gebhart/patrepeval huggingface dataset:
Induction of apoptotic cell death in hen granulosa cells by ceramide. (1996)

Recent studies have demonstrated that ovarian follicle atresia occurs extensively before follicle selection into the avian preovulatory hierarchy, and that this process is mediated via granulosa cell apoptosis. Subsequent to follicle selection, granulosa cells are inherently resistant to apoptosis, and such resistance is correlated with increased expression of death suppressor genes such as bcl-xlong. In the present studies we used this avian ovary model system to 1) identify cellular characteristics and mechanisms related to apoptotic cell death of granulosa cells in vitro, and 2) further characterize functional differences between apoptosis-susceptible (4- to 8-mm follicle) and apoptosis-resistant (preovulatory follicle) granulosa cells. Treatment of granulosa cells from the largest preovulatory follicle with N-octanoylsphingosine (C8-ceramide) results in pronounced oligonucleosome formation, a hallmark of apoptosis. That this is indicative of programmed cell death is supported by an increased incidence of pyknotic nuclei and apoptotic bodies in C8-ceramide-treated samples compared to that in control cultured cells. Tumor necrosis factor-alpha, a stimulator of ceramide production, actively promotes oligonucleosome formation in apoptosis-susceptible, but not in apoptosis-resistant, granulosa cells. Induction of apoptosis is also observed after exposure of apoptosis-resistant granulosa cells to sphingomyelinase treatment and UV irradiation, which are known to stimulate endogenous ceramide production, and to the anticancer drug, daunorubicin, which initiates de novo ceramide biosynthesis via activation of ceramide synthase. Although treatment of granulosa cells with fumonisin B1, a specific ceramide synthase inhibitor, blocks daunorubicin-stimulated oligonucleosome formation, UV-induced cell death is unaffected. Taken together, these results demonstrate that pharmacological factors known to mimic the actions of ceramide or stimulate ceramide production can induce oligonucleosome formation and programmed cell death in granulosa cells. More importantly, however, the ability of a physiologically relevant initiator of ceramide biosynthesis, tumor necrosis factor-alpha, to promote cell death is evident only in apoptosis-susceptible granulosa cells collected from atresia-prone prehierarchal follicles. These data provide support for ceramide as an important intracellular signaling mechanism, mediating granulosa cell apoptosis and follicle atresia.
Identification of SoxS-Regulated Genes in Salmonella enterica Serovar Typhimurium (2000)

Salmonella enterica serovar Typhimurium responds to superoxide-generating agents through soxR-mediated activation of the soxS gene, whose product, SoxS, is necessary for resistance to oxidative stress. The S. enterica serovar Typhimurium soxRS system also mediates redox-inducible resistance to diverse antibiotics, which may be relevant to clinical infections. In order to identify SoxS-regulated genes in S. enterica serovar Typhimurium, a lacI-regulated expression system for the S. enterica serovar Typhimurium soxS gene was developed. This system was used to demonstrate that soxS expression is sufficient for the induction of resistance to the superoxide-generating drug paraquat and for the transcriptional activation of the sodA and micF genes. In addition, a library of random lacZ insertions was generated and screened for clones displaying differential beta-galactosidase activity in the presence or absence of SoxS. This selection yielded six independent chromosomal lacZ transcriptional fusions that were activated by either artificial expression of SoxS or exposure of wild-type cells to micromolar concentrations of paraquat. Moreover, disruption of the inducible genes by the insertions rendered S. enterica serovar Typhimurium hypersensitive to millimolar concentrations of paraquat. Nucleotide sequence determination identified the disrupted genes as sodA (Mn-containing superoxide dismutase), fpr (NADPH:ferredoxin oxidoreductase), and ydbK (a putative Fe-S-containing reductase).
Role of Transforming Growth Factor Beta in Corneal Function, Biology and Pathology (2010)

Transforming growth factor-beta (TGFbeta) is a pleiotropic multifunctional cytokine that regulates several essential cellular processes in many parts of the body including the cornea. Three isoforms of TGFbeta are known in mammals and the human cornea expresses all of them. TGFbeta1 has been shown to play a central role in scar formation in adult corneas whereas TGFbeta2 and TGFbeta3 have been implicated to play a critical role in corneal development and scarless wound healing during embryogenesis. The biological effects of TGFbeta in the cornea have been shown to follow Smad dependent as well as Smad-independent signaling pathways depending upon cellular responses and microenvironment. Corneal TGFbeta expression is necessary for maintaining corneal integrity and corneal wound healing. On the other hand, TGFbeta is perhaps the most important cytokine in the pathogenesis of fibrotic disease in the cornea. Although the transformation of keratocytes to myofibroblasts induced by TGFbeta is largely believed to cause corneal fibrosis or scarring, the precise molecular mechanism(s) involved in this process is still unknown. Currently no drugs are available to treat corneal scarring effectively without causing significant side effects. Many approaches to treat TGFbeta-mediated corneal scarring are under investigation. These include blocking of TGFbeta, TGFbeta receptor, TGFbeta function and/or TGFbeta maturation. Other strategies such as modulating keratocyte proliferation, apoptosis, transcription and DNA condensation are also being investigated. The potential of gene therapy to neutralize the pathologic effects of TGFbeta has also been demonstrated recently.
Getting Mechanics Plugged in With Training (2008)

This article describes efforts by transit agencies to upgrade their mechanic training programs to reflect the increased complexity of transit bus mechanical systems, the aging of the maintenance mechanic population, and the difficulty in finding funds to pay for system maintenance and training of maintenance personnel. While the federal government will pay for up to 80 percent of the capital cost of a piece of equipment, there is no federal program to pay for maintenance or training. The result has been a learning gap, especially when it comes to electrical and electronic systems. Various agencies have put together partnerships with local colleges, unions and other parties to create training programs for current staff and to attract new employees to the transit maintenance field. Some observers predict that as much as 40 percent of the mechanic workforce will be retiring in the next five to 10 years, so that their younger successors need to be brought up to standards in the newest systems. Groups that have formed consortia for training initiatives are described, along with several agency programs that have developed in-house.
Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K +  channel GIRK2 (1997)

G protein-gated, inwardly rectifying K+ channels (GIRK) are effectors of G protein-coupled receptors for neurotransmitters and hormones and may play an important role in the regulation of neuronal excitability. GIRK channels may be important in neurodevelopment, as suggested by the recent finding that a point mutation in the pore region of GIRK2 (G156S) is responsible for the weaver (wv) phenotype. The GIRK2 G156S gene gives rise to channels that exhibit a loss of K+ selectivity and may also exert dominant-negative effects on G(betagamma)-activated K+ currents. To investigate the physiological role of GIRK2, we generated mutant mice lacking GIRK2. Unlike wv/wv mutant mice, GIRK2 -/- mice are morphologically indistinguishable from wild-type mice, suggesting that the wv phenotype is likely due to abnormal GIRK2 function. Like wv/wv mice, GIRK2 -/- mice have much reduced GIRK1 expression in the brain. They also develop spontaneous seizures and are more susceptible to pharmacologically induced seizures using a gamma-aminobutyric acid antagonist. Moreover, wv/- mice exhibit much milder cerebellar abnormalities than wv/wv mice, indicating a dosage effect of the GIRK2 G156S mutation. Our results indicate that the weaver phenotypes arise from a gain-of-function mutation of GIRK2 and that GIRK1 and GIRK2 are important mediators of neuronal excitability in vivo.
The pathway of L-ascorbic acid biosynthesis in the colourless microalga Prototheca moriformis (2003)

When mutant strain UV77-247 of Prototheca moriformis Kruger was fed d-[1-13C]Glc, it synthesized l-ascorbic acid (AA) with approximately three-quarters of the label at the C-1 position and the remaining label at the C-6 position, showing that AA is made by a non-inversion (retention) pathway, i.e. C-1 of Glc becomes C-1 of AA. The label present at C-6 is consistent with the glycolytic conversion of Glc to 3-carbon intermediates and subsequent gluconeogenesis. Compounds suggested as intermediates in inversion-type pathways were not converted to AA. Most strains converted Man to AA at a rate greater than they did Glc. Enzyme activities leading from Fru-6-P to the formation of GDP-Man were identified in all strains, but none of these activities correlated with the mutants' abilities to accumulate AA. However, there was a strong correlation between GDP-Man-3,5-epimerase activity and AA accumulation. Wild-type P. moriformis ATCC 75669 and mutant strains of varying AA-synthesizing abilities rapidly converted l-Gal or l-galactono-1,4-lactone to AA. Based on this data, a biosynthetic pathway from Glc to AA is proposed in which the epimerase is the rate-limiting activity in AA synthesis.
Ascorbate inhibits iNOS expression in endotoxin‐ and IFNγ‐stimulated rat skeletal muscle endothelial cells (2002)

Lipopolysaccharide endotoxin and interferon-gamma induced inducible nitric oxide synthase (iNOS) protein expression and nitrite/nitrate formation in microvascular endothelial cell cultures (ECs) derived from rat skeletal muscle. Pretreatment of ECs with ascorbate accumulated a large amount of ascorbate inside the cells and consequently decreased both intracellular oxidant level and iNOS induction. These effects of ascorbate were abolished in the presence of exogenous superoxide generated by xanthine oxidase/xanthine plus catalase but were not altered when N-nitro-L-arginine methyl ester was applied to inhibit nitric oxide synthesis. Ascorbate also attenuated the activation of transcription factor IRF-1 but not NF kappa B. These results indicate that ascorbate inhibits iNOS expression in ECs by an antioxidant mechanism independent of both NF kappa B activation and the reported negative feedback effect of nitric oxide.
A CD8 genomic fragment that directs subset-specific expression of CD8 in transgenic mice (1997)

Helper and cytotoxic T cell subsets require the expression of different coreceptors (CD4 and CD8, respectively) for their development and function. We have cloned the CD8 gene locus from genomic cosmid and P1 libraries and analyzed the region around the CD8alpha and CD8beta genes for gene expression regulatory elements. DNase I (DNase I) hypersensitivity analysis of 80 kb in the CD8 locus identified four clusters of putative regulatory regions, three of which are thymocyte specific. Transgenic mice carrying the cloned CD8alphabeta genomic locus and containing the identified DNase I-hypersensitive site clusters express the transgenic CD8 in a developmentally regulated, tissue-specific, and CD8 T cell subset-specific manner.
Nitrosated peptides and polyamines as endogenous mutagens in O6- alkylguanine-DNA alkyltransferase deficient cells (1997)

Mutants of Escherichia coli and Saccharomyces cerevisiae that lack O6-alkylguanine-DNA alkyltransferase activities have increased spontaneous mutation rates, indicating the presence of a cellular metabolite that can alkylate DNA. Bacterially catalysed nitrosation has been implicated previously in producing the endogenous alkylating agent(s). Here, nitrosated polyamines and azaserine, a model compound for nitrosated peptides, are shown to be mutagenic to E. coli ada ogt mutants deficient in O6-alkylguanine-DNA alkyltransferase activity. The mutagenicity of azaserine may be explained by its ability to methylate DNA, whereas nitrosated spermidine causes DNA damage that is susceptible to both nucleotide excision repair and O6-alkylguanine-DNA alkyltransferase activity, which indicates the generation of more bulky DNA adducts. Nitrosated peptides and polyamines are therefore potential endogenous mutagens that are harmful particularly in O6-alkylguanine-DNA alkyltransferase deficient cells.
New hydrophilicity scale derived from high-performance liquid chromatography peptide retention data: correlation of predicted surface residues with antigenicity and x-ray-derived accessible sites (1986)

A new set of hydrophilicity high-performance liquid chromatography (HPLC) parameters is presented. These parameters were derived from the retention times of 20 model synthetic peptides, Ac-Gly-X-X-(Leu)3-(Lys)2-amide, where X was substituted with the 20 amino acids found in proteins. Since hydrophilicity parameters have been used extensively in algorithms to predict which amino acid residues are antigenic, we have compared the profiles generated by our new set of hydrophilic HPLC parameters on the same scale as nine other sets of parameters. Generally, it was found that the HPLC parameters obtained in this study correlated best with antigenicity. In addition, it was shown that a combination of the three best parameters for predicting antigenicity further improved the predictions. These predicted surface sites or, in other words, the hydrophilic, accessible, or mobile regions were then correlated to the known antigenic sites from immunological studies and accessible sites determined by X-ray crystallographic data for several proteins.
Dispersive readout of a flux qubit at the single-photon level (2011)

A superconducting flux qubit is inductively coupled to a superconducting quantum interference device (SQUID) magnetometer, capacitively shunted to form a 1.294-GHz resonator. The qubit-state-dependent resonator frequency is weakly probed with a microwave signal and detected with a microstrip SQUID amplifier. At a mean resonator occupation $\overline{n}=1.5$ photons, the readout visibility is increased by a factor of 4.5 over that using a cryogenic semiconductor amplifier. As $\overline{n}$ is increased from 0.008 to 0.1, no reduction in ${T}_{1}$ is observed, potentially enabling continuous monitoring of the qubit state.
Myeloid specific human CD33 is an inhibitory receptor with differential ITIM function in recruiting the phosphatases SHP-1 and SHP-2 (2000)

CD33 is a myeloid specific member of the sialic acid-binding receptor family and is expressed highly on myeloid progenitor cells but at much lower levels in differentiated cells. Human CD33 has two tyrosine residues in its cytoplasmic domain (Y340 and Y358). When phosphorylated, these tyrosines could function as docking sites for the phosphatases, SHP-1 and/or SHP-2, enabling CD33 to function as an inhibitory receptor. Here we demonstrate that CD33 is tyrosine phosphorylated in the presence of the phosphatase inhibitor, pervanadate, and recruits SHP-1 and SHP-2. Co-expression studies suggest that the Src-family kinase Lck is effective at phosphorylating Y340, but not Y358, suggesting that these residues may function in the selective recruitment of adapter molecules and have distinct functions. Further support for overlapping, but nonredundant, roles for Y340 and Y358 comes from peptide-binding studies that revealed the recruitment of both SHP-1 and SHP-2 to Y340 but only SHP-2 to Y358. Analysis using mutants of SHP-1 demonstrated that binding Y340 of CD33 was primarily to the amino Src homology-2 domain of SHP-1. The potential of CD33 to function as an inhibitory receptor was demonstrated by its ability to down-regulate CD64-induced calcium mobilization in U937. The dependence of this inhibition on SHP-1 was demonstrated by blocking CD33-mediated effects with dominant negative SHP-1. This result implies that CD33 is an inhibitory receptor and also that SHP-1 phosphatase has a significant role in mediating CD33 function. Further studies are essential to identify the receptor(s) that CD33 inhibits in vivo and its function in myeloid lineage development. (Blood. 2000;96:483-490)
Low Density Lipoprotein Binds to Proprotein Convertase Subtilisin/Kexin Type-9 (PCSK9) in Human Plasma and Inhibits PCSK9-mediated Low Density Lipoprotein Receptor Degradation (2013)

Proprotein convertase subtilisin/kexin type-9 (PCSK9) is a secreted protein that binds to the epidermal growth factor-like-A domain of the low density lipoprotein receptor (LDLR) and mediates LDLR degradation in liver. Gain-of-function mutations in PCSK9 are associated with autosomal dominant hypercholesterolemia in humans. Size-exclusion chromatography of human plasma has shown PCSK9 to be partly associated with undefined high molecular weight complexes within the LDL size range. We used density gradient centrifugation to isolate LDL in plasma pooled from 5 normolipidemic subjects and report that >40% of total PCSK9 was associated with LDL. Binding of fluorophore-labeled recombinant PCSK9 to isolated LDL in vitro was saturable with a K(D) ∼ 325 nM. This interaction was competed >95% by excess unlabeled PCSK9, and competition binding curves were consistent with a one-site binding model. An N-terminal region of the PCSK9 prodomain (amino acids 31-52) was required for binding to LDL in vitro. LDL dose-dependently inhibited binding and degradation of cell surface LDLRs by exogenous PCSK9 in HuH7 cells. LDL also inhibited PCSK9 binding to mutant LDLRs defective at binding LDL. These data suggest that association of PCSK9 with LDL particles in plasma lowers the ability of PCSK9 to bind to cell surface LDLRs, thereby blunting PCSK9-mediated LDLR degradation.
Thermo-driven light controller by using thermal modulation of diffraction wavelength in holographic polymer dispersed liquid crystal grating (2014)

A microperiodic structure composed of polymer and liquid crystal (LC) phases, called holographic polymer dispersed liquid crystal (HPDLC), was fabricated based on a photo-induced phase separation technique by laser interferometric exposure. The diffraction wavelength of HPDLC gratings formed by different LC composites and grating structures was experimentally investigated by spectroscopic measurements as a function of temperature at around 30 &deg;C. The HPDLC gratings composed of nematic LC having low nematic to isotropic temperature (T<sub>NI</sub>) and film thickness of 25 &mu;m showed the switch of diffraction wavelength between visible and infrared lights by the change of temperature. The optical characteristics achieved in HPDLC gratings are expected to be applicable for the basis of diffractive type of thermodriven light controller which can supply visibility constantly for solar-ray control windows.
A rapid alkaline extraction procedure for screening recombinant plasmid DNA (1979)

A procedure for extracting plasmid DNA from bacterial cells is described. The method is simple enough to permit the analysis by gel electrophoresis of 100 or more clones per day yet yields plasmid DNA which is pure enough to be digestible by restriction enzymes. The principle of the method is selective alkaline denaturation of high molecular weight chromosomal DNA while covalently closed circular DNA remains double-stranded. Adequate pH control is accomplished without using a pH meter. Upon neutralization, chromosomal DNA renatures to form an insoluble clot, leaving plasmid DNA in the supernatant. Large and small plasmid DNAs have been extracted by this method.
2016 S/S 패션에 나타난 트렌드 컬러를 활용한 젤 네일아트 디자인연구 (2016)

현대인의 문화적인 잠재능력을 지지하는 생산과 소비기반의 산업적 경제구조는 의류 와 미용패션의 트렌드를 소비자 중심으로 대중화하는데 기여하고 있다. 의류와 미용 패션의 중심적인 명제는 개성과 유행을 아우르는 아름다움의 표현이다. 이러한 표현 욕구는 메이크업에 영향을 주어 다양한 문화적 소재로부터 색채, 재료, 방법, 디자인 등을 추출하여 모방적 또는 융합적으로 네일아트를 창조할 수 있는 기회를 제공하고 있다. 또한 시대적인 요구를 반영한 문화적인 욕구를 충족하기 위해서 네일아트에 의 류와 미용패션을 응용하는 경향이 증가하고 있어 이러한 경향을 반영하여 2016 패션 에 나타난 트렌드 컬러를 활용한 네일아트를 디자인하였다. 네일아트에 적합한 패턴 과 컬러 디자인을 선발하기 위해 2016 S/S 패션에 나타난 컬러 트렌드를 조사 및 분 석하였고 패션 섬유의 분석결과 얻어진 자료를 모티브로 제작한 젤 네일아트 작품은 독창성, 형태, 색상, 패션균형 등을 기준으로 평가하였다. 이와 같이 패션의 경향과 디 자인을 응용한 네일아트 작품을 연구, 제작, 분석, 평가하는 것은 미용학적 관점에서 메이크업의 예술적 수준을 향상시키는데 필요한 작업이라고 생각한다. 향후 의류패션 이외에도 다양한 예술적 소재를 반영한 네일아트의 구성과 표현을 위한 연구가 지속 되어야 할 것으로 사료된다.
Sacral nerve stimulation increases activation of the primary somatosensory cortex by anal canal stimulation in an experimental model (2011)

Brief sacral neuromodulation induces profound changes in anal canal representation on the primary somatosensory cortex, providing a plausible hypothesis concerning the mechanism of action of neuromodulation in the treatment of faecal incontinence.
Cancer cachexia and immunomodulation. (2012)

Cachexia is derived from the Greek words "kakos" meaning "bad" and "hexis" meaning "condition". Cachexia is a debilitating state of involuntary weight loss complicating malignant, infectious and inflammatory diseases. Several hypotheses for its etiology have been suggested including cytokines, circulating hormones, neuropeptides, neurotransmitters, and tumor-derived factors. Cachexia syndrome is caused predominantly by cytokines either produced by cancer or released by the immune system cells as a response to the presence of cancer, as well as other tumor products that induce profound lipolysis or protein degradation. Several strategies have been applied in the management of cachexia and related immunodeficiency including: 1.hypercaloric feeding;2.administration of glucocorticoids;3.progrestational drugs;4.cyproheptadine and other antiserotonergic drugs;5.branched-chain aminoacids;6.prokinetic agents;7.eicosapentanoic acid (EPA);8.cannabinoids;9.5'-deoxy-5-fluorouridine;10.emerging drugs: melatonin, thalidomide, beta2-agonists, non-steroidal anti-inflammatory drugs (NSAIDs);11.others:pentoxifylline, hydrazine sulfate, anabolic steroids. Better understanding of the mechanisms underlying cancer and cachexia leading to immune dysfunction has guided immunomodulatory strategies to reverse cachexia and immunodeficiency. The oncept is that the tumor itself may lead to cachexia and immune dysfunction but also cachexia is related and mediated with immune dysfunction. Thus the purpose is to affect the tumor itself and cachexia immune pathways in order to restore immune efficiency. However, more experimental and clinical studies are needed to evaluate the efficacy of immunomodulatory intervention in cancer cachexia and related immunodeficiency.