http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Chim, Harvey,Zoghbi, Yasmina,Nugent, Ajani George,Kassira, Wrood,Askari, Morad,Salgado, Christopher John Korean Society of Plastic and Reconstructive Surge 2018 Archives of Plastic Surgery Vol.45 No.1
Background Free muscle flaps are a mainstay for reconstruction of distal third leg wounds and for large lower extremity wounds with exposed bone. However a major problem is the significant postoperative flap swelling, which may take months to resolve. We studied the efficacy and safety of immediate application of a vacuum assisted closure (VAC) dressing after a free muscle flap to the lower extremity. Methods Over a 19 months period, all consecutive free muscle flaps for lower extremity reconstruction at a Level I trauma center were evaluated prospectively for postoperative flap thickness, complications and flap survival. Immediate application of a VAC dressing was performed in 9 patients, while the flap was left exposed for monitoring in 8 patients. Results There was no statistically significant difference in flap survival between both cohorts. Mean flap thickness at postoperative day 5 for the VAC group was $6.4{\pm}6.4mm$, while flap thickness for the exposed flap group was $29.6{\pm}13.5mm$. Flap thickness was significantly decreased at postoperative day 5 for the VAC dressing group. Conclusions Immediate application of VAC dressing following free muscle flaps to the lower extremity does not compromise flap survival or outcomes and results in decreased flap thickness and a better aesthetic outcome.
Harvey Chim,Yasmina Zoghbi,Ajani George Nugent,Wrood Kassira,Morad Askari,Christopher John Salgado 대한성형외과학회 2018 Archives of Plastic Surgery Vol.45 No.1
Background Free muscle flaps are a mainstay for reconstruction of distal third leg wounds and for large lower extremity wounds with exposed bone. However a major problem is the significant postoperative flap swelling, which may take months to resolve. We studied the efficacy and safety of immediate application of a vacuum assisted closure (VAC) dressing after a free muscle flap to the lower extremity. Methods Over a 19 months period, all consecutive free muscle flaps for lower extremity reconstruction at a Level I trauma center were evaluated prospectively for postoperative flap thickness, complications and flap survival. Immediate application of a VAC dressing was performed in 9 patients, while the flap was left exposed for monitoring in 8 patients. Results There was no statistically significant difference in flap survival between both cohorts. Mean flap thickness at postoperative day 5 for the VAC group was 6.4±6.4 mm, while flap thickness for the exposed flap group was 29.6±13.5 mm. Flap thickness was significantly decreased at postoperative day 5 for the VAC dressing group. Conclusions Immediate application of VAC dressing following free muscle flaps to the lower extremity does not compromise flap survival or outcomes and results in decreased flap thickness and a better aesthetic outcome.
Kim, Eunji,Lu, Hsiang-Chih,Zoghbi, Huda Y.,Song, Ji-Joon Cold Spring Harbor Laboratory Press 2013 Genes & development Vol.27 No.6
<P>The interaction of ATAXIN-1 (ATXN1) with the transcriptional repressor Capicua (CIC) plays a critical role in the pathogenesis of spinocerebellar ataxia type 1 (SCA1), a polyglutamine expansion neurodegenerative disease. This study presents the crystal structure of the AXH domain of ATXN1 bound to CIC and then provides evidence showing that CIC binding to ATXN1 disrupts homodimerization of ATXN1 and induces a new form of dimerization mediated by CIC. These results indicate the interdependent nature of ATXN1–CIC complex formation and provide a possible target for modulating SCA1 pathogenesis.</P>
Propofol decreases in vivo binding of 11C-PBR28 to translocator protein (18 kDa) in the human brain.
Hines, Christina S,Fujita, Masahiro,Zoghbi, Sami S,Kim, Jin Su,Quezado, Zenaide,Herscovitch, Peter,Miao, Ning,Ferraris Araneta, Maria D,Morse, Cheryl,Pike, Victor W,Labovsky, Julia,Innis, Robert B Society of Nuclear Medicine 2013 The Journal of nuclear medicine Vol.54 No.1
<P>The PET radioligand (11)C-PBR28 targets translocator protein (18 kDa) (TSPO) and is a potential marker of neuroimmune activation in vivo. Although several patient populations have been studied using (11)C-PBR28, no investigators have studied cognitively impaired patients who would require anesthesia for the PET procedure, nor have any reports investigated the effects that anesthesia may have on radioligand uptake. The purpose of this study was to determine whether the anesthetic propofol alters brain uptake of (11)C-PBR28 in healthy subjects.</P>
Han, Kihoon,Chen, Hogmei,Gennarino, Vincenzo A.,Richman, Ronald,Lu, Hui-Chen,Zoghbi, Huda Y. IRL Press 2015 Human molecular genetics Vol.24 No.7
<P>Silencing of fragile X mental retardation 1 (<I>FMR1</I>) gene and loss of fragile X mental retardation protein (FMRP) cause fragile X syndrome (FXS), a genetic disorder characterized by intellectual disability and autistic behaviors. FMRP is an mRNA-binding protein regulating neuronal translation of target mRNAs. Abnormalities in actin-rich dendritic spines are major neuronal features in FXS, but the molecular mechanism and identity of FMRP targets mediating this phenotype remain largely unknown. Cytoplasmic FMR1-interacting protein 2 (Cyfip2) was identified as an interactor of FMRP, and its mRNA is a highly ranked FMRP target in mouse brain. Importantly, Cyfip2 is a component of WAVE regulatory complex, a key regulator of actin cytoskeleton, suggesting that Cyfip2 could be implicated in the dendritic spine phenotype of FXS. Here, we generated and characterized <I>Cyfip2</I>-mutant (<I>Cyfip2<SUP>+/−</SUP></I>) mice. We found that <I>Cyfip2<SUP>+/−</SUP></I> mice exhibited behavioral phenotypes similar to <I>Fmr1</I>-null (<I>Fmr1<SUP>−/y</SUP></I>) mice, an animal model of FXS. Synaptic plasticity and dendritic spines were normal in <I>Cyfip2<SUP>+/−</SUP></I> hippocampus. However, dendritic spines were altered in <I>Cyfip2<SUP>+/−</SUP></I> cortex, and the dendritic spine phenotype of <I>Fmr1<SUP>−/y</SUP></I> cortex was aggravated in <I>Fmr1<SUP>−/y</SUP></I>; <I>Cyfip2<SUP>+/−</SUP></I> double-mutant mice. In addition to the spine changes at basal state, metabotropic glutamate receptor (mGluR)-induced dendritic spine regulation was impaired in both <I>Fmr1<SUP>−/y</SUP></I> and <I>Cyfip2<SUP>+/−</SUP></I> cortical neurons. Mechanistically, mGluR activation induced mRNA translation-dependent increase of Cyfip2 in wild-type cortical neurons, but not in <I>Fmr1<SUP>−/y</SUP></I> or <I>Cyfip2<SUP>+/−</SUP></I> neurons. These results suggest that misregulation of Cyfip2 function and its mGluR-induced expression contribute to the neurobehavioral phenotypes of FXS.</P>
Gennarino, Vincenzo A.,Singh, Ravi K.,White, Joshua J.,De Maio, A.,Han, K.,Kim, J.Y.,Jafar-Nejad, P.,di Ronza, A.,Kang, H.,Sayegh, Layal S.,Cooper, Thomas A.,Orr, Harry T.,Sillitoe, Roy V.,Zoghbi, Hud Cell Press ; MIT Press 2015 Cell Vol.160 No.6
Spinocerebellar ataxia type 1 (SCA1) is a paradigmatic neurodegenerative proteinopathy, in which a mutant protein (in this case, ATAXIN1) accumulates in neurons and exerts toxicity; in SCA1, this process causes progressive deterioration of motor coordination. Seeking to understand how post-translational modification of ATAXIN1 levels influences disease, we discovered that the RNA-binding protein PUMILIO1 (PUM1) not only directly regulates ATAXIN1 but also plays an unexpectedly important role in neuronal function. Loss of Pum1 caused progressive motor dysfunction and SCA1-like neurodegeneration with motor impairment, primarily by increasing Ataxin1 levels. Breeding Pum1<SUP>+/-</SUP> mice to SCA1 mice (Atxn1<SUP>154Q/+</SUP>) exacerbated disease progression, whereas breeding them to Atxn1<SUP>+/-</SUP> mice normalized Ataxin1 levels and largely rescued the Pum1<SUP>+/-</SUP> phenotype. Thus, both increased wild-type ATAXIN1 levels and PUM1 haploinsufficiency could contribute to human neurodegeneration. These results demonstrate the importance of studying post-transcriptional regulation of disease-driving proteins to reveal factors underlying neurodegenerative disease.