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Sökning: WFRF:(Parham P)

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1.
  • Dankert, André, 1986, et al. (författare)
  • Spin-Polarized Tunneling through Chemical Vapor Deposited Multilayer Molybdenum Disulfide
  • 2017
  • Ingår i: ACS Nano. - : AMER CHEMICAL SOC. - 1936-086X .- 1936-0851. ; 11:6, s. 6389-6395
  • Tidskriftsartikel (refereegranskat)abstract
    • The two-dimensional (2D) semiconductor molybdenum disulfide (MoS2) has attracted widespread attention for its extraordinary electrical-, optical-, spin-, and valley-related properties. Here, we report on spin-polarized tunneling through chemical vapor deposited multilayer MoS2 (∼7 nm) at room temperature in a vertically fabricated spin-valve device. A tunnel magnetoresistance (TMR) of 0.5–2% has been observed, corresponding to spin polarization of 5–10% in the measured temperature range of 300–75 K. First-principles calculations for ideal junctions result in a TMR up to 8% and a spin polarization of 26%. The detailed measurements at different temperature, bias voltages, and density functional theory calculations provide information about spin transport mechanisms in vertical multilayer MoS2 spin-valve devices. These findings form a platform for exploring spin functionalities in 2D semiconductors and understanding the basic phenomena that control their performance.
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  • Johansson, Linda, et al. (författare)
  • Cathelicidin LL-37 in Severe Streptococcus pyogenes Soft Tissue Infections in Humans
  • 2008
  • Ingår i: Infection and Immunity. - : American Society for Microbiology. - 1098-5522. ; 76:8, s. 3399-3404
  • Tidskriftsartikel (refereegranskat)abstract
    • Severe soft tissue infections, such as necrotizing fasciitis and severe cellulitis, caused by group A streptococcus (GAS) are rapidly progressing life-threatening infections characterized by massive bacterial load in the tissue even late after onset of infection. Antimicrobial peptides are important components of the innate host defence and cathelicidins have been shown to protect against murine necrotic skin infection caused by GAS. However, the streptococcal cysteine protease SpeB has been demonstrated to proteolytically inactivate the human cathelicidin LL-37 in vitro. Here we have investigated the expression of LL-37 and its interaction with GAS and SpeB during acute severe soft tissue infections by analyses of patient tissue biopsies. The results showed high amounts of LL-37, both the proform (hCAP18) and the mature peptide, present in the tissue. Confocal microscopy identified neutrophils as the main source of the peptide. A distinct co-localization between the bacteria and LL-37 could be noted, and bacterial load showed a positive correlation to the LL-37 levels. Areas with high LL-37 levels coincided with areas with high amounts of SpeB. Confocal microscopy confirmed a strong co-localization of GAS, SpeB and LL-37 at the bacterial surface. Taken together the findings of this study provides in vivo support that SpeB-mediated inactivation of LL-37 at the streptococcal surface represent a bacterial resistance mechanism at the infected tissue site in patients with severe GAS tissue infections.
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3.
  • Johansson, Linda, et al. (författare)
  • HMGB1 in severe soft tissue infections caused by Streptococcus pyogenes.
  • 2014
  • Ingår i: Frontiers in cellular and infection microbiology. - : Frontiers Media S. A.. - 2235-2988. ; 4:Jan 30
  • Tidskriftsartikel (refereegranskat)abstract
    • Extracellular High Mobility Group Box 1 (HMGB1) has been associated with acute and chronic inflammatory conditions. However, little is known about HMGB1 in necrotizing bacterial infections. We hypothesized that the local HMGB1 response is excessive in severe soft tissue infections (STIs), which are characterized by necrosis and hyperinflammation. To explore this, tissue biopsies were collected from patients with varying severity of Streptococcus pyogenes skin and STIs, including erysipelas, cellulitis, and necrotizing fasciitis. Tissue sections were immunostained for HMGB1, S. pyogenes, and inflammatory cell infiltrates and results quantified by acquired computerized image analysis (ACIA). HMGB1 expression increased in parallel to disease severity and was significantly higher in necrotizing fasciitis than in erysipelas (p = 0.0023). Confocal microscopy of sections co-stained for HMGB1 and cell markers revealed both extracellular and cytoplasmic HMGB1, the latter of which was found predominantly in macrophages. To further verify macrophages as main source of activation triggered HMGB1 release, human macrophages were infected with clinical S. pyogenes isolates. The results demonstrated infection triggered release of HMGB1. Dual staining's visualized HMGB1 in areas close to, but not overlapping, with neutrophils, indicating a potential chemotactic role. In vitro transmigration experiments showed a chemotactic effect of HMGB1 on neutrophils. The data furthermore provided in vivo support that HGMB1 may form immunostimulatory complexes with IL-1β. Taken together, the findings provide the first in vivo evidence that HMGB1 is abundant at the local site of severe bacterial STIs and its levels correlated to severity of infections; hence, indicating its potential value as a biomarker for tissue pathology.
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4.
  • Nordebo, S., et al. (författare)
  • An adjoint field approach to Fisher information-based sensitivity analysis in electrical impedance tomography
  • 2010
  • Ingår i: Inverse Problems. - : IOP Publishing. - 0266-5611 .- 1361-6420. ; 26:12
  • Tidskriftsartikel (refereegranskat)abstract
    • An adjoint field approach is used to formulate a general numerical framework for Fisher information-based sensitivity analysis in electrical impedance tomography. General expressions are given for the gradients used in standard least-squares optimization, i.e. the Jacobian related to the forward problem, and it is shown that these gradient expressions are compatible with commonly used electrode models such as the shunt model and the complete electrode model. By using the adjoint field formulations together with a variational analysis, it is also shown how the computation of the Fisher information can be integrated with the gradient calculations used for optimization. It is furthermore described how the Fisher information analysis and the related sensitivity map can be used in a preconditioning strategy to obtain a well-balanced parameter sensitivity and improved performance for gradient-based quasi-Newton optimization algorithms in electrical impedance tomography. Numerical simulations as well as reconstructions based on experimental data are used to illustrate the sensitivity analysis and the performance of the improved inversion algorithm in a four-electrode measurement set-up.
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  • Ebrahimi-Fakhari, Darius, et al. (författare)
  • Defining the clinical, molecular and imaging spectrum of adaptor protein complex 4-associated hereditary spastic paraplegia
  • 2020
  • Ingår i: Brain. - OXFORD ENGLAND. - 0006-8950 .- 1460-2156. ; 143:10, s. 2929-2944
  • Tidskriftsartikel (refereegranskat)abstract
    • Bi-allelic loss-of-function variants in genes that encode subunits of the adaptor protein complex 4 (AP-4) lead to prototypical yet poorly understood forms of childhood-onset and complex hereditary spastic paraplegia: SPG47 (AP4B1), SPG50 (AP4M1), SPG51 (AP4E1) and SPG52 (AP4S1). Here, we report a detailed cross-sectional analysis of clinical, imaging and molecular data of 156 patients from 101 families. Enrolled patients were of diverse ethnic backgrounds and covered a wide age range (1.0-49.3 years). While the mean age at symptom onset was 0.8 +/- 0.6 years [standard deviation (SD), range 0.2-5.0], the mean age at diagnosis was 10.2 +/- 8.5 years (SD, range 0.1-46.3). We define a set of core features: early-onset developmental delay with delayed motor milestones and significant speech delay (50% non-verbal); intellectual disability in the moderate to severe range; mild hypotonia in infancy followed by spastic diplegia (mean age: 8.4 +/- 5.1 years, SD) and later tetraplegia (mean age: 16.1 +/- 9.8 years, SD); postnatal microcephaly (83%); foot deformities (69%); and epilepsy (66%) that is intractable in a subset. At last follow-up, 36% ambulated with assistance (mean age: 8.9 +/- 6.4 years, SD) and 54% were wheelchair-dependent (mean age: 13.4 +/- 9.8 years, SD). Episodes of stereotypic laughing, possibly consistent with a pseudobulbar affect, were found in 56% of patients. Key features on neuroimaging include a thin corpus callosum (90%), ventriculomegaly (65%) often with colpocephaly, and periventricular white-matter signal abnormalities (68%). Iron deposition and polymicrogyria were found in a subset of patients. AP4B1-associated SPG47 and AP4M1-associated SPG50 accounted for the majority of cases. About two-thirds of patients were born to consanguineous parents, and 82% carried homozygous variants. Over 70 unique variants were present, the majority of which are frameshift or nonsense mutations. To track disease progression across the age spectrum, we defined the relationship between disease severity as measured by several rating scales and disease duration. We found that the presence of epilepsy, which manifested before the age of 3 years in the majority of patients, was associated with worse motor outcomes. Exploring genotype-phenotype correlations, we found that disease severity and major phenotypes were equally distributed among the four subtypes, establishing that SPG47, SPG50, SPG51 and SPG52 share a common phenotype, an 'AP-4 deficiency syndrome'. By delineating the core clinical, imaging, and molecular features of AP-4-associated hereditary spastic paraplegia across the age spectrum our results will facilitate early diagnosis, enable counselling and anticipatory guidance of affected families and help define endpoints for future interventional trials.
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  • Resultat 1-10 av 16
  • [1]2Nästa

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