15 research outputs found

    Evaluating the effect of training along with fit testing on earmuff users in a Chinese textile factory

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    <p>A hearing protection fit testing was conducted on workers (n = 189) in a textile factory in southern China. The 3M E-A-Rfit Dual-Ear Validation System was used to measure the personal attenuation rating (PAR) on an over-the-head style earmuff at the work site. In addition, PARs were obtained several times throughout the same work shift to capture different fits on 39 workers. Follow-up visits were conducted in approximate 6-month or 12-month intervals to repeat the fit testing. Both the immediate and residual effects of training on the field attenuation of hearing protection devices obtained by workers, and the effects of training toward improving the attenuation and protection of earmuffs after a period of daily use, were observed. A questionnaire survey was used to assess the awareness of hearing health and motivation toward the use of earmuffs in a high temperature environment. The results showed that there were wide variations in PARs among the workers tested. The one-on-one training together with fit testing improved PAR and helped to reduce the negative impact caused by use of protective hair covers. Since earmuffs are often used for long periods of time (>1 year), repeating fit tests could be helpful in order to verify the attenuation received throughout their useful life.</p

    Periodic Fluorescent Silver Clusters Assembled by Rolling Circle Amplification and Their Sensor Application

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    A simple method for preparing DNA-stabilized Ag nanoclusters (NCs) nanowires is presented. To fabricate the Ag NCs nanowires, we use just two unmodified component strands and a long enzymatically produced scaffold. These nanowires form at room temperature and have periodic sequence units that are available for fluorescence Ag NCs assembled which formed three-way junction (TWJ) structure. These Ag NCs nanowires can be clearly visualized by confocal microscopy. Furthermore, due to the high efficiency of rolling circle amplification reaction in signal amplification, the nanowires exhibit high sensitivity for the specific DNA detection with a wide linear range from 6 to 300 pM and a low detection limit of 0.84 pM, which shows good performance in the complex serum samples. Therefore, these Ag NCs nanowires might have great potential in clinical and imaging applications in the future

    Image_2_Impacts of Acute Hypoxia on Alzheimer's Disease-Like Pathologies in APPswe/PS1dE9 Mice and Their Wild Type Littermates.TIF

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    <p>Alzheimer's disease (AD) is the most common form of dementia and pathologically featured by β-amyloid (Aβ) plaque deposition and hyper-phosphorylated tau aggregation in the brain. Environmental factors are believed to contribute to the pathogenesis and progression of AD. In the present study, we investigated the impacts of acute hypoxia on Aβ and tau pathologies, neuroinflammation, mitochondrial function, and autophagy in APP<sup>swe</sup>/PS1<sup>dE9</sup> AD mouse model. Male APP<sup>swe</sup>/PS1<sup>dE9</sup> transgenic (Tg) mice and their age-matched wild type (Wt) littermates were exposed to one single acute hypoxic episode (oxygen 7%) for 24 h. We found that acute hypoxia exposure increased the expressions of amyloid precursor protein (APP), anterior pharynx-defective 1 (APH1) and cyclin-dependent kinase 5 (CDK5), and promoted tau phosphorylation at T181 and T231 residues in both Tg and Wt mice. In addition, acute hypoxia also induced autophagy through the mammalian target of rapamycin (mTOR) signaling, elicited abnormal mitochondrial function and neuroinflammation in both Tg and Wt mice. In summary, all these findings suggest that acute hypoxia could induce the AD-like pathological damages in the brain of APP<sup>swe</sup>/PS1<sup>dE9</sup> mice and Wt mice to some extent.</p

    Data_Sheet_1_Impacts of Acute Hypoxia on Alzheimer's Disease-Like Pathologies in APPswe/PS1dE9 Mice and Their Wild Type Littermates.PDF

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    <p>Alzheimer's disease (AD) is the most common form of dementia and pathologically featured by β-amyloid (Aβ) plaque deposition and hyper-phosphorylated tau aggregation in the brain. Environmental factors are believed to contribute to the pathogenesis and progression of AD. In the present study, we investigated the impacts of acute hypoxia on Aβ and tau pathologies, neuroinflammation, mitochondrial function, and autophagy in APP<sup>swe</sup>/PS1<sup>dE9</sup> AD mouse model. Male APP<sup>swe</sup>/PS1<sup>dE9</sup> transgenic (Tg) mice and their age-matched wild type (Wt) littermates were exposed to one single acute hypoxic episode (oxygen 7%) for 24 h. We found that acute hypoxia exposure increased the expressions of amyloid precursor protein (APP), anterior pharynx-defective 1 (APH1) and cyclin-dependent kinase 5 (CDK5), and promoted tau phosphorylation at T181 and T231 residues in both Tg and Wt mice. In addition, acute hypoxia also induced autophagy through the mammalian target of rapamycin (mTOR) signaling, elicited abnormal mitochondrial function and neuroinflammation in both Tg and Wt mice. In summary, all these findings suggest that acute hypoxia could induce the AD-like pathological damages in the brain of APP<sup>swe</sup>/PS1<sup>dE9</sup> mice and Wt mice to some extent.</p

    Image_1_Impacts of Acute Hypoxia on Alzheimer's Disease-Like Pathologies in APPswe/PS1dE9 Mice and Their Wild Type Littermates.TIF

    No full text
    <p>Alzheimer's disease (AD) is the most common form of dementia and pathologically featured by β-amyloid (Aβ) plaque deposition and hyper-phosphorylated tau aggregation in the brain. Environmental factors are believed to contribute to the pathogenesis and progression of AD. In the present study, we investigated the impacts of acute hypoxia on Aβ and tau pathologies, neuroinflammation, mitochondrial function, and autophagy in APP<sup>swe</sup>/PS1<sup>dE9</sup> AD mouse model. Male APP<sup>swe</sup>/PS1<sup>dE9</sup> transgenic (Tg) mice and their age-matched wild type (Wt) littermates were exposed to one single acute hypoxic episode (oxygen 7%) for 24 h. We found that acute hypoxia exposure increased the expressions of amyloid precursor protein (APP), anterior pharynx-defective 1 (APH1) and cyclin-dependent kinase 5 (CDK5), and promoted tau phosphorylation at T181 and T231 residues in both Tg and Wt mice. In addition, acute hypoxia also induced autophagy through the mammalian target of rapamycin (mTOR) signaling, elicited abnormal mitochondrial function and neuroinflammation in both Tg and Wt mice. In summary, all these findings suggest that acute hypoxia could induce the AD-like pathological damages in the brain of APP<sup>swe</sup>/PS1<sup>dE9</sup> mice and Wt mice to some extent.</p

    Table_1_Impacts of Acute Hypoxia on Alzheimer's Disease-Like Pathologies in APPswe/PS1dE9 Mice and Their Wild Type Littermates.pdf

    No full text
    <p>Alzheimer's disease (AD) is the most common form of dementia and pathologically featured by β-amyloid (Aβ) plaque deposition and hyper-phosphorylated tau aggregation in the brain. Environmental factors are believed to contribute to the pathogenesis and progression of AD. In the present study, we investigated the impacts of acute hypoxia on Aβ and tau pathologies, neuroinflammation, mitochondrial function, and autophagy in APP<sup>swe</sup>/PS1<sup>dE9</sup> AD mouse model. Male APP<sup>swe</sup>/PS1<sup>dE9</sup> transgenic (Tg) mice and their age-matched wild type (Wt) littermates were exposed to one single acute hypoxic episode (oxygen 7%) for 24 h. We found that acute hypoxia exposure increased the expressions of amyloid precursor protein (APP), anterior pharynx-defective 1 (APH1) and cyclin-dependent kinase 5 (CDK5), and promoted tau phosphorylation at T181 and T231 residues in both Tg and Wt mice. In addition, acute hypoxia also induced autophagy through the mammalian target of rapamycin (mTOR) signaling, elicited abnormal mitochondrial function and neuroinflammation in both Tg and Wt mice. In summary, all these findings suggest that acute hypoxia could induce the AD-like pathological damages in the brain of APP<sup>swe</sup>/PS1<sup>dE9</sup> mice and Wt mice to some extent.</p

    Porous Collagen Sponge Loaded with Large Efficacy-Potentiated Exosome-Mimicking Nanovesicles for Diabetic Skin Wound Healing

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    Diabetic skin wounds are difficult to heal quickly due to insufficient angiogenesis and prolonged inflammation, which is an urgent clinical problem. To address this clinical problem, it becomes imperative to develop a dressing that can promote revascularization and reduce inflammation during diabetic skin healing. Herein, a multifunctional collagen dressing (CTM) was constructed by loading large efficacy-potentiated exosome-mimicking nanovesicles (L-Meseomes) into a porous collagen sponge with transglutaminase (TGase). L-Meseomes were constructed in previous research with the function of promoting cell proliferation, migration, and angiogenesis and inhibiting inflammation. CTM has a three-dimensional porous network structure with good biocompatibility, swelling properties, and degradability and could release L-Meseome slowly. In vitro experiments showed that CTM could promote the proliferation of fibroblasts and the polarization of macrophages to the anti-inflammatory phenotype. For in vivo experiments, on the 21st day after surgery, the wound healing rates of the control and CTM were 83.026 ± 4.17% and 93.12 ± 2.16%, respectively; the epidermal maturation and dermal differentiation scores in CTM were approximately four times that of the control group, and the skin epidermal thickness of the CTM group was approximately 20 μm, which was closest to that of normal rats. CTM could significantly improve wound healing in diabetic rats by promoting anti-inflammation, angiogenesis, epidermal recovery, and dermal collagen deposition. In summary, the multifunctional collagen dressing CTM could significantly promote the healing of diabetic skin wounds, which provides a new strategy for diabetic wound healing in the clinic

    Table_1_A normative modeling approach to quantify white matter changes and predict functional outcomes in stroke patients.docx

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    ObjectivesThe diverse nature of stroke necessitates individualized assessment, presenting challenges to case-control neuroimaging studies. The normative model, measuring deviations from a normal distribution, provides a solution. We aim to evaluate stroke-induced white matter microstructural abnormalities at group and individual levels and identify potential prognostic biomarkers.MethodsForty-six basal ganglia stroke patients and 46 healthy controls were recruited. Diffusion-weighted imaging and clinical assessment were performed within 7 days after stroke. We used automated fiber quantification to characterize intergroup alterations of segmental diffusion properties along 20 fiber tracts. Then each patient was compared to normative reference (46 healthy participants) by Mahalanobis distance tractometry for 7 significant fiber tracts. Mahalanobis distance-based deviation loads (MaDDLs) and fused MaDDLmulti were extracted to quantify individual deviations. We also conducted correlation and logistic regression analyses to explore relationships between MaDDL metrics and functional outcomes.ResultsDisrupted microstructural integrity was observed across the left corticospinal tract, bilateral inferior fronto-occipital fasciculus, left inferior longitudinal fasciculus, bilateral thalamic radiation, and right uncinate fasciculus. The correlation coefficients between MaDDL metrics and initial functional impairment ranged from 0.364 to 0.618 (p multi. Furthermore, MaDDLmulti demonstrated a significant enhancement in predictive efficacy compared to MaDDL (integrated discrimination improvement [IDI] = 9.62%, p = 0.005) and FA (IDI = 34.04%, p ConclusionMaDDLmulti allows for assessing behavioral disorders and predicting prognosis, offering significant implications for personalized clinical decision-making and stroke recovery. Importantly, our method demonstrates prospects for widespread application in heterogeneous neurological diseases.</p

    Photoinduced Electron Transfer Mediated by Coordination between Carboxyl on Carbon Nanodots and Cu<sup>2+</sup> Quenching Photoluminescence

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    Carbon nanodots (C-dots) have been widely used in sensing, such as detection of ions, small molecules and biomolecules, based on their photoluminescence (PL) quenching by metal ions. Though C-dots prepared by different methods exhibited various sensitives to metal ions, it is labor intensiveness and time-consuming for selecting synthetic route to obtain C-dots that meet requirements of practical applications. Hence, for the high selective and sensitive applications of C-dots, it is the effective approach to reveal the structure–property relationships in the quenching process. Herein, we present an insight into the mechanism of the PL quenching of C-dots by Cu<sup>2+</sup>. According to the results of PL, UV–vis absorption, time-resolved PL, and femtosecond transient absorbance measurements, we confirmed that the quenching occurs by a photoinduced electron transfer (PET) process from the photoexcited C-dots to the empty d orbits of Cu<sup>2+</sup> combining with C-dots. Meanwhile, through separate protecting functional groups on the surface of C-dots, the structure of C-dots coordinating with Cu<sup>2+</sup> is revealed to be carboxyl rather than hydroxyl groups. This study leads to a better understanding of the quenching of C-dots and takes an important step toward more rational design of C-dots-based sensor with high performance

    Achieving High-Performance Surface-Enhanced Raman Scattering through One-Step Thermal Treatment of Bulk MoS<sub>2</sub>

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    We present a strong Raman enhancement substrate through one-step thermal treatment of bulk MoS<sub>2</sub>. The substrate provides very efficient hot spots by using the rhodamine 6G (R6G) molecule as a probe. Raman and photoluminescence spectra of modified MoS<sub>2</sub> reveal the detailed mechanism for enhancing Raman signal of R6G. It is found that both the substrate roughness and the slight chemical bond broken on the surface are the main driven forces to induce the surface enhanced Raman scattering (SERS) effects. The minimum detectable concentration of R6G on the most optimized thermally treated MoS<sub>2</sub> can be as low as 10<sup>–8</sup> M. This synthetic approach is facile, sensitive, and reliable, which shows great potential to be an excellent SERS substrate for biological and chemical detection
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