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| 1 | Small molecule-based disruption of the Axin/β-catenin protein complex regulates mesenchymal stem cell differentiation显示文摘 | Jungsug Gwak Sun Gwan Hwang Hyung-Soon Park Sang Rak Choi Sun-Hee Park Hyunjoon Kim Nam-Chul Ha Sung Jin Bae Jin-Kwan Han Dong-Eun Kim Jeong Woo Cho Sangtaek Oh | 2012 | Cell Research2012，22，1： | 11 |
| 2 | Mesenchymal stem cell-derived small extracellular vesicles mitigate oxidative stress-induced senescence in endothelial cells via regulation of miR-146a/Src显示文摘Senescent endothelial cells (ECs) could impair the integrity of the blood vessel endothelium, leading to vascular aging and a series of diseases, such as atherosclerosis, diabetes. Preventing or mitigating EC senescence might serve as a promising therapeutic paradigm for these diseases. Recent studies showed that small extracellular vesicles (sEV) have the potential to transfer bioactive molecules into recipient cells and induce phenotypic changes. Since mesenchymal stem cells (MSCs) have long been postulated as an important source cell in regenerative medicine, herein we investigated the role and mechanism of MSC-derived sEV (MSC-sEV) on EC senescence. In vitro results showed that MSC-sEV reduced senescent biomarkers, decreased senescence-associated secretory phenotype (SASP), rescued angiogenesis, migration and other dysfunctions in senescent EC induced by oxidative stress. In the In vivo natural aging and type-2 diabetes mouse wound-healing models (both of which have senescent ECs), MSC-sEV promoted wound closure and new blood vessel formation. Mechanically, miRNA microarray showed that miR-146a was highly expressed in MSC-sEV and also upregulated in EC after MSC-sEV treatment. miR-146a inhibitors abolished the stimulatory effects of MSC-sEV on senescence. Moreover, we found miR-146a could suppress Src phosphorylation and downstream targets VE-cadherin and Caveolin-1. Collectively, our data indicate that MSC-sEV mitigated endothelial cell senescence and stimulate angiogenesis through miR-146a/Src. | Xian Xiao Meiqian Xu Hongliang Yu Liping Wang Xiaoxia Li Janusz Rak Shihua Wang Robert Chunhua Zhao | 2021 | Signal Transduction and Targeted Therapy2021，6，11： | 5 |
| 3 | Surface and Hydrogen Sorption Characteristics of Various Activated Carbons Developed from Rat Coal Mine (Zonguldak) and Anthracite显示文摘激活的碳样品从从一个煤矿获得的煤样品被开发,老鼠(Zonguldak,土耳其) 并且白煤(西伯利亚,俄国) ,在 600900 | Atakan Top rak Turkan Kopac | 2011 | Chinese Journal of Chemical Engineering2011，19，6： | 4 |
| 4 | Chronological age when health care transition skills are mastered in adolescents/young adults with inflammatory bowel disease显示文摘AIM To describe the longitudinal course of acquisition of healthcare transition skills among adolescents and young adults with inflammatory bowel diseases.METHODS We recruited adolescents and young adults(AYA) with inflammatory bowel diseases(IBD), from the pediatric IBD clinic at the University of North Carolina. Participants completed the TRx ANSITION Scale? at least once during the study period(2006-2015). We used the electronic medical record to extract participants' clinical and demographic data. We used ordinary least square regressions with robust standard error clustered at patient level to explore the variations in the levels and growths of healthcare transition readiness.RESULTS Our sample(n = 144) ranged in age from 14-22 years. Age was significantly and positively associated with both the level and growth of TRx ANSITION Scale? scores(P < 0.01). Many healthcare transition(HCT) skills were acquired between ages 12 and 14 years, but others were not mastered until after age 18, including self-management skills.CONCLUSION This is one of the first studies to describe the longitudinal course of HCT skill acquisition among AYA with IBD, providing benchmarks for evaluating transition interventions. | Natalie Stollon Yi Zhong Maria Ferris Suneet Bhansali Brian Pitts Eniko Rak Maureen Kelly Sandra Kim Miranda AL van Tilburg | 2017 | World Journal of Gastroenterology2017，23，18： | 2 |
| 5 | Attenuated FOLFIRINOX in the salvage treatment of gemcitabine-refractory advanced pancreatic cancer: a phase II study显示文摘Background:Combination therapy with oxaliplatin,irinotecan,fluorouracil,and leucovorin(FOLFIRINOX)chemotherapy drastically improves survival of advanced pancreatic cancer patients.However,the efficacy of FOLFIRINOX as a second-line treatment after gemcitabine failure has not been tested prospectively.We investigated the feasibility and safety of attenuated FOLFIRINOX in patients with gemcitabine-refractory advanced pancreatic cancer.Methods:A multicenter phase II prospective open-label,single-arm study was conducted at 14 hospitals.Patients with histologically proven invasive ductal pancreatic adenocarcinoma,a measurable or evaluable lesion,Eastern Cooperative Oncology Group performance status 0 or 1,adequate organ function,and aged 19 years or older were eligible.Attenuated FOLFIRINOX consisted of oxaliplatin 65 mg/m2,irinotecan 135 mg/m2,and leucovorin 400 mg/m2 injected intravenously on day 1 and 5-fluorouracil 2000 mg/m2 continuously infused intravenously over 46 h on days 1-2,repeated every 2 weeks.The primary endpoint was progression-free survival from the initiation of FOLFIRINOX.Secondary endpoints were the objective response rate,disease control rate,overall survival,safety,and tolerability.We estimated overall survival and progression-free survival using the Kaplan-Meier methods.Results:We enrolled 39 patients from 14 institutions.The objective response rate was 10.3%,while the disease control rate was 64.1%.The 6-month and 1-year overall survival rates were 59.0%and 15.4%,respectively.Median progression-free survival and overall survival were 3.8 months(95%confidence interval[CI]1.5-6.0 months)and 8.5 months(95%CI 5.6-11.4 months),respectively.Grade 3 or 4 adverse events were neutropenia(41.0%),nausea(10.3%),anorexia(10.3%),anemia(7.7%),mucositis(7.7%),pneumonia/pleural effusion(5.1%),and fatigue(5.1%).One treatment-related death attributable to septic shock occurred.Conclusion:Attenuated FOLFIRINOX may be promising as a second-line therapy for gemcitabine-refractory pancre-atic cancer. | Jung Hoon Kim Sang-Cheol Lee Sung Yong Oh Seo-Young Song Namsu Lee Eun Mi Nam Soonil Lee In Gyu Hwang Hyo Rak Lee Kyu Taek Lee Sang-Byung Bae Han Jo Kim Joung Soon Jang Do Hyoung Lim Hyun Woo Lee Seok Yun Kang Jung Hun Kang | 2018 | Cancer Communications2018，38，1： | 2 |
| 6 | AIF-regulated oxidative phosphorylation supports lung cancer development显示文摘Cancer is a major and still increasing cause of death in humans. Most cancer cells have a fundamentally different metabolic profile from that of normal tissue. This shift away from mitochondrial ATP synthesis via oxidative phosphorylation towards a high rate of glycolysis, termed Warburg effect, has long been recognized as a paradigmatic hallmark of cancer, supporting the increased biosynthetic demands of tumor cells. Here we show that deletion of apoptosis-inducing factor (AIF) in a Kras^G12D-driven mouse lung cancer model resulted in a marked survival advantage, with delayed tumor onset and decreased malignant progression. Mechanistically, Aif deletion leads to oxidative phosphorylation (OXPHOS) deficiency and a switch in cellular metabolism towards glycolysis in non-transformed pneumocytes and at early stages of tumor development. Paradoxically, although Aif-deficient cells exhibited a metabolic Warburg profile, this bioenergetic change resulted in a growth disadvantage of Kras^G12D-driven as well as Kras wild-type lung cancer cells. Cell-autonomous re-expression of both wild-type and mutant AIF (displaying an intact mitochondrial, but abrogated apoptotic function) in Aif-knockout Kras^G12D mice restored OXPHOS and reduced animal survival to the same level as AIF wild-type mice. In patients with non-small cell lung cancer, high AIF expression was associated with poor prognosis. These data show that AIF-regulated mitochondrial respiration and OXPHOS drive the progression of lung cancer. | Shuan Rao Laura Mondragon Blanka Pranjic Toshikatsu Hanada Gautier Stoll Thomas Kocher Peng Zhang Alexander Jais Alexander Lercher Andreas Bergthaler Daniel Schramek Katharina Haigh Valentina Sica Marion Leduc Nazanine Modjtahedi Tsung-Pin Pai Masahiro Onji Iris Uribesalgo Reiko Hanada Ivona Kozieradzki Rubina Koglgruber Shane J. Cronin Zhigang She Franz Quehenberger Helmut Popper Lukas Kenner Jody J. Haigh Oliver Kepp Malgorzata Rak Kaican Cai Guido Kroemer Josef M. Penninger | 2019 | Cell Research2019，29，7： | 2 |
| 7 | Massive hemoptysis after a bronchoscopic biopsy in patients with endobronchial tuberculosis显示文摘Endobronchial tuberculosis (EBTB) is an infectious disease occurring in the trachea or the bronchus with microbiological and histological evidences of tuberculosis.It is assumed a specific form or complication of tuberculosis.EBTB is combined in 10% to 40% of patients with active pulmonary tuberculosis. | Eun Seok Kang Young Rak Choi Ki Man Lee Kang Hyeon Choe Jin Young An | 2014 | Chinese Medical Journal2014，，21： | 2 |
| 8 | 十五肽BPC157减弱慢性苯丙胺诱导的行为障碍(英文)显示文摘AIM: To investigate the effect of pentadecapeptide BPC 157 on chronic exposure to amphetamine in rats, particularly the changes commonly referred in chronic amphetamine studies as tolerance ( lesser grade of stereotyped behavior, without increased excitability) and reverse tolerance (ie, prominent stereotyped behavior and heightened startle response upon late amphetamine challenges). METHODS: After initial application (initial single dose-regimen), amphetamine (10 mg/kg, ip) was given once daily till d 5 ( continuous administration-regimen), and thereafter on d 8, 16, and 46 (intermittent administration regimen). For stereotyped behavior and heightened startle response the observation period was 120 min after amphetamine application, and each animal was observed for 10 s in 5 min intervals. Pentadecapeptide BPC 157 (10 μg/kg or 10 ng/kg, ip) or saline (5.0 mL/kg, ip) were given only at the beginning of the experiment, simultaneously with the initial dose of amphetamine. RESULTS: In relation to | Predrag SIKIRIC, Nikola JELOVAC, Andjelka JELOVAC-GJELDUM, Goran DODIG, Mario STARESINIC, Tornislav ANIC, Ivan ZORICIC, Davor RAK, Darko PEROVIC, Gorana ARALICA, Gojko BULJAT, Ingrid PRKACEV, Martina LOVRIC-BENCIC, Jadranka SEPAROVIC, Sven SEIWERTH, Rudolf RUCMAN, Marijan PETEK, Branko TURKOVIC, Tihomil ZIGER, AJenka BOBAN-BLAGAIC, Vlado BEDEKOVIC, Ante TONKIC, Slaven BABIC ( Department of Pharmacology, Medical Faculty University of Zagreb, Croatia) | 2002 | Acta Pharmacologica Sinica2002，23，5： | 2 |
| 9 | Marked induction of the IAP family antiapoptosis proteins Survivin and XIAP by VEGF in vascular endothelial cells显示文摘 | Tran J Rak J Sheehan C | 1999 | Biochem Biophys Res Commun1999，264，： | 1 |
| 10 | Mutant ras oncogenes upregu- late VEGF/VPF expression:implications for induction and inhibition of tumor angiogenesis显示文摘 | Rak J Mitsuhashi Y Bayko L | 1995 | Cancer Res1995，55，20： | 1 |
| 11 | Production of cytokines and stimulation of resistance to viral infection in human leukocytes by Scutellaria baicalensis flavones显示文摘 | Btach-Olszewska Z Jatczak B Rak A | 2008 | J Interferon Cytokine Res2008，25，9： | 1 |
| 12 | From critical care to comfort care:the sustaining value of humour显示文摘 | Dean RAK Major JE | 2008 | J Clin Nurs2008，17，8： | 1 |
| 13 | Oncogenes and tumor angiogenesis:the question of vascular 'supply' and vascular 'demand'显示文摘 | Rak J Yu JL | 2004 | Semin Cancer Biol2004，14，2： | 1 |
| 14 | Continuous low-dose therapy with vinblastine and VEGF receptor-2 antibody induces sustained tumor regression without overt toxieity显示文摘 | Klement G Baruchel S Rak J | 2000 | J Clin Invest2000，105，8： | 1 |
| 15 | Effect of p53 status on tumor response to antiangiogenie therapy显示文摘 | Yu JL Rak JW Coomber BL | 2002 | Science2002，295，： | 1 |
| 16 | Operative treatment of intra-articular calcaneal fractures with calcaneal plates and its complications显示文摘 | Rak V Ira D | 2009 | Indian Orthop2009，3，： | 1 |
| 17 | Marked induction of the IAP fami- ly antiapoptotic proteins Survivin and XIAP by VEGF in vascular endothelial cells显示文摘 | Tran J Rak J Sheehan C | 1999 | Biochem Biophys Res Commun1999，264，5： | 1 |
| 18 | Continuous low-dose thera-py with vinblastine and VEGF receptor-2 antibody induces sustained tumorregression without overt toxicity 显示文摘 | Klement G Baruchel S Rak J | 2000 | J Clin Invest2000，105，8： | 1 |
| 19 | Production of cytokines and stimulation of resistance to viral infection in human leukocytes by Scutellaria baicalensis flavones显示文摘 | Blach-Olszewska Z Jatczak B Rak A | 2008 | Interferon Cytokine Res2008，28，9： | 1 |
| 20 | Distributivity equation for nullnorms 显示文摘 | Rak E | 2005 | J Electr Eng2005，56，12： | 1 |
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