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Kim, T.,Jin, C.E.,Sung, H.,Koo, B.,Park, J.,Kim, S.-M.,Kim, J.Y.,Chong, Y.P.,Lee, S.-O.,Choi, S.-H.,Kim, Y.S.,Woo, J.H.,Lee, J.-H.,Lee, J.-H.,Lee, K.-H.,Shin, Y.,Kim, S.-H. Elsevier 2017 The Journal of hospital infection Vol.97 No.4
<P><B>Summary</B></P> <P><B>Background</B></P> <P>Although fomites or contaminated surfaces have been considered as transmission routes, the role of environmental contamination by human parainfluenza virus type 3 (hPIV-3) in healthcare settings is not established.</P> <P><B>Aim</B></P> <P>To describe an hPIV-3 nosocomial outbreak and the results of environmental sampling to elucidate the source of nosocomial transmission and the role of environmental contamination.</P> <P><B>Methods</B></P> <P>During an hPIV-3 outbreak between May and June 2016, environmental surfaces in contact with clustered patients were swabbed and respiratory specimens used from infected patients and epidemiologically unlinked controls. The epidemiologic relatedness of hPIV-3 strains was investigated by sequencing of the haemagglutinin–neuraminidase and fusion protein genes.</P> <P><B>Findings</B></P> <P>Of 19 hPIV-3-infected patients, eight were haematopoietic stem cell recipients and one was a healthcare worker. In addition, four had upper and 12 had lower respiratory tract infections. Of the 19 patients, six (32%) were community-onset infections (symptom onset within <7 days of hospitalization) and 13 (68%) were hospital-onset infections (≥7 days of hospitalization). Phylogenetic analysis identified two major clusters: five patients, and three patients plus one healthcare worker. Therefore, seven (37%) were classified as nosocomial transmissions. hPIV-3 was detected in 21 (43%) of 49 environmental swabs up to 12 days after negative respiratory polymerase chain reaction conversion.</P> <P><B>Conclusion</B></P> <P>At least one-third of a peak season nosocomial hPIV-3 outbreak originated from nosocomial transmission, with multiple importations of hPIV-3 from the community, providing experimental evidence for extensive environmental hPIV-3 contamination. Direct contact with the contaminated surfaces and fomites or indirect transmission from infected healthcare workers could be responsible for nosocomial transmission.</P>
SUH, YOO-HUN,CHONG, YOUNG HAE,KIM, SEONG-HUN,CHOI, WOONG,MIN, KYEONGSIK,JEONG, SUNG-JIN,FRASER, S. P.,DJAMGOZ, M. B. A. 이화여자대학교 생명과학연구소 1996 생명과학연구논문집 Vol.7 No.-
APP may be associated with defense mechanisms in the central nervous system involving the immune system.^1 The finding of low levels of APP was initially described in proportion to lymphocytes.^2 We examined APP expression in human lymphocytes and spleen and compared APP expression in lymphocytes from Alzheimer's patients to that in lymphocytes from age-matched controls. In spleen, the majority of cells showing A? immunoreactivity was found in the T cell-dependent zone. Fluorescence activated cell sort analysis(FACS) indicated that around 90% of CD4^+ T cells and 60% of CD8^+ T cells were immunoreactive to A? specific monoclonal antibody (mAb) 4G8. Northern blot analysis showed that lymphocyte APP mRNA was gradually increased to reach a maximum at 3 days