cells. By constructing a series of chimeric mouse (Mo)/SHaPrP genes, we developed an epitopically tagged functional variant of the MoPrP gene, which can efficiently form protease‐resistant PrP molecules upon expression in ScN2a cells. The presence of a defined epitope for an SHa‐specific monoclonal antibody allows the products of this chimeric gene to be discriminated from endogenous MoPrP and creates a useful reagent for exploring structure/function relationships via targeted mutagenesis. In addition, we developed a transgenic mouse expression vector by manipulation of an SHaPrP cosmid clone. This vector permits the efficient expression of foreign PrP genes in the brains of transgenic animals, enabling pathological consequences of in vitro mutagenesis to be studied.
Innervation of the carotid body: Immunohistochemical, denervation, and retrograde tracing studies

This review presents information about multiple neurochemical substances in the carotid body. Nerve fibers around blood vessels and glomus cells within the chemoreceptive organ contain immunoreactivities (IR) for tyrosine hydroxylase (TH), calcitonin gene‐related peptide (CGRP), substance P (SP), galanin (GAL), vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY), calretinin (CR), calbindin D‐28k (CB), parvalbumin (PV), and nitric oxide synthase (NOS). Parasympathetic neurons scattered around the carotid body contain VIP, choline acetyltransferase, and vanilloid receptor 1‐like receptor. In the mammalian carotid body, transection of the carotid sinus nerve (CSN) causes the absence or decrease of CGRP‐, SP‐, and NOS‐immunoreactive (IR) nerve fibers, whereas all NPY‐IR nerve fibers disappear after removal of the superior cervical ganglion. Most VIP‐IR nerve fibers disappear but a few persist after sympathetic ganglionectomy. In addition, the CSN transection appears to cause the acquisition of GAL‐IR in originally immunonegative glomus cells and nerve fibers within the rat carotid body. On the other hand, 4%, 25%, 17%, and less than 1% of petrosal neurons retrogradely labeled from the rat CSN contain TH‐, CGRP‐, SP‐, and VIP‐IR, respectively. In the chicken carotid body, many CGRP‐ and SP‐IR nerve fibers disappear after vagus nerve transection or nodose ganglionectomy. GAL‐, NPY‐, and VIP‐IR nerve fibers mostly disappear after removal of the 14th cervical ganglion of the sympathetic trunk. The origin and functional significance of the various neurochemical substances present in the carotid body is discussed. Microsc. Res. Tech. 59:188–195, 2002. © 2002 Wiley‐Liss, Inc.
Sequence-dependent Structural Variation in DNA Undergoing Intrahelical Inspection by the DNA glycosylase MutM*

Background: The molecular basis for sequence-dependent variation in DNA repair is poorly understood. Results: A systematic study of lesion encounter by MutM reveals major differences in stacking of the target oxoG. Conclusion: Sequence-dependent changes in base stacking may contribute to lesion extrusion and repair. Significance: This is the first structural study of sequence context effects on lesion recognition for a DNA repair enzyme. MutM, a bacterial DNA-glycosylase, plays a critical role in maintaining genome integrity by catalyzing glycosidic bond cleavage of 8-oxoguanine (oxoG) lesions to initiate base excision DNA repair. The task faced by MutM of locating rare oxoG residues embedded in an overwhelming excess of undamaged bases is especially challenging given the close structural similarity between oxoG and its normal progenitor, guanine (G). MutM actively interrogates the DNA to detect the presence of an intrahelical, fully base-paired oxoG, whereupon the enzyme promotes extrusion of the target nucleobase from the DNA duplex and insertion into the extrahelical active site. Recent structural studies have begun to provide the first glimpse into the protein-DNA interactions that enable MutM to distinguish an intrahelical oxoG from G; however, these initial studies left open the important question of how MutM can recognize oxoG residues embedded in 16 different neighboring sequence contexts (considering only the 5′- and 3′-neighboring base pairs). In this study we set out to understand the manner and extent to which intrahelical lesion recognition varies as a function of the 5′-neighbor. Here we report a comprehensive, systematic structural analysis of the effect of the 5′-neighboring base pair on recognition of an intrahelical oxoG lesion. These structures reveal that MutM imposes the same extrusion-prone (“extrudogenic”) backbone conformation on the oxoG lesion irrespective of its 5′-neighbor while leaving the rest of the DNA relatively free to adjust to the particular demands of individual sequences.
Comparison of SISO and MIMO techniques in 802.11n wireless local area network

In this paper we are introducing a new generation of 802.11n wireless network standard. The objective is to obtain numerical values for various measures of networking performance of 802.11n by simulating the system using Simulink. Our initial approach was to investigate the abilities of 802.11n standard to model a transmitter and receiver that communicated over a user defined channel. Traditional wireless communication systems use a single antenna for transmission and a single antenna for reception. Such systems are known as single input single output (SISO) systems. In recent years, significant progress has been made in developing systems that use multiple antennas at the transmitter and the receiver to achieve better performance. Such systems are known as multiple inputs multiple output (MIMO) systems [1]. We simulated a single OFDM symbol SISO system followed by Multiple Input Multiple Output system (MIMO). We tested the performance of the system using Matlab's built in bit-error rate (BER) tool in both SISO and MIMO Techniques. We also calculated different Variation in BER on varying Parameters like Delay and K factor.