114 research outputs found

    Iterative morphological and mollifier-based baseline correction for Raman spectra

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    In vivo Raman spectroscopy with low signal-to-noise ratio and strong, irregularly shaped fluorescence background imposes a challenge for automatic baseline correction methods. In this work, an approach that enables fast and efficient batch baseline correction has been developed, which is based on a morphological operation in combination with a mollifier algorithm. As this algorithm relies only on three parameters, which are determined by the given experimental conditions, it can be used for automatic and objective processing of many Raman spectra. The applicability of the baseline correction is demonstrated on resonance Raman spectra of beta-carotene mixed with fluorescent red ink as model system, on carotenoids in human skin, and on an excitation–emission map of the green alga Haematococcus pluvialis. In the future, the algorithm opens the potential for wide application in Raman spectra analysis in biological contexts. In particular, it greatly facilitates data processing in cases where special photochemical sample preparation or complex experimental baseline removal was required before. Similarly, processing data of experiments using resonant excitation techniques yielding strong fluorescence background is possible. This is the peer reviewed version of the following article: Koch, M.; Suhr, C.; Roth, B.; Meinhardt-Wollweber, M.: Iterative morphological and mollifier-based baseline correction for Raman spectra. In: Journal of Raman Spectroscopy 48 (2016), Nr. 2, S. 336-342, which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1002/jrs.5010/abstract. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.BMBF/MeDiOO/03V0826BMBF/03V082

    Informal caregivers during the COVID-19 pandemic perceive additional burden: findings from an ad-hoc survey in Germany

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    Background: While the relation between care involvement of informal caregivers and caregiver burden is well-known, the additional psychosocial burden related to care involvement during the COVID-19 pandemic has not yet been investigated. Methods: A total of 1000 informal caregivers, recruited offline, participated in a cross-sectional online survey from April 21 to May 2, 2020. Questionnaires were used to assess COVID-19-specific changes in the care situation, negative feelings in the care situation, problems with implementation of COVID-19 measures, concerns/excessive demands, loss of support, change in informal caregivers' own involvement in care and problems with provision, comprehension & practicability of COVID-19 information, and to relate these issues to five indicators of care involvement (i.e., being the main caregiver, high expenditure of time, high level of care, dementia, no professional help). Binomial and multiple regression analyses were applied. Results: Across indicators of care involvement, 25.5-39.7% reported that the care situation rather or greatly worsened during the COVID-19 pandemic, especially for those caring for someone with dementia or those usually relying on professional help. In a multiple regression model, the mean number of involvement indicators met was associated with age (beta = .18; CI .10-.25), excessive demands (beta = .10, CI .00-.19), problems with implementation of COVID-19 measures (beta = .11, CI .04-.19), an increase in caregiving by the informal caregivers themselves (beta = .14, CI .03-.24) as well as with no change in the amount of caregiving (beta = .18, CI .07-.29) and loss of support (beta = -.08, CI -.16-.00). No significant associations with the mean number of involvement indicators met were found for gender, educational level, change in the care situation, negative feelings, and provision, comprehension & practicability of COVID-19 information. Conclusion: Those caregivers who perceived extensive care burden were those who suffered most during the pandemic, calling for structural support by the healthcare system now and in the future

    Hvordan oplever vi kærlighed? Mikrofænomenologi som metode til beskrivelse af subjektive oplevelser

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    Det mikrofænomenologiske interview tilbyder antropologien en tilgang til at undersøge, hvordan vi som mennesker oplever den verden, vi er en del af. Metoden tager udgangspunkt i konkrete og som regel ganske korte subjektive oplevelser. Gennem en ikke-inducerende interviewteknik guides den interviewede til at genkalde sig en konkret oplevelse, hvorefter intervieweren systematisk spørger ind til, hvordan oplevelsen udfoldede sig. Teknikken gør det muligt at beskrive aspekter i en oplevelse, som vi ellers normalt ikke er opmærksomme paĚŠ. I denne artikel demonstreres metoden gennem eksempler fra et antropologisk forskningsprojekt om oplevelser af kærlighed

    90K, an interferon-stimulated gene product, reduces the infectivity of HIV-1

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    BACKGROUND: In response to viral infections, interferons induce the transcription of several hundred genes in mammalian cells. Specific antiviral functions, however, have only been attributed to a few of them. 90K/LGALS3BP has been reported to be an interferon-stimulated gene that is upregulated in individuals with cancer or HIV-1 infection. RESULTS: Here, we show that 90K expression dose-dependently decreased the particle infectivity of HIV-1 progeny. The lower infectivity of released particles correlated with reduced virion incorporation of mature envelope glycoproteins gp120 and gp41. Further, proteolytic processing of the gp160 precursor and surface expression of gp120 in the producer cell were impaired in the presence of 90K expression. In contrast, expression of Gag, Nef and Vpu, and virus release were not grossly affected by 90K expression. 90K-imposed restriction occurred in the absence of direct interaction of 90K with HIV-1 Env or entrapment of Env in the ER. The cell-associated, but not the secreted species of 90K, mediated the antiviral effect. A truncated version of human 90K, solely consisting of the two intermediate domains, displayed a similar antiviral activity as the full-length wildtype 90K, indicating that the N-terminal SRCR-like domain and the C-terminal domain are dispensable for 90K’s antiviral activity. The murine homolog of 90K, CypCAP (Cyclophilin C-associated protein), neither modulated particle infectivity of HIV-1 nor lowered the virion incorporation of mature gp120, suggesting a species-specific mode of action. 90K was expressed at basal levels in TZM-bl cells and in primary macrophages, and at low levels in CD4(+) T-cells and PBMCs. 90K’s susceptibility to IFN-mediated stimulation of expression was cell type-specific. siRNA-mediated knockdown of 90K in TZM-bl cells and primary macrophages enhanced the incorporation of Env glycoproteins into progeny virions, boosted the particle infectivity of released HIV-1, and accelerated HIV-1 spread. Conversely, treatment of HIV-1 infected macrophages with IFN-α induced 90K expression and lowered the particle infectivity of HIV-1. CONCLUSIONS: Thus, 90K constitutes a novel antiviral factor that reduces the particle infectivity of HIV-1, involving interference with the maturation and incorporation of HIV-1 Env molecules into virions

    Adenosine/A2B receptor signaling ameliorates the effects of ageing and counteracts obesity

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    The combination of aging populations with the obesity pandemic results in an alarming rise in non-communicable diseases. Here, we show that the enigmatic adenosine A2B receptor (A2B) is abundantly expressed in skeletal muscle (SKM) as well as brown adipose tissue (BAT) and might be targeted to counteract age-related muscle atrophy (sarcopenia) as well as obesity. Mice with SKM-specific deletion of A2B exhibited sarcopenia, diminished muscle strength, and reduced energy expenditure (EE), whereas pharmacological A2B activation counteracted these processes. Adipose tissue-specific ablation of A2B exacerbated age-related processes and reduced BAT EE, whereas A2B stimulation ameliorated obesity. In humans, A2B expression correlated with EE in SKM, BAT activity, and abundance of thermogenic adipocytes in white fat. Moreover, A2B agonist treatment increased EE from human adipocytes, myocytes, and muscle explants. Mechanistically, A2B forms heterodimers required for adenosine signaling. Overall, adenosine/A2B signaling links muscle and BAT and has both anti-aging and anti-obesity potential
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