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  • 1
    ISSN: 0960-894X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0968-0896
    Keywords: acylation and deacylation ; amino acids. ; d-aminoacylase ; d-methionine ; enantioselectivity
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background  Epidermolytic palmoplantar keratoderma (EPPK) is an autosomal dominant inherited skin disorder characterized by diffuse yellow thickening of the skin of the palms and soles, sharply bordered with erythematous margins. Histologically and ultrastructurally, EPPK presents cytolysis of keratinocytes and abnormal aggregation of tonofilaments in the suprabasal layers of the epidermis. To date, 15 different mutations of the keratin 9 gene (KRT9) have been demonstrated to cause most cases of EPPK.Objectives  To identify the KRT9 mutation in a large Chinese family with EPPK.Methods  Denaturing high-performance liquid chromatography (DHPLC), DNA sequencing and allele-specific polymerase chain reaction (AS-PCR) were used to screen exon 1 of the KRT9 gene for sequence variations.Results  The DHPLC elution profiles of the DNA fragments amplified from the affected samples differed from those obtained from unaffected individuals, indicating that a sequence variation existed within the analysed fragment of KRT9. DNA sequencing revealed a novel insertion–deletion mutation in the exon 1 of KRT9, 497delAinsGGCT, resulting in the change of tyrosine166 to tryptophan and leucine (Y166delinsWL). AS-PCR confirmed the mutation was not a common polymorphism.Conclusions  The results suggest the molecular basis of EPPK in this Chinese family and provide further evidence that mutations in the helix initiation motif of keratin 9 underlie Chinese EPPK.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 77 (2000), S. 2982-2984 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Thermotropic nematic and chiral-nematic poly(p-phenylene)s were prepared into well-aligned films between fused-silica substrates in which conjugated backbones were uniaxially and helically oriented. With unpolarized photoexcitation at 350 nm, a nematic film produced a degree of linear polarization of 9 near the emission peak at 410 nm with no evidence of excimer formation. With the same photoexcitation of a chiral-nematic film, the degree of circular polarization was found to vary from −1.3 in the 390–430 nm spectral region to between +0.3 and +0.9 beyond the edge of the selective reflection band. The crossover behavior unique to light emission from the selective reflection region remains inexplicable with existing theories on light propagation through periodically structured films. © 2000 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We have measured the photoreflectance spectrum at 300 K from a lattice-matched InAlAs/InGaAs heterostructure bipolar transistor grown by molecular beam epitaxy. The energy features of photoreflectance spectra have been identified and the built-in dc electric fields and associated doping profiles have been evaluated in the n-InAlAs emitter from the observed Franz–Keldysh oscillations. The undoped InGaAs spacer between emitter and base was added on to change the built-in electric field. The results showed that the energy features above the InGaAs band gap are the transitions from the valence band to the quantized state of the conduction band. The quantum well of the conduction band is in the interface of the InAlAs and InGaAs heterojunction. The interface charge densities in the spacer channel are determined to be 3.54×1011 cm−2 and 4.22×1011 cm−2, corresponding to the samples with spacer thicknesses of 300 and 500 A(ring), respectively. A triangular potential profile model was used to calculate the microstructure in the potential well and electron energy transition. The theoretical and experimental results were compared and good agreements were also found.
    Type of Medium: Electronic Resource
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  • 6
    Publication Date: 2018-04-10
    Description: Airway epithelial cell death and inflammation are pathological features of chronic obstructive pulmonary disease (COPD). Mechanistic target of rapamycin (MTOR) is involved in inflammation and multiple cellular processes, e.g., autophagy and apoptosis, but little is known about its function in COPD pathogenesis. In this article, we illustrate how MTOR regulates cigarette smoke (CS)–induced cell death, airway inflammation, and emphysema. Expression of MTOR was significantly decreased and its suppressive signaling protein, tuberous sclerosis 2 (TSC2), was increased in the airway epithelium of human COPD and in mouse lungs with chronic CS exposure. In human bronchial epithelial cells, CS extract (CSE) activated TSC2, inhibited MTOR, and induced autophagy. The TSC2–MTOR axis orchestrated CSE-induced autophagy, apoptosis, and necroptosis in human bronchial epithelial cells; all of which cooperatively regulated CSE-induced inflammatory cytokines IL-6 and IL-8 through the NF-B pathway. Mice with a specific knockdown of Mtor in bronchial or alveolar epithelial cells exhibited significantly augmented airway inflammation and airspace enlargement in response to CS exposure, accompanied with enhanced levels of autophagy, apoptosis, and necroptosis in the lungs. Taken together, these data demonstrate that MTOR suppresses CS-induced inflammation and emphysema—likely through modulation of autophagy, apoptosis, and necroptosis—and thus suggest that activation of MTOR may represent a novel therapeutic strategy for COPD.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 7
    Publication Date: 2018-04-10
    Description: Increasing toxicological and epidemiological studies have demonstrated that ambient particulate matter (PM) could cause adverse health effects including inflammation in the lung. Alveolar macrophages represent a major type of innate immune responses to foreign substances. However, the detailed mechanisms of inflammatory responses induced by PM exposure in macrophages are still unclear. We observed that coarse PM treatment rapidly activated mechanistic target of rapamycin (MTOR) in mouse alveolar macrophages in vivo, and in cultured mouse bone marrow–derived macrophages, mouse peritoneal macrophages, and RAW264.7 cells. Pharmacological inhibition or genetic knockdown of MTOR in bone marrow–derived macrophages leads to an amplified cytokine production upon PM exposure, and mice with specific knockdown of MTOR or ras homolog enriched in brain in myeloid cells exhibit significantly aggregated airway inflammation. Mechanistically, PM activated MTOR through modulation of ERK, AKT serine/threonine kinase 1, and tuberous sclerosis complex signals, whereas MTOR deficiency further enhanced the PM-induced necroptosis and activation of subsequent NF light-chain–enhancer of activated B cells (NFKB) signaling. Inhibition of necroptosis or NFKB pathways significantly ameliorated PM-induced inflammatory response in MTOR-deficient macrophages. The present study thus demonstrates that MTOR serves as an early adaptive signal that suppresses the PM-induced necroptosis, NFKB activation, and inflammatory response in lung macrophages, and suggests that activation of MTOR or inhibition of necroptosis in macrophages may represent novel therapeutic strategies for PM-related airway disorders.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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