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Free Tissue Transfer in Sickle Cell Disease: A Case Report and Systematic Review
Huang Anne,Patel Ronak A.,Gottlieb Lawrence J. 대한성형외과학회 2023 Archives of Plastic Surgery Vol.50 No.3
Hemoglobinopathies such as sickle cell disease (SCD) are traditionally considered a relative contraindication to free tissue transfer, due to concerns that erythrocyte sickling will increase the risk of microvascular thrombosis and flap failure. This article describes a case report with the successful use of free tissue transfer in a patient with SCD and provides a systematic literature review on free tissue transfer in SCD. A retrospective chart review was performed of a patient with SCD who underwent free tissue transfer at the authors' institution. A systematic literature review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was performed using the keywords “free tissue transfer,” “free flap,” or “microsurgery” and “sickle cell” on PubMed, Ovid/Medline, and Scopus. A 29-year-old male with delayed presentation of an electrical burn to the face and scalp underwent wound closure with a free anterolateral thigh flap. Key management principles included red blood cell transfusion to keep hemoglobin S under 30% and hemoglobin greater than 10 g/dL, maintenance of hydration, normothermia, adequate analgesia, and postoperative anticoagulation. Systematic literature review identified 7 articles describing 13 cases of free tissue transfer in 10 patients with SCD, with combined complete free flap success in 10 of the 13 flaps. Free tissue transfer can be successfully performed in patients with SCD. However, evidence on the optimal management of this unique patient population in the perioperative period after free tissue transfer is limited to case reports in the literature.
Ann, Xiao-Hua,Lun, Yong-Zhi,Zhang, Wei,Liu, Ben,Li, Xing-Yun,Zhong, Min-Tao,Wang, Xiao-Li,Cao, Jing,Ning, An-Hong,Huang, Min Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.12
In this study, an anti-oxidant and anti-tumor protein Latcripin-3 of Lentinula edodes C91-3 was expressed in Escherichia coli. for the first time. According to the cDNA library, the full-length gene of Latcripin-3 was cloned by the methods of 3'-full rapid amplification of cDNA Ends (RACE) and 5'-full RACE. The structural domain gene of Latcripin-3 was inserted into the pET32 a(+). The functional protein of Latcripin-3 was expressed in Rosetta-gami (DE3) E. coli, evaluated by Western blotting and mass spectrometry. DPPH testing showed that the protein Latcripin-3 can scavenge free radicals remarkably well. The activity of functional protein Latcripin-3 on A549 cells was studied with flow cytometry and the MTT method. The MTT assay results showed that there was a decreases in cell viability in a dose-dependent and time-dependent manner in protein Latcripin-3 treated groups. Flow cytometry demonstrated that Latcripin-3 can induce apoptosis and block S phase dramatically in human A549 lung cancer cells as compared to the control group. At the same time, the cell ultrastructure observed by transmission electron microscopy supported the results of flow cytometry. This research offers new insights and advantages for identifying anti-oxidant and anti-tumor proteins.
Atypical Teratoid Rhabdoid Tumour : From Tumours to Therapies
Richardson, Elizabeth Anne,Ho, Ben,Huang, Annie The Korean Neurosurgical Society 2018 Journal of Korean neurosurgical society Vol.61 No.3
Atypical teratoid rhabdoid tumours (ATRTs) are the most common malignant central nervous system tumours in children ${\leq}1year$ of age and represent approximately 1-2% of all pediatric brain tumours. ATRT is a primarily monogenic disease characterized by the bi-allelic loss of the SMARCB1 gene, which encodes the hSNF5 subunit of the SWI/SNF chromatin remodeling complex. Though conventional dose chemotherapy is not effective in most ATRT patients, high dose chemotherapy with autologous stem cell transplant, radiotherapy and/or intrathecal chemotherapy all show significant potential to improve patient survival. Recent epigenetic and transcriptional studies highlight three subgroups of ATRT, each with distinct clinical and molecular characteristics with corresponding therapeutic sensitivities, including epigenetic targeting, and inhibition of tyrosine kinases or growth/lineage specific pathways.
Lee, Mee-Hyun,Huang, Zunnan,Kim, Dong Joon,Kim, Sung-Hyun,Kim, Myoung Ok,Lee, Sung-Young,Xie, Hua,Park, Si Jun,Kim, Jae Young,Kundu, Joydeb Kumar,Bode, Ann M.,Surh, Young-Joon,Dong, Zigang American Association for Cancer Research 2013 Cancer prevention research Vol.6 No.5
<P>Abnormal functioning of multiple gene products underlies the neoplastic transformation of cells. Thus, chemopreventive and/or chemotherapeutic agents with multigene targets hold promise in the development of effective anticancer drugs. Silybin, a component of milk thistle, is a natural anticancer agent. In the present study, we investigated the effect of silybin on melanoma cell growth and elucidated its molecular targets. Our study revealed that silybin attenuated the growth of melanoma xenograft tumors in nude mice. Silybin inhibited the kinase activity of mitogen-activated protein kinase (MEK)-1/2 and ribosomal S6 kinase (RSK)-2 in melanoma cells. The direct binding of silybin with MEK1/2 and RSK2 was explored using a computational docking model. Treatment of melanoma cells with silybin attenuated the phosphorylation of extracellular signal-regulated kinase (ERK)-1/2 and RSK2, which are regulated by the upstream kinases MEK1/2. The blockade of MEK1/2-ERK1/2-RSK2 signaling by silybin resulted in a reduced activation of NF-κB, activator protein-1, and STAT3, which are transcriptional regulators of a variety of proliferative genes in melanomas. Silybin, by blocking the activation of these transcription factors, induced cell-cycle arrest at the G<SUB>1</SUB> phase and inhibited melanoma cell growth <I>in vitro</I> and <I>in vivo</I>. Taken together, silybin suppresses melanoma growth by directly targeting MEK- and RSK-mediated signaling pathways. <I>Cancer Prev Res; 6(5); 455–65. ©2013 AACR</I>.</P>
Manju Chandran,Yun Ann Chin,Kuan Swen Choo,Wan Chen Ang,Xiao Feng Huang,Xiao Ming Liu,Donovan Tay,Tin Kyaw Kyaw Aung,Amin Ali,Win Pa Pa Thu,Susan Logan,Sean Xuexian Yan,Sarath Lekamwasam,Ying Hao 대한골다공증학회 2020 Osteoporosis and Sarcopenia Vol.6 No.2
Objectives: The accuracy of FRAX® as a screening tool to identify osteoporosis and how it compares with tools such as Osteoporosis Self-Assessment Tool for Asians (OSTA), in Southeast Asian women has so far been unexplored. We aimed to determine the FRAX® thresholds that accurately identify densitometric osteoporosis and to compare its performance with that of OSTA for this purpose. Methods: Singaporean postmenopausal women (n ¼ 1056) were evaluated. FRAX® Major Osteoporotic Fracture Probability (MOFP), Hip Fracture Probability (HFP) scores, and OSTA indices were calculated. Receiver operating characteristic (ROC) curves were constructed and via the Youden index, the optimal cut-off points of balanced sensitivity and specificity for dual energy X-ray absorptiometry (DXA)-defined osteoporosis were identified and the performance characteristics were compared. Results: A FRAX® MOFP threshold of ≥3.7% had sensitivity, specificity, positive predictive value and negative predictive value of 0.78 (0.73-0.83), 0.63 (0.59-0.66), 0.4 (0.36-0.44), and 0.9 (0.87-0.92), respectively in identifying osteoporosis. The corresponding values for a HFP threshold of 0.6% were 0.85 (0.80-0.89), 0.58 (0.55-0.62), 0.39 (0.35-0.43), and 0.92 (0.9-0.94) and that for an OSTA index cut-off of ≥ -1.2 were 0.76 (0.70-0.81), 0.74 (0.71-0.77), 0.48 (0.43-0.54), and 0.91 (0.88-0.93). The area under the ROC curves were 82.8% (79.9%-85.6%), 77.6% (74.2%-81%), and 79.6% (76.5%-82.8%) for OSTA, MOFP, and HFP thresholds respectively. Conclusions: FRAX® and OSTA perform comparably in identifying osteoporosis in our population. OSTA has only 2 parameters and may be simpler to use. However, FRAX® may also have a role in primary screening to identify the postmenopausal woman to be referred for DXA scanning and may help facilitate fracture risk reduction discussions with the patient.
Curcumin Suppresses Proliferation of Colon Cancer Cells by Targeting CDK2
Lim, Tae-Gyu,Lee, Sung-Young,Huang, Zunnan,Lim, Do Young,Chen, Hanyong,Jung, Sung Keun,Bode, Ann M.,Lee, Ki Won,Dong, Zigang American Association for Cancer Research 2014 CANCER PREVENTION RESEARCH Vol.7 No.4
<P>Curcumin, the yellow pigment of turmeric found in Southeast Indian food, is one of the most popular phytochemicals for cancer prevention. Numerous reports have demonstrated modulation of multiple cellular signaling pathways by curcumin and its molecular targets in various cancer cell lines. To identify a new molecular target of curcumin, we used shape screening and reverse docking to screen the Protein Data Bank against curcumin. Cyclin-dependent kinase 2 (CDK2), a major cell-cycle protein, was identified as a potential molecular target of curcumin. Indeed, <I>in vitro</I> and <I>ex vivo</I> kinase assay data revealed a dramatic suppressive effect of curcumin on CDK2 kinase activity. Furthermore, curcumin induced G<SUB>1</SUB> cell-cycle arrest, which is regulated by CDK2 in HCT116 cells. Although the expression levels of CDK2 and its regulatory subunit, cyclin E, were not changed, the phosphorylation of retinoblastoma (Rb), a well-known CDK2 substrate, was reduced by curcumin. Because curcumin induced cell-cycle arrest, we investigated the antiproliferative effect of curcumin on HCT116 colon cancer cells. In this experiment, curcumin suppressed HCT116 cell proliferation effectively. To determine whether CDK2 is a direct target of curcumin, CDK2 expression was knocked down in HCT116 cells. As expected, HCT116 sh-CDK2 cells exhibited G<SUB>1</SUB> arrest and reduced proliferation. Because of the low levels of CDK2 in HCT116 sh-CDK2 cells, the effects of curcumin on G<SUB>1</SUB> arrest and cell proliferation were not substantially relative to HCT116 sh-control cells. From these results, we identified CDK2 as a direct target of curcumin in colon cancer cells. <I>Cancer Prev Res; 7(4); 466–74. ©2014 AACR</I>.</P>
APMP.QM-K111-propane in nitrogen
Lin, Tsai-Yin,Liu, Hsin-Wang,Huang, Chiung-Kun,Kang, Namgoo,Bae, Hyun Kil,Woo, Jin Chun,Bi, Zhe,Zhou, Zeyi,Sinweeruthai, Ratirat,Wongjuk, Arnuttachai,Li, Hou,Keat, Teo Beng,Hui, Liu,Wu, Thomas,Ann, Ch BUREAU INTERNATIONAL DES POIDS ET MESURES 2018 METROLOGIA -BERLIN- Vol.55 No.1
Liu, Haidan,Hwang, Joonsung,Li, Wei,Choi, Tae Woong,Liu, Kangdong,Huang, Zunnan,Jang, Jae-Hyuk,Thimmegowda, N.R.,Lee, Ki Won,Ryoo, In-Ja,Ahn, Jong-Seog,Bode, Ann M.,Zhou, Xinmin,Yang, Yifeng,Erikson, American Association for Cancer Research 2014 CANCER PREVENTION RESEARCH Vol.7 No.1
<P>Mitogen- and stress-activated kinase 1 (MSK1) is a nuclear serine/threonine protein kinase that acts downstream of both extracellular signal-regulated kinases and p38 mitogen-activated protein kinase in response to stress or mitogenic extracellular stimuli. Increasing evidence has shown that MSK1 is closely associated with malignant transformation and cancer development. MSK1 should be an effective target for cancer chemoprevention and chemotherapy. However, very few MSK1 inhibitors, especially natural compounds, have been reported. We used virtual screening of a natural products database and the active conformation of the C-terminal kinase domain of MSK1 (PDB id 3KN) as the receptor structure to identify chrysin and its derivative, compound 69407, as inhibitors of MSK1. Compared with chrysin, compound 69407 more strongly inhibited proliferation and 12-<I>O</I>-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic transformation of JB6 P+ cells with lower cytotoxicity. Western blot data demonstrated that compound 69407 suppressed phosphorylation of the MSK1 downstream effector histone H3 in intact cells. Knocking down the expression of MSK1 effectively reduced the sensitivity of JB6 P+ cells to compound 69407. Moreover, topical treatment with compound 69407 before TPA application significantly reduced papilloma development in terms of number and size in a two-stage mouse skin carcinogenesis model. The reduction in papilloma development was accompanied by the inhibition of histone H3 phosphorylation at Ser10 in tumors extracted from mouse skin. The results indicated that compound 69407 exerts inhibitory effects on skin tumorigenesis by directly binding with MSK1 and attenuates the MSK1/histone H3 signaling pathway, which makes it an ideal chemopreventive agent against skin cancer. <I>Cancer Prev Res; 7(1); 74–85. ©2013 AACR</I>.</P>
( Nagamu Inoue ),( Kiyonori Kobayashi ),( Makoto Naganuma ),( Fumihito Hirai ),( Morio Ozawa ),( Dilek Arikan ),( Bidan Huang ),( Anne M. Robinson ),( Roopal B. Thakkar ),( Toshifumi Hibi ) 대한장연구학회 2017 Intestinal Research Vol.15 No.3
Background/Aims: Intestinal Behcet`s disease (BD) is an immune-mediated inflammatory disorder. We followed up the patients and evaluated safety profile and effectiveness of adalimumab for the treatment of intestinal BD through 100 weeks rolled over from the 52 week clinical trial (NCT01243671). Methods: Patients initiated adalimumab therapy at 160 mg at week 0, followed by 80 mg at week 2, followed by 40 mg every other week until the end of the study. Long-term safety and all adverse events (AEs) were examined. The efficacy was assessed on the basis of marked improvement (MI) and complete remission (CR) using a composite efficacy index, which combined global gastrointestinal symptoms and endoscopic assessments. Re-sults: Twenty patients were enrolled in this study; 15 patients received adalimumab treatment until study completion. The incidence of AEs through week 100 was 544.4 events/100 person-years, which was comparable to the incidence through week 52 (560.4 events/100 person-years). No unexpected trend was observed and adalimumab was well tolerated. At weeks 52 and 100, 60.0% and 40.0% of patients showed MI, respectively, and 20.0% and 15.0% of patients showed CR, respectively. Conclusions: This report demonstrates 2 years safety and effectiveness of adalimumab in intestinal BD patients. Patients with intestinal BD refractory to conventional treatment receiving up to 2 years of adalimumab treatment demonstrated safety outcomes consistent with the known profile of adalimumab, and the treatment led to sustained reduction of clinical and endoscopic disease activity. (Intest Res 2017;15:395-401)