474 research outputs found

    A Qualitative Examination of the Needs of Mothers in College in the Rural Southeast

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    The purpose of my study was to understand student mothers that attended college in the rural southeast by using an ecological framework to examine the barriers and challenges that they encounter on college campuses. Additionally, the study identified support and the lack of support that the mothers received. The theoretical concepts of intensive mothering, role strain, and role conflict were also used to comprehend how parental obligations can conflict with the expectations of being a college student. In total, 14 participants that attended a mid-size university in the rural southeast agreed to be a part of the study. The criteria to participate was that a college student had to be at least 18 years of age, currently enrolled or last enrolled at a university or college within the last five years, parent to at least one child that is 18 years or younger. They all identified as mothers from various demographic backgrounds. A qualitative study was then conducted using a thematic analysis to compare the narrative experiences of the participants. The four primary themes that emerged from the data analysis included accommodations, campus restrictions, events and activities, and feeling uncomfortable. In summary, the results of the study may be used to develop programs and services to assist the needs of mothers that attend colleges and universities in rural communities. However, the study does have limitations such as no males agreed to participate and the sample size of the participants is too small to make the results generalizable

    Nonresonant hyper‐Raman and hyper‐Rayleigh scattering in benzene and pyridine

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    This is the publisher's version, also available electronically from http://scitation.aip.org/content/aip/journal/jcp/90/9/10.1063/1.456592.Nonresonant hyper‐Raman and hyper‐Rayleigh spectra excited at 1064 nm are reported for neat benzene and pyridine. The theory of Herzberg–Teller vibronic coupling in nonresonant and preresonant hyper‐Raman scattering is developed. Nonresonant hyper‐Raman scattering is shown to be vibronically induced by modes that efficiently couple strongly allowed one‐photon and two‐photon transitions. A weak and broad (55 cm− 1) hyper‐Rayleigh band was observed in benzene and attributed to collective scattering, while in pyridine, a much more intense and much narrower hyper‐Rayleigh band was observed. Only the a 2u vibration (ν1 1) was observed in the hyper‐Raman spectrum of benzene, while several strong bands were observed in pyridine. Possible vibronic‐coupling pathways are discussed for these modes. In addition, the observed hyper‐Raman spectrum of pyridine is compared to a recent calculation

    Reduced GABAergic Neuron Excitability, Altered Synaptic Connectivity, and Seizures in a KCNT1 Gain-of-Function Mouse Model of Childhood Epilepsy.

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    Gain-of-function (GOF) variants in K+ channels cause severe childhood epilepsies, but there are no mechanisms to explain how increased K+ currents lead to network hyperexcitability. Here, we introduce a human Na+-activated K+ (KNa) channel variant (KCNT1-Y796H) into mice and, using a multiplatform approach, find motor cortex hyperexcitability and early-onset seizures, phenotypes strikingly similar to those of human patients. Although the variant increases KNa currents in cortical excitatory and inhibitory neurons, there is an increase in the KNa current across subthreshold voltages only in inhibitory neurons, particularly in those with non-fast-spiking properties, resulting in inhibitory-neuron-specific impairments in excitability and action potential (AP) generation. We further observe evidence of synaptic rewiring, including increases in homotypic synaptic connectivity, accompanied by network hyperexcitability and hypersynchronicity. These findings support inhibitory-neuron-specific mechanisms in mediating the epileptogenic effects of KCNT1 channel GOF, offering cell-type-specific currents and effects as promising targets for therapeutic intervention

    Distinct degassing pulses during magma invasion in the stratified Karoo Basin – New insights from hydrothermal fluid flow modelling

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    Magma emplacement in organic‐rich sedimentary basins is a main driver of past environmental crises. Using a 2D numerical model, we investigate the process of thermal cracking in contact aureoles of cooling sills and subsequent transport and emission of thermogenic methane by hydrothermal fluids. Our model includes a Mohr‐Coulomb failure criterion to initiate hydrofracturing and a dynamic porosity/permeability. We investigate the Karoo Basin, taking into account host‐rock material properties from borehole data, realistic total organic carbon content, and different sill geometries. Consistent with geological observations, we find that thermal plumes quickly rise at the edges of saucer‐shaped sills, guided along vertically fractured high permeability pathways. Contrastingly, less focused and slower plumes rise from the edges and the central part of flat‐lying sills. Using a novel upscaling method based on sill‐to‐sediment ratio we find that degassing of the Karoo Basin occurred in two distinct phases during magma invasion. Rapid degassing triggered by sills emplaced within the top 1.5 km emitted ~1.6·103 Gt of thermogenic methane, while thermal plumes originating from deeper sills, carrying a 12‐times greater mass of methane, may not reach the surface. We suggest that these large quantities of methane could be re‐mobilized by the heat provided by neighboring sills. We conclude that the Karoo LIP may have emitted as much as ~22.3·103 Gt of thermogenic methane in the half million years of magmatic activity, with emissions up to 3 Gt/year. This quantity of methane and the emission rates can explain the negative δ13C excursion of the Toarcian environmental crisis. Key Points Sill geometry and emplacement depth as well as intruded host rock type are the main factors controlling methane mobilization and degassing Dehydration‐related porosity increase and pore‐pressure‐induced hydrofracturing are important mechanisms for a quick transport of methane from sill to the surface The Karoo Basin may have degassed ~22.3·103 Gt of thermogenic methane in the half million years of magmatic activit

    AXR1-ECR1 and AXL1-ECR1 heterodimeric RUB-activating enzymes diverge in function in Arabidopsis thaliana

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    RELATED TO UBIQUITIN (RUB) modification of CULLIN (CUL) subunits of the CUL-RING ubiquitin E3 ligase (CRL) superfamily regulates CRL ubiquitylation activity. RUB modification requires E1 and E2 enzymes that are analogous to, but distinct from, those activities required for UBIQUITIN (UBQ) attachment. Gene duplications are widespread in angiosperms, and in line with this observation, components of the RUB conjugation pathway are found in multiples in Arabidopsis. To further examine the extent of redundancy within the RUB pathway, we undertook biochemical and genetic characterizations of one such duplication event- the duplication of the genes encoding a subunit of the RUB E1 into AUXIN RESISTANT1 (AXR1) and AXR1-LIKE1 (AXL1). In vitro, the two proteins have similar abilities to function with E1 C-TERMINAL-RELATED1 (ECR1) in catalyzing RUB1 activation and RUB1-ECR1 thioester formation. Using mass spectrometry, endogenous AXR1 and AXL1 proteins were found in complex with 3HA-RUB1, suggesting that AXR1 and AXL1 exist in parallel RUB E1 complexes in Arabidopsis. In contrast, AXR1 and AXL1 differ in ability to correct phenotypic defects in axr1-30, a severe loss-of-function AXR1 mutant, when the respective coding sequences are expressed from the same promoter, suggesting differential in vivo functions. These results suggest that while both proteins function in the RUB pathway and are biochemically similar in RUB-ECR1 thioester formation, they are not functionally equivalent

    Optimisation of the RT-PCR detection of immunomagnetically enriched carcinoma cells

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    BACKGROUND: Immunomagnetic enrichment followed by RT-PCR (immunobead RT-PCR) is an efficient methodology to identify disseminated carcinoma cells in the blood and bone marrow. The RT-PCR assays must be both specific for the tumor cells and sufficiently sensitive to enable detection of single tumor cells. We have developed a method to test RT-PCR assays for any cancer. This has been investigated using a panel of RT-PCR markers suitable for the detection of breast cancer cells. METHODS: In the assay, a single cell line-derived tumor cell is added to 100 peripheral blood mononuclear cells (PBMNCs) after which mRNA is isolated and reverse transcribed for RT-PCR analysis. PBMNCs without added tumor cells are used as specificity controls. The previously studied markers epidermal growth factor receptor (EGFR), mammaglobin 1 (MGB1), epithelial cell adhesion molecule (EpCAM/TACSTD1), mucin 1 (MUC1), carcinoembryonic antigen (CEA) were tested. Two new epithelial-specific markers ELF3 and EphB4 were also tested. RESULTS: MUC1 was unsuitable as strong amplification was detected in 100 cell PBMNC controls. Expression of ELF3, EphB4, EpCAM, EGFR, CEA and MGB1 was found to be both specific for the tumor cell, as demonstrated by the absence of a signal in most 100 cell PBMNC controls, and sensitive enough to detect a single tumor cell in 100 PBMNCs using a single round of RT-PCR. CONCLUSIONS: ELF3, EphB4, EpCAM, EGFR, CEA and MGB1 are appropriate RT-PCR markers for use in a marker panel to detect disseminated breast cancer cells after immunomagnetic enrichment

    Modern Electronic Techniques Applied to Physics and Engineering

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    Contains reports on seven research projects.Office of Scientific Research and Development (OSRD) OEMsr-26

    Dystrophin Is Required for the Normal Function of the Cardio-Protective KATP Channel in Cardiomyocytes

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    Duchenne and Becker muscular dystrophy patients often develop a cardiomyopathy for which the pathogenesis is still unknown. We have employed the murine animal model of Duchenne muscular dystrophy (mdx), which develops a cardiomyopathy that includes some characteristics of the human disease, to study the molecular basis of this pathology. Here we show that the mdx mouse heart has defects consistent with alteration in compounds that regulate energy homeostasis including a marked decrease in creatine-phosphate (PC). In addition, the mdx heart is more susceptible to anoxia than controls. Since the cardio-protective ATP sensitive potassium channel (KATP) complex and PC have been shown to interact we investigated whether deficits in PC levels correlate with other molecular events including KATP ion channel complex presence, its functionality and interaction with dystrophin. We found that this channel complex is present in the dystrophic cardiac cell membrane but its ability to sense a drop in the intracellular ATP concentration and consequently open is compromised by the absence of dystrophin. We further demonstrate that the creatine kinase muscle isoform (CKm) is displaced from the plasma membrane of the mdx cardiac cells. Considering that CKm is a determinant of KATP channel complex function we hypothesize that dystrophin acts as a scaffolding protein organizing the KATP channel complex and the enzymes necessary for its correct functioning. Therefore, the lack of proper functioning of the cardio-protective KATP system in the mdx cardiomyocytes may be part of the mechanism contributing to development of cardiac disease in dystrophic patients
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