285 research outputs found

    Occupational Skin Diseases in Korea

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    Skin disease is the most common occupational disease, but the reported number is small in Korea due to a difficulty of detection and diagnosis in time. We described various official statistics and data from occupational skin disease surveillance system, epidemiological surveys and cases published in scientific journals. Until 1981, 2,222 cases of occupational skin disease were reported by Korean employee's regular medical check-up, accounting for 4.9% of the total occupational diseases. There was no subsequent official statistics to figure out occupational skin diseases till 1998. From 1999, the Korea Occupational Safety and Health Agency (KOSHA) published the number of occupational skin diseases through the statistics of Cause Investigation for Industrial Accidents. A total of 301 cases were reported from 1999 to 2007. Recent one study showed the figures of compensated occupational skin diseases. Many of them belonged to daily-paid workers in the public service, especially forestry workers. Also, it described the interesting cases such as vitiligo and trichloroethylene-induced Stevens-Johnson Syndrome. Skin diseases are still important though the number of cases has decreased, and therefore it is recommended to grasp the status of occupational skin diseases through continuous surveillance system and to make policy protecting high-risk group

    Prevalence of Allergic Diseases and Risk Factors of Wheezing in Korean Military Personnel

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    The objective of this study was to evaluate the prevalence of asthma, allergic rhinitis, and atopic dermatitis, as well as the risk factors of wheezing among young adults in the Korean military. Young military conscripts in five areas completed a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire. For subjects with current wheeze in one sample area, baseline spirometry and bronchodilator response were measured. For subjects without a significant response to bronchodilator (improvement in FEV1 of more than 200 mL and 12%), methacholine challenge tests (MCT) were also performed. Of 3,359 subjects that completed the questionnaire, 354 (10.5%) had current wheeze, 471 (14.0%) had current allergic rhinitis, and 326 (9.7%) had current eczema. Current wheeze was associated with family history of allergic disease, overweight, current smoking, allergic rhinitis, and atopic dermatitis. Of 36 subjects with current wheeze who underwent PFT with or without MCT in the Anyang area, 24 (66.7%) were confirmed to have current asthma. In conclusion, the prevalence of allergic disease in young adults of Korean military is not low, and the risk factors of wheezing include family history of allergic disease, overweight, current smoking, allergic rhinitis, and atopic dermatitis

    Carbon-nanotube-interfaced glass fiber scaffold for regeneration of transected sciatic nerve.

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    Carbon nanotubes (CNTs), with their unique and unprecedented properties, have become very popular for the repair of tissues, particularly for those requiring electrical stimuli. Whilst most reports have demonstrated in vitro neural cell responses of the CNTs, few studies have been performed on the in vivo efficacy of CNT-interfaced biomaterials in the repair and regeneration of neural tissues. Thus, we report here for the first time the in vivo functions of CNT-interfaced nerve conduits in the regeneration of transected rat sciatic nerve. Aminated CNTs were chemically tethered onto the surface of aligned phosphate glass microfibers (PGFs) and CNT-interfaced PGFs (CNT-PGFs) were successfully placed into three-dimensional poly(l/d-lactic acid) (PLDLA) tubes. An in vitro study confirmed that neurites of dorsal root ganglion outgrew actively along the aligned CNT-PGFs and that the CNT interfacing significantly increased the maximal neurite length. Sixteen weeks after implantation of a CNT-PGF nerve conduit into the 10mm gap of a transected rat sciatic nerve, the number of regenerating axons crossing the scaffold, the cross-sectional area of the re-innervated muscles and the electrophysiological findings were all significantly improved by the interfacing with CNTs. This first in vivo effect of using a CNT-interfaced scaffold in the regeneration process of a transected rat sciatic nerve strongly supports the potential use of CNT-interfaced PGFs at the interface between the nerve conduit and peripheral neural tissues

    CO2 capture from syngas by an adsorption process at a biomass gasification CHP plant: Its comparison with amine-based CO2 capture

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    AbstractAn exemplary 10MWth biomass-fuelled CHP plant equipped with a FICFB (Fast Internally Circulating Fluidised Bed) gasifier and a Jenbacher type 6 gas engine was simulated using Honeywell UniSim R400 to estimate the power and thermal outputs. The biomass gasification CHP plant was integrated with either a pre-combustion adsorptive capture process or a conventional post-combustion amine process to achieve carbon-negative power and heat generation. The practical maximum of carbon capture rate achievable with an adsorptive CO2 capture process applied to a syngas stream was 49% in overall while the amine process could boost the carbon capture rate up to 59%. However, it was found that the two-stage, two-bed PVSA (Pressure Vacuum Swing Adsorption) unit would have a clear advantage over the conventional amine processes in that the CHP plant integrated with the PVSA unit could achieve 1.7% points higher net electrical efficiency and 12.8% points higher net thermal efficiency than the CHP plant integrated with the amine process

    Remdesivir for 5 or 10 Days in Patients With Severe Covid-19

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    Background: Remdesivir is an RNA polymerase inhibitor with potent antiviral activity in vitro and efficacy in animal models of coronavirus disease 2019 (Covid-19). Methods: We conducted a randomized, open-label, phase 3 trial involving hospitalized patients with confirmed SARS-CoV-2 infection, oxygen saturation of 94% or less while they were breathing ambient air, and radiologic evidence of pneumonia. Patients were randomly assigned in a 1:1 ratio to receive intravenous remdesivir for either 5 days or 10 days. All patients received 200 mg of remdesivir on day 1 and 100 mg once daily on subsequent days. The primary end point was clinical status on day 14, assessed on a 7-point ordinal scale. Results: In total, 397 patients underwent randomization and began treatment (200 patients for 5 days and 197 for 10 days). The median duration of treatment was 5 days (interquartile range, 5 to 5) in the 5-day group and 9 days (interquartile range, 5 to 10) in the 10-day group. At baseline, patients randomly assigned to the 10-day group had significantly worse clinical status than those assigned to the 5-day group (P = 0.02). By day 14, a clinical improvement of 2 points or more on the ordinal scale occurred in 64% of patients in the 5-day group and in 54% in the 10-day group. After adjustment for baseline clinical status, patients in the 10-day group had a distribution in clinical status at day 14 that was similar to that among patients in the 5-day group (P = 0.14). The most common adverse events were nausea (9% of patients), worsening respiratory failure (8%), elevated alanine aminotransferase level (7%), and constipation (7%). Conclusions: In patients with severe Covid-19 not requiring mechanical ventilation, our trial did not show a significant difference between a 5-day course and a 10-day course of remdesivir. With no placebo control, however, the magnitude of benefit cannot be determined. (Funded by Gilead Sciences; GS-US-540-5773 ClinicalTrials.gov number, NCT04292899.)

    Pathogenic NR2F1 variants cause a developmental ocular phenotype recapitulated in a mutant mouse model

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    Pathogenic NR2F1 variants cause a rare autosomal dominant neurodevelopmental disorder referred to as the Bosch-Boonstra-Schaaf Optic Atrophy Syndrome. Although visual loss is a prominent feature seen in affected individuals, the molecular and cellular mechanisms contributing to visual impairment are still poorly characterized. We conducted a deep phenotyping study on a cohort of 22 individuals carrying pathogenic NR2F1 variants to document the neurodevelopmental and ophthalmological manifestations, in particular the structural and functional changes within the retina and the optic nerve, which have not been detailed previously. The visual impairment became apparent in early childhood with small and/or tilted hypoplastic optic nerves observed in 10 cases. High-resolution optical coherence tomography imaging confirmed significant loss of retinal ganglion cells with thinning of the ganglion cell layer, consistent with electrophysiological evidence of retinal ganglion cells dysfunction. Interestingly, for those individuals with available longitudinal ophthalmological data, there was no significant deterioration in visual function during the period of follow-up. Diffusion tensor imaging tractography studies showed defective connections and disorganization of the extracortical visual pathways. To further investigate how pathogenic NR2F1 variants impact on retinal and optic nerve development, we took advantage of an Nr2f1 mutant mouse disease model. Abnormal retinogenesis in early stages of development was observed in Nr2f1 mutant mice with decreased retinal ganglion cell density and disruption of retinal ganglion cell axonal guidance from the neural retina into the optic stalk, accounting for the development of optic nerve hypoplasia. The mutant mice showed significantly reduced visual acuity based on electrophysiological parameters with marked conduction delay and decreased amplitude of the recordings in the superficial layers of the visual cortex. The clinical observations in our study cohort, supported by the mouse data, suggest an early neurodevelopmental origin for the retinal and optic nerve head defects caused by NR2F1 pathogenic variants, resulting in congenital vision loss that seems to be non-progressive. We propose NR2F1 as a major gene that orchestrates early retinal and optic nerve head development, playing a key role in the maturation of the visual system

    Health – related quality of life of Kuwaiti women with breast cancer: a comparative study using the EORTC Quality of Life Questionnaire

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    <p>Abstract</p> <p>Background</p> <p>The Kuwaiti perspective on quality of life (QOL) in breast cancer is important because it adds the contribution from a country where the disease affects women at a relatively younger age and seems to be more aggressive. We used the EORTC QLQ – C30 and its breast-specific module (BR-23) to highlight the health-related QOL of Kuwaiti women with breast cancer, in comparison with the international data, and assessed the socio-demographic and clinical variables that predict the five functional scales and global QOL (GQOL) scale of the QLQ – C30.</p> <p>Methods</p> <p>Participants were consecutive clinic attendees for chemotherapy, in stable condition, at the Kuwait Cancer Control Center.</p> <p>Results</p> <p>The 348 participants were aged 20–81 years (mean 48.3, SD 10.3); 58.7% had stages III and IV disease. Although the mean scores for QLQ – C30 (GQOL, 45.3; and five functional scales, 52.6%–61.2%) indicated that the patients had poor to average functioning, only 5.8% to 11.2% had scores that met the </= 33% criterion for problematic functioning, while 12.0% to 40.0% met the >66% criterion for more severe symptoms. Most (47.8%–70.1%) met the >66% criterion for "good functioning" on the BR-23 functional scales. The mean scores of the QLQ – C30 indicated that, despite institutional supports, Kuwaiti women had clinically significantly poorer global QOL and functional scale scores, and more intense symptom experience, in comparison with the international data (i.e., </= 10% difference between groups). For the BR-23, Kuwaiti women seemed to have clinically significantly better functional scale scores, but more severe symptoms, especially systemic side effects and breast symptoms. Younger women had poorer HRQOL scores. In regression analysis, social functioning accounted for the highest proportion of variance for GQOL.</p> <p>Conclusion</p> <p>The relatively high number that met the criterion for good functioning on the functional scales is an evidence base to boost national health education about psychosocial prognosis in cancer. In view of the poor performance on the symptom scales, clinicians treating Kuwaiti women with breast cancer should prepare them for the acute toxicities of treatment and address fatigue. The findings call for the institution of a psycho-oncology service to address psycho-social issues.</p

    PP2A inactivation is a crucial step in triggering apoptin-induced tumor-selective cell killing

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    Apoptin (apoptosis-inducing protein) harbors tumor-selective characteristics making it a potential safe and effective anticancer agent. Apoptin becomes phosphorylated and induces apoptosis in a large panel of human tumor but not normal cells. Here, we used an in vitro oncogenic transformation assay to explore minimal cellular factors required for the activation of apoptin. Flag-apoptin was introduced into normal fibroblasts together with the transforming SV40 large T antigen (SV40 LT) and SV40 small t antigen (SV40 ST) antigens. We found that nuclear expression of SV40 ST in normal cells was sufficient to induce phosphorylation of apoptin. Mutational analysis showed that mutations disrupting the binding of ST to protein phosphatase 2A (PP2A) counteracted this effect. Knockdown of the ST-interacting PP2A–B56γ subunit in normal fibroblasts mimicked the effect of nuclear ST expression, resulting in induction of apoptin phosphorylation. The same effect was observed upon downregulation of the PP2A–B56δ subunit, which is targeted by protein kinase A (PKA). Apoptin interacts with the PKA-associating protein BCA3/AKIP1, and inhibition of PKA in tumor cells by treatment with H89 increased the phosphorylation of apoptin, whereas the PKA activator cAMP partially reduced it. We infer that inactivation of PP2A, in particular, of the B56γ and B56δ subunits is a crucial step in triggering apoptin-induced tumor-selective cell death

    The complement cascade as a mediator of tissue growth and regeneration

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    Recent evidence has demonstrated that the complement cascade is involved in a variety of physiologic and pathophysiologic processes in addition to its role as an immune effector. Research in a variety of organ systems has shown that complement proteins are direct participants in maintenance of cellular turnover, healing, proliferation and regeneration. As a physiologic housekeeper, complement proteins maintain tissue integrity in the absence of inflammation by disposing of cellular debris and waste, a process critical to the prevention of autoimmune disease. Developmentally, complement proteins influence pathways including hematopoietic stem cell engraftment, bone growth, and angiogenesis. They also provide a potent stimulus for cellular proliferation including regeneration of the limb and eye in animal models, and liver proliferation following injury. Here, we describe the complement cascade as a mediator of tissue growth and regeneration
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