New-onset or Exacerbated Occupational Hand Eczema among Healthcare Workers During the COVID-19 Pandemic: A Growing Health Problem

Hand hygiene is one of the cornerstones in ensuring effective infection control during the Coronavirus disease 2019 (COVID-19) outbreak. We aimed to investigate the prevalence of new-onset occupational HE during the COVID-19 outbreak in healthcare workers (HCWs) and the clinical course, clinical features, and risk factors of occupational hand eczema (HE). A total of 159 volunteer HCWs (female: n=112; male: n=47, mean age=35.55±7.03 years) working in a pandemic hospital were included. Participants were questioned in terms of daily hand hygiene, use of gloves, and signs and symptoms associated with HE before and during the COVID-19 pandemic. HCWs were divided into two groups classified as non-COVID and COVID, according to the unit they worked in. In our study, 55 participants reported new-onset signs and/or symptoms associated with HE during the COVID-19 pandemic. 59 participants described an increase in signs and/or symptoms associated with HE. The presence of newly-formed or increased signs and/or symptoms associated with HE was found to be 71.7%. A significant increase in dryness, itching, pain/burning, erythema, and scaling was observed (P<0.05). No difference was found between the COVID and non-COVID groups in terms of newly formed and/or increased signs and symptoms (P>0.05). The study included a limited number of participants, and the participants self-reported the signs and symptoms associated with HE. During the COVID-19 period, there has been a significant increase in the signs and symptoms of occupational HE as a result of increased hand hygiene practices in HCWs

New-onset or Exacerbated Occupational Hand Eczema among Healthcare Workers During the COVID-19 Pandemic: A Growing Health Problem

Hand hygiene is one of the cornerstones in ensuring effective infection control during the Coronavirus disease 2019 (COVID-19) outbreak. We aimed to investigate the prevalence of new-onset occupational HE during the COVID-19 outbreak in healthcare workers (HCWs) and the clinical course, clinical features, and risk factors of occupational hand eczema (HE). A total of 159 volunteer HCWs (female: n=112; male: n=47, mean age=35.55±7.03 years) working in a pandemic hospital were included. Participants were questioned in terms of daily hand hygiene, use of gloves, and signs and symptoms associated with HE before and during the COVID-19 pandemic. HCWs were divided into two groups classified as non-COVID and COVID, according to the unit they worked in. In our study, 55 participants reported new-onset signs and/or symptoms associated with HE during the COVID-19 pandemic. 59 participants described an increase in signs and/or symptoms associated with HE. The presence of newly-formed or increased signs and/or symptoms associated with HE was found to be 71.7%. A significant increase in dryness, itching, pain/burning, erythema, and scaling was observed (P<0.05). No difference was found between the COVID and non-COVID groups in terms of newly formed and/or increased signs and symptoms (P>0.05). The study included a limited number of participants, and the participants self-reported the signs and symptoms associated with HE. During the COVID-19 period, there has been a significant increase in the signs and symptoms of occupational HE as a result of increased hand hygiene practices in HCWs

Zelluläre Regulation des AT1a-Rezeptors in aortalen glatten Gefäßmuskelzellen der Ratte

Während Sepsis ist die Blutdruckwirksamkeit des vasokonstriktiven Hormons Angiotensin II deutlich reduziert. Der Mechanismus dieser vaskulären Hyporeaktivität auf Angiotensin II, auch Vasoplegie genannt, ist derzeit nicht schlüssig bekannt. Untersuchungen am Tiermodell haben gezeigt, daß nach Induktion einer Gram-negativen Sepsis die Expression der AT1-Rezeptoren unterdrückt war. Möglicherweise liegt die verminderte Blutdruckwirksamkeit von Angiotensin II während Sepsis daher an einer veränderten Genexpression der AT1-Rezeptoren. Deshalb war es Ziel dieser Arbeit, die Regulation des AT1a-Rezeptors durch Sepsis-typische Mediatoren wie proinflammatorische Zytokine und Stickstoffmonoxid auf zellulärer Ebene näher zu charakterisieren. Als in vitro-Modell wurden in dieser Arbeit primäre glatte Gefäßmuskelzellen aus der Aorta der Ratte verwendet. Die Zytokine TNF-alpha und IFN-gamma wie auch Stickstoffmonoxid führten zu einer Herabregulation der mRNA-Expression des AT1a-Rezeptors, während IL-1beta keinen Einfluß auf die Expression der AT1a-Rezeptor mRNA hatte. Verschiedene Kombinationen dieser drei Zytokine führten alle zu einer Hemmung der Expression, wobei die Herabregulation der AT1a-Rezeptor mRNA Expression durch die Kombination aus den drei Zytokinen am stärksten ausfiel. Es ist bekannt, daß die proinflammatorischen Zytokine TNF-alpha, IFN-gamma und IL-1beta u.a. den Transkriptionsfaktor NF-kappaB und die drei wichtigsten MAP-Kinasen - die p42/44, die SAPK/JNK und die p38 - aktivieren. Die in dieser Arbeit erhobenen Befunde zeigen aber, daß diese bei der Hemmung der AT1a-Rezeptor mRNA Expression durch Zytokine wohl keine Rolle spielen. Ferner konnte eine Destabilisierung der AT1a-Rezeptor mRNA für die Zytokin- und NO- vermittelte AT1a-Rezeptor Genexpression ausgeschlossen werden. Weiterführende Versuche haben ergeben, daß die verminderte mRNA Expression durch die Zytokine TNF-alpha und IFN-gamma wie auch durch Stickstoffmonoxid auf einer Hemmung der transkriptionellen Aktivität des AT1a-Rezeptor Promotors beruht. Anhand von Promotor-Reporter-Konstrukten konnten die jeweiligen regulatorischen Sequenzen eingegrenzt werden. Desweiteren wurde in den glatten Gefäßmuskelzellen die Ca2+-Freisetzung aus dem endoplasmatischen Retikulum ins Zytosol durch Angiotensin II untersucht. In dieser Arbeit konnte gezeigt werden, daß Angiotensin II in Zellen, die zuvor mit dem Zytokin-Mix behandelt wurden, im Gegensatz zu unbehandelten Zellen keine Ca2+-Freisetzung bewirkte. Dies könnte eine sehr gute Erklärung dafür sein, daß Angiotensin II bei Sepsis eine verminderte Blutdruckantwort zeigt. In weiterführenden Versuchen muß mit Hilfe von weiteren Deletionen und Mutationen des AT1a-Rezeptor Promotors geklärt werden, über welche regulatorischen Sequenzen die Hemmung der transkriptionellen Aktivität durch TNF-alpha, IFN-gamma und Stickstoffmonoxid vermittelt wird, und welche Signalwege dafür verantwortlich sind

Evaluation of sex hormones in epilepsy patients

31st International Epilepsy Congress -- SEP 05-09, 2015 -- Istanbul, TURKEYWOS: 000365756500134

Brominated flame retardants in a computer technical service: Indoor air gas phase, submicron (PM1) and coarse (PM10) particles, associated inhalation exposure, and settled dust

Brominated flame retardants (BFRs) are found in multi-media indoors, therefore, may pose serious risks to human health. This study investigated the occurrence of BFRs in particulate matter (PM1 and PM10) and gas phase by active and passive sampling, and settled dust to estimate potential exposure in a computer technical service. Polybrominated diphenyl ethers (PBDEs) and their alternatives (novel BFRs, NBFRs) were studied. PM and gas phase were collected on glass fiber filters and polyurethane foam plugs, respectively, and analyzed with a GC/MS after extraction, clean-up, and concentration. Inhalation exposure of the staff was estimated based on the measured concentrations using Monte Carlo simulation. BDE-209 was the dominating PBDE congener in all media while bis(2-ethylhexyl)-3,4,5,6-tetrabromophthalate and 1,2-bis(2,4,6-tribromophenoxy)ethane were those of NBFRs. Submicron particulate matter (PM1) BFR levels constituted about one half of the PM10-associated concentrations, while average PM10 mass concentration (69.9 μg m−3) was nine times that of PM1 (7.73 μg m−3). Calculated log10 dust-gas and PM-gas partitioning coefficients ranged from −5.03 to −2.10, −2.21 to −0.55, and −2.26 to −1.04 for settled dust, PM10, and PM1, respectively. The indoor/outdoor concentration ratios were >1 for all compounds indicating the strength of indoor sources in the service. The estimated potential inhalation exposures, for future chronic-toxic and carcinogenic risk assessments, indicated that the levels of gas-phase and PM1-associated exposures were similar at approximately one half of PM10-associated levels. Results of this study indicate that the occurrence of BFRs in all studied media should be taken into consideration for occupational health mitigation efforts

Inducible deletion of connexin 40 in adult mice causes hypertension and disrupts pressure control of renin secretion

Genetic loss-of-function defects of connexin 40 in renal juxtaglomerular cells are associated with renin-dependent hypertension. The dysregulation of renin secretion results from an intrarenal displacement of renin cells and an interruption of the negative feedback control of renin secretion by blood pressure. It is unknown whether this phenotype is secondary to developmental defects of juxtaglomerular renin cells due to connexin 40 malfunction, or whether acute functional defects of connexin 40 in the normal adult kidney can also lead to a similar dysregulation of renin secretion and hypertension. To address this question, we generated mice with an inducible deletion of connexin 40 in the adult kidney by crossing connexin 40-floxed mice with mice harboring a ubiquitously expressed tamoxifen-inducible Cre recombinase. Tamoxifen treatment in these mice strongly reduced connexin 40 mRNA and protein expression in the kidneys. These mice displayed persistent hypertension with renin expression shifted from the media layer of afferent arterioles to juxtaglomerular periglomerular cells. Control of renin secretion by the perfusion pressure was abolished in vitro, whereas in vivo plasma renin concentrations were increased. Thus, interruption of the connexin 40 gene in the adult kidney produced very similar changes in the renin system as had embryonic deletion. Hence, impairments of connexin 40 function in the normal adult kidney can cause renin-dependent hypertension