18 results on '"Chong, Shan"'
Search Results
2. Contributors
- Author
-
Ascierto, Paolo A., primary, Bertolotti, Milena, additional, Borkowsky, William, additional, Coussens, Lisa M., additional, Esclatine, Audrey, additional, Festino, Lucia, additional, Gershon, Anne A., additional, Hayat, M.A., additional, He, Ming-Xiao, additional, He, You-Wen, additional, Ibrahim, Nuhad K., additional, Jagannath, Chinnaswamy, additional, Jia, Wei, additional, Kehrl, John H., additional, Khan, Arshad, additional, Lal, Girdhari, additional, Lang, Mark L., additional, Liudahl, Shannon M., additional, Lussignol, Marion, additional, Marciani, Dante J., additional, McLeod, Ian, additional, Murray, James L., additional, Nabar, Neel R., additional, Norian, Lyse, additional, Orlandella, Rachael, additional, Paul, Sourav, additional, Rampuria, Pragya, additional, Shi, Chong-Shan, additional, Sitia, Roberto, additional, Strudel, Martina, additional, Vanella, Vito, additional, Venkatesh, Yeldur P., additional, Wang, Jin, additional, and Yang, Chuanwei, additional
- Published
- 2018
- Full Text
- View/download PDF
3. Autophagy Accompanies Inflammasome Activation to Moderate Inflammation by Eliminating Active Inflammasomes
- Author
-
Nabar, Neel R., primary, Shi, Chong-Shan, additional, and Kehrl, John H., additional
- Published
- 2017
- Full Text
- View/download PDF
4. Contributors
- Author
-
Amer, Amal O., primary, Ávalos, Yenniffer, additional, Belyayev, Alexander, additional, Caution, Kyle, additional, Cenci, Simone, additional, Cecconi, Francesco, additional, Choksi, Swati, additional, Cianfanelli, Valentina, additional, Cook, Katherine L., additional, Clarke, Robert, additional, Cornet-Boyaka, Estelle, additional, Cragg, Mark S., additional, Dakhlallah, Duaa, additional, Erenpreisa, Jekaterina, additional, Esaki, Masatoshi, additional, Feun, Lynn G., additional, Fink, Mark Y., additional, Gottlieb, Roberta A., additional, Guo, Jessie Y., additional, Harimoto, Norifumi, additional, Harris, James, additional, Hayat, M.A., additional, Hayashi, Toshihiko, additional, Hernández-Cáceres, Maria P., additional, Ikegami, Toru, additional, Ikejima, Takashi, additional, Inashkina, Inna, additional, Itoh, Shinji, additional, Ivanov, Andrei I., additional, Kehrl, John H., additional, Kuo, M.T., additional, Lang, Tali, additional, Franco Leal, Raquel, additional, Liu, Zhenggang, additional, Lipatova, Zhanna, additional, Luo, Jia, additional, Maehara, Yoshihiko, additional, Manque, Patricio, additional, Markaki, Maria, additional, Matsumoto, Yoshihiro, additional, Metaxakis, Athansios, additional, MeKee-Muir, Olivia C., additional, Morselli, Eugenia, additional, Nabar, Neel R., additional, Nassif, Melissa, additional, Nguyen, Dao, additional, Pengo, Niccolò, additional, Protasoni, Margherita, additional, Russell, Ryan C., additional, Salmina, Kristine, additional, Savaraj, Niramol, additional, Segev, Nava, additional, Shi, Chong-Shan, additional, Shirabe, Ken, additional, Ramos Silva, Francesca A., additional, Snyder, Michelle L., additional, Sukkar, Maria B., additional, Taanman, Jan-Willem, additional, Tavernarakis, Nektarios, additional, Toledo, Lilian, additional, Toshima, Takeo, additional, Tsung, Allan, additional, Wangpaichitr, Medhi, additional, Weichseldorfer, Matthew R., additional, White, Theresa L., additional, Woelhbier, Ute, additional, Wu, Chunjing, additional, Yoshizumi, Tomoharu, additional, You, Min, additional, Zhang, Lemeng, additional, and Zhang, Yan, additional
- Published
- 2017
- Full Text
- View/download PDF
5. Impact of increasing alanine aminotransferase levels within normal range on incident diabetes
- Author
-
Chong-Shan Wang, Ting-Tsung Chang, Wei-Jen Yao, Shan-Tair Wang, and Pesus Chou
- Subjects
alanine aminotransferase ,cohort study ,incident type 2 diabetes ,Medicine (General) ,R5-920 - Abstract
Abnormal alanine aminotransferase level (ALT) levels might be associated with type 2 diabetes, but whether higher ALT levels within the normal range predict the risk is unknown. Methods: We followed a community-based cohort of 3446 individuals who were ≥35 years old without diabetes and hepatitis B or C in southern Taiwan for 8 years (1997–2004) to study the risk for type 2 diabetes with different normal ALT levels. Results: Among the 337 incident diabetes cases, 16.0% were from those with ALT levels
- Published
- 2012
- Full Text
- View/download PDF
6. Contributors
- Author
-
Carroll, Bernadette, primary, Codogno, Patrice, additional, Colombo, María I., additional, Durcan, Thomas M., additional, Eckhart, Leopold, additional, Esclatine, Audrey, additional, Falk, Matthias M., additional, Frühbeck, Gema, additional, Fujita, Masayo, additional, Ghislat, Ghita, additional, Gozuacik, Devrim, additional, Grose, Charles, additional, Harris, James, additional, Hashimoto, Makoto, additional, Hayat, M.A., additional, Hewitt, Graeme, additional, Iwamaru, Yoshifumi, additional, Jones, Sarah A., additional, Kehrl, John H., additional, Kitani, Hiroshi, additional, Knecht, Erwin, additional, Korolchuk, Viktor I., additional, Lee, Jongdae, additional, López de Armentia, María Milagros, additional, Lorin, Séverine, additional, Lussignol, Marion, additional, Marinković, Mija, additional, Meijer, Alfred J., additional, Méndez-Giménez, Leire, additional, Münz, Christian, additional, Novak, Ivana, additional, Ou, Jing-hsiung James, additional, Ozturk, Deniz Gulfem, additional, Peral de Castro, Celia, additional, Raz, Eyal, additional, Rodríguez, Amaia, additional, Sekiyama, Kazunari, additional, Shi, Chong-Shan, additional, Sugama, Shuei, additional, Sukseree, Supawadee, additional, Takenouchi, Takato, additional, Tang, Matthew Y., additional, Tekirdag, Kumsal Ayse, additional, Tian, Yongjun, additional, Tsukimoto, Mitsutoshi, additional, Vural, Ali, additional, and Wang, Lin-ya, additional
- Published
- 2015
- Full Text
- View/download PDF
7. Toll-Like Receptors Serve as Activators for Autophagy in Macrophages Helping to Facilitate Innate Immunity
- Author
-
Vural, Ali, primary, Shi, Chong-Shan, additional, and Kehrl, John H., additional
- Published
- 2015
- Full Text
- View/download PDF
8. Signaling by the Toll-Like Receptors Induces Autophagy Through Modification of Beclin 1
- Author
-
Neel R. Nabar, Chong-Shan Shi, and John H. Kehrl
- Subjects
0301 basic medicine ,Toll-like receptor ,Innate immune system ,Autophagy ,Pattern recognition receptor ,Signal transducing adaptor protein ,Biology ,Cell biology ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Immune system ,TRIF ,030220 oncology & carcinogenesis ,Intracellular - Abstract
The innate immune system employs germline-encoded pattern recognition receptors (PRRs) that can detect pathogens and initiate the immune response. The Toll-like receptors (TLRs) are the best studied PRRs and they act by initiating an intracellular signaling cascade that is dependent on the adaptor proteins MyD88 and TRIF. This response activates the critical transcription factors NF-κB and IRF3, and functions to prime both the innate and adaptive immune effector cells for pathogen clearance. Macrophages are one of the major effector cell types of innate immunity. They help clear extracellular infections by phagocytosis and eventual phagosome–lysosome fusion, and intracellular infections by enclosing microbes in autophagic vesicles for delivery to the lysosome. Initiation of autophagy requires phosphatidylinositol 3-phosphate [PtdIns(3)P], which is generated by the phosphatidylinositol 3-kinase class III (PtdIns3KC3/Vps34) complex. This chapter discusses the detailed molecular mechanisms through which TLR signaling primes macrophages for intracellular pathogen clearance by initiating autophagy. We focus on Beclin 1, a key component of the PtdIsn3KC3 complex, which is recruited to the TLR signalosome upon TLR stimulation and subsequently posttranslationally modified to disrupt its binding with its inhibitor, Bcl-2.
- Published
- 2018
9. Contributors
- Author
-
Paolo A. Ascierto, Milena Bertolotti, William Borkowsky, Lisa M. Coussens, Audrey Esclatine, Lucia Festino, Anne A. Gershon, M.A. Hayat, Ming-Xiao He, You-Wen He, Nuhad K. Ibrahim, Chinnaswamy Jagannath, Wei Jia, John H. Kehrl, Arshad Khan, Girdhari Lal, Mark L. Lang, Shannon M. Liudahl, Marion Lussignol, Dante J. Marciani, Ian McLeod, James L. Murray, Neel R. Nabar, Lyse Norian, Rachael Orlandella, Sourav Paul, Pragya Rampuria, Chong-Shan Shi, Roberto Sitia, Martina Strudel, Vito Vanella, Yeldur P. Venkatesh, Jin Wang, and Chuanwei Yang
- Published
- 2018
10. Contributors
- Author
-
Amal O. Amer, Yenniffer Ávalos, Alexander Belyayev, Kyle Caution, Simone Cenci, Francesco Cecconi, Swati Choksi, Valentina Cianfanelli, Katherine L. Cook, Robert Clarke, Estelle Cornet-Boyaka, Mark S. Cragg, Duaa Dakhlallah, Jekaterina Erenpreisa, Masatoshi Esaki, Lynn G. Feun, Mark Y. Fink, Roberta A. Gottlieb, Jessie Y. Guo, Norifumi Harimoto, James Harris, M.A. Hayat, Toshihiko Hayashi, Maria P. Hernández-Cáceres, Toru Ikegami, Takashi Ikejima, Inna Inashkina, Shinji Itoh, Andrei I. Ivanov, John H. Kehrl, M.T. Kuo, Tali Lang, Raquel Franco Leal, Zhenggang Liu, Zhanna Lipatova, Jia Luo, Yoshihiko Maehara, Patricio Manque, Maria Markaki, Yoshihiro Matsumoto, Athansios Metaxakis, Olivia C. MeKee-Muir, Eugenia Morselli, Neel R. Nabar, Melissa Nassif, Dao Nguyen, Niccolò Pengo, Margherita Protasoni, Ryan C. Russell, Kristine Salmina, Niramol Savaraj, Nava Segev, Chong-Shan Shi, Ken Shirabe, Francesca A. Ramos Silva, Michelle L. Snyder, Maria B. Sukkar, Jan-Willem Taanman, Nektarios Tavernarakis, Lilian Toledo, Takeo Toshima, Allan Tsung, Medhi Wangpaichitr, Matthew R. Weichseldorfer, Theresa L. White, Ute Woelhbier, Chunjing Wu, Tomoharu Yoshizumi, Min You, Lemeng Zhang, and Yan Zhang
- Published
- 2017
11. Autophagy Accompanies Inflammasome Activation to Moderate Inflammation by Eliminating Active Inflammasomes
- Author
-
John H. Kehrl, Chong-Shan Shi, and Neel R. Nabar
- Subjects
0301 basic medicine ,Innate immune system ,Autophagy ,Cellular homeostasis ,Inflammation ,Inflammasome ,Biology ,Systemic inflammation ,Cell biology ,03 medical and health sciences ,AIM2 ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Lysosome ,medicine ,medicine.symptom ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Inflammation is an important physiological response to noxious stimuli, but unchecked inflammation is pathophysiological and can result in tissue destruction and autoimmune disease. Inflammasomes are large multimeric signaling complexes of the innate immune system involved in the proteolytic cleavage and activation of interleukin-1 beta (IL-1β) and IL-18. Inflammasome signaling is a key early step in generating the inflammatory response as IL-1β is a critical cytokine in mediating systemic inflammation and has a variety of downstream effects. Aberrant inflammasome activation is the basis of many human autoinflammatory diseases, thus delineation of feedback loops regulating inflammasome signaling is of great importance to understanding autoinflammatory conditions. Autophagy is a conserved degradation pathway that delivers damaged organelles and aged protein complexes to the lysosome for destruction. It evolved both as a cellular recycling system and as a quality control system to ensure cellular homeostasis. This chapter covers the dynamic interplay between inflammasome activation and autophagy induction, with a specific focus on the cellular and molecular mechanisms by which autophagy feedback inhibits inflammasome signaling.
- Published
- 2017
12. Toll-Like Receptors Serve as Activators for Autophagy in Macrophages Helping to Facilitate Innate Immunity
- Author
-
Ali Vural, John H. Kehrl, and Chong-Shan Shi
- Subjects
Chemokine ,Innate immune system ,Downregulation and upregulation ,biology ,Intracellular parasite ,Autophagy ,biology.protein ,Signal transducing adaptor protein ,Receptor ,Cell biology ,Interferon regulatory factors - Abstract
Toll-like receptors (TLRs) play critical roles in host defense by recognizing specific molecular patterns from a wide variety of pathogens. Using a small set of adaptor proteins TLR engagement leads to the activation of nuclear factor-κB (NF-κB) and interferon regulatory factors (IRFs). This results in the upregulation of downstream target genes including an array of pro-inflammatory cytokines, chemokines, and interferon-responsive genes. In macrophages TLR signaling also induces autophagy. Autophagy is a cellular response to starvation that helps remove damaged organelles and long-lived proteins from the cytosol. It also has a cytoprotective function helping to limit the replication of intracellular pathogens. Many pathogens target the autophagy pathway to thwart its effectiveness. This review focuses on how TLRs can activate autophagosome formation in macrophages and briefly reviews the role of autophagy in innate immunity.
- Published
- 2015
13. Abemaciclib increases the risk of venous thromboembolism in breast cancer: Integrate meta-analysis, pharmacovigilance database analysis, and in vitro validation.
- Author
-
Hua M, Xiong F, Chong S, Zhang Z, Liu Q, Hou J, Zhang Z, Gu Z, Cui X, Cui Y, Xu L, and Xiang Q
- Abstract
Background: Recently, cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) have emerged as a novel treatment strategy for breast cancer. However, increasing reports of CDK4/6i-associated venous thromboembolism (VTE) have garnered attention. This study assessed CDK4/6i-associated VTE in breast cancer, and examined the effect of CDK4/6i on platelet/coagulation function for the first time in vitro., Methods: PubMed and Embase databases were searched for studies published from the establishment of the database to December 31, 2022 for randomized controlled trials (RCTs) and real-world studies of CDK4/6i in patients with breast cancer, and the data obtained from the included studies were used for meta-analysis. A disproportionality analysis by extracting adverse drug reaction signals of CDK4/6i-associated VTE from the FDA Adverse Event Reporting System (FAERS) database was also conducted. Additionally, the in vitro effect of CDK4/6i on platelet function was assessed based on platelet aggregation tests and flow cytometry, and coagulation function was assessed based on the blood clotting function test., Findings: A total of 16,903 patients in 13 RCTs and 6,490 patients in 9 real-world studies were included in the meta-analysis. In RCTs, VTE occurred in 193 (2.1 %) and 55 (0.7 %) patients in the CDK4/6i and control groups, respectively. In real-world studies, the aggregate incidence rate of VTE was 4.2 % (95 % CI: 2.1, 6.3). The meta-analysis of RCTs revealed that abemaciclib (Odds ratio [OR]: 4.40 [95 % CI: 2.74,7.05], p < 0.001) and palbociclib (OR: 2.35 [95 % CI: 1.34, 4.12], p < 0.01) significantly increased the risk of VTE in patients with breast cancer compared to placebo. FAERS database analysis revealed that abemaciclib (reporting odds ratio [ROR]: 1.63 [95 % CI: 1.36, 1.97]; IC
025 : 0.67) and ribociclib (ROR: 1.17 [95 % CI: 1.0, 1.39]; IC025 : 0.18) demonstrated a significantly increased signal of VTE. Similarly, findings from in vitro experiments demonstrated that abemaciclib enhanced agonist-induced platelet activation, especially when collagen was used as the inducer, and this effect became more prominent with increasing its concentration., Interpretation: Use of abemaciclib may increase the risk of VTE in patients with breast cancer, which may be partially attributed to the effect of abemaciclib on platelet function. Close monitoring of VTE occurrence is highly recommended while using abemaciclib, especially in patients at a high risk of VTE., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)- Published
- 2024
- Full Text
- View/download PDF
14. The effects of repeated freezing and thawing on bovine sperm morphometry and function.
- Author
-
Min CG, Ma X, Wang YC, Zhong CK, Yuan CS, Zhang KY, Zhan CL, Hou SK, Wang XH, Wang J, Zhao J, Fang Y, Liu HY, Ding H, Guo J, and Lu WF
- Subjects
- Animals, Male, Cattle, Cell Membrane, Cell Survival, Acrosome, Cryopreservation veterinary, Cryopreservation methods, Sperm Motility, Semen Preservation veterinary, Semen Preservation methods, Spermatozoa physiology, Fertilization in Vitro veterinary, Freezing adverse effects, Oxidative Stress, Apoptosis
- Abstract
Refreezing the remaining genetic resources after in vitro fertilization (IVF) can conserve genetic materials. However, the precise damage inflicted by repeated freezing and thawing on bovine sperm and its underlying mechanism remain largely unexplored. Thus, this study investigates the impact of repeated freeze-thaw cycles on sperm. Our findings indicate that such cycles significantly reduce sperm viability and motility. Furthermore, the integrity of the sperm plasma membrane and acrosome is compromised during this process, exacerbating the advanced apoptosis triggered by oxidative stress. Additionally, transmission electron microscopy exposed severe damage to the plasma membranes of both the sperm head and tail. Notably, the "9 + 2" structure of the tail was disrupted, along with a significant decrease in the level of the axonemal protein DNAH10, leading to reduced sperm motility. IVF outcomes revealed that repeated freeze-thaw cycles considerably impair sperm fertilization capability, ultimately reducing the blastocyst rate. In summary, our research demonstrates that repeated freeze-thaw cycles lead to a decline in sperm viability and motility, attributed to oxidative stress-induced apoptosis and DNAH10-related dynamic deficiency. As a result, the utility of semen is compromised after repeated freezing., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Society for Cryobiology. Published by Elsevier Inc. All rights reserved.)
- Published
- 2024
- Full Text
- View/download PDF
15. Executive function predict the quality of life and negative emotion in older adults with diabetes: A longitudinal study.
- Author
-
Ho HT, Lin SI, Guo NW, Yang YC, Lin MH, and Wang CS
- Subjects
- Aged, Emotions, Humans, Longitudinal Studies, Pain diagnosis, Pain etiology, Quality of Life psychology, Diabetes Mellitus diagnosis, Executive Function
- Abstract
Aims: To investigate the influence of executive function (EF) on current and future quality of life (QoL) and negative emotion (NE) in older adults with diabetes., Methods: A total of 128 older adults with diabetes were recruited. Independent variables (demographic information, health and medical conditions, cognitive function, life function) were collected in the first year. Dependent variables (QoL and NE) were collected for 3 years. Pearson's correlation coefficient analysis and stepwise multiple linear regression analysis were performed to identify the predictors of QoL and NE., Results: EF was the strongest predictor for overall QoL and NE in all 3 years, and accounted for 23.0-36.2% and 11.1-17.1% of the variance, respectively. The second strongest predictor for overall QoL in all 3 years was pain interference, which accounted for 3.2-5.8% of the variance. Pain interference was also the second strongest predictor for NE in the second year, accounting for 5.5% of the variance., Conclusions: The present study revealed that EF is more predictive than pain for current and future QoL and NE in older adults with diabetes. We recommend that EF be included as an indicator for diabetes surveillance, and that prevention of EF decline be a part of diabetes management plans., (Copyright © 2022 Primary Care Diabetes Europe. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2022
- Full Text
- View/download PDF
16. Downregulation of TRPC6 expression is a critical molecular event during FK506 treatment for overactive bladder.
- Author
-
Chang C, Li K, Jiang S, Li B, Cao L, and Wang P
- Subjects
- Animals, Disease Models, Animal, Female, Humans, Rats, Rats, Wistar, Down-Regulation drug effects, TRPC Cation Channels biosynthesis, TRPC6 Cation Channel biosynthesis, Tacrolimus pharmacology, Urinary Bladder, Overactive drug therapy, Urinary Bladder, Overactive metabolism, Urinary Bladder, Overactive pathology, Urodynamics drug effects
- Abstract
Purpose: It has been suggested that FK506 could improve some symptoms of OAB in both clinical settings and animal models; however, its mechanism of action is not well-understood. Here, we investigated the effect of FK506 on TRPC6 in bladder smooth muscle, and explored the possible involvement of TRPC6 in OAB., Methods: FK506 was injected intraperitoneally into rats in which OAB was induced via BOO, and urodynamic indices were recorded. Rats and human bladder smooth muscle tissues with or without OAB were examined for TRPC6 expression by western blot, RT-PCR and IF staining. Cultured BSMCs were treated with PDGF, TRPC6 siRNAs and FK506. Then the TRPC6 expression and cellular proliferation were examined, and the Ca
2+ influx and contractility of BSMCs were examined by time-lapse Ca2+ imaging and collagen gel contraction. Finally, IF and Co-IP were performed to test the effects of FK506 on NFAT translocation to the nucleus and the interaction of TRPC6 with FKBP12, respectively., Results: FK506 improved urodynamic indices of OAB rats, and TRPC6 was expressed in rats and human bladder tissues. TRPC6 elevation in OAB rats was inhibited by FK506, and this inhibition coincided with improvements in urodynamic indices. PDGF enhanced TRPC6 expression, cellular proliferation, Ca2+ influx and contractility of BSMCs, and these effects were inhibited by TRPC6 siRNAs and FK506. FK506 inhibited NFAT translocation to the nucleus and disrupted the interaction of TRPC6 with FKBP12., Conclusions: Our results collectively indicate that FK506 may be used to treat OAB, and that TRPC6 may serve as an attractive target for therapeutic intervention in OAB., (Copyright © 2018 Elsevier Ltd. All rights reserved.)- Published
- 2019
- Full Text
- View/download PDF
17. Diclofenac degradation in water by FeCeO x catalyzed H 2 O 2 : Influencing factors, mechanism and pathways.
- Author
-
Chong S, Zhang G, Zhang N, Liu Y, Huang T, and Chang H
- Abstract
The degradation of diclofenac in a like Fenton system, FeCeO
x -H2 O2 , was studied in details. The influencing factors, reaction kinetics, reaction mechanism and degradation pathways of diclofenac were investigated. The optimum conditions were at a solution pH of 5.0, H2 O2 concentration of 3.0mmol/L, diclofenac initial concentration of 0.07mmol/L, FeCeOx dosage of 0.5g/L, and 84% degradation of diclofenac was achieved within 40min. The kinetics of FeCeOx catalyzed H2 O2 process involved adsorption-dominating and degradation-dominating stages and fitted pseudo-second order model and pseudo-first order model, respectively. Singlet oxygen1 O2 was the primary intermediate oxidative species in the degradation process; superoxide radical anion O2 - also participated in the reaction. The surface cerium and iron sites and the oxygen vacancies in the FeCeOx catalyst were proposed to play an important role in H2 O2 decomposition and active species generation. The detected intermediates were identified as hydroxylated derivatives (m/z of 310, 326 and 298), quinone imine compounds (m/z of 308, 278 and 264) and hydroxyl phenylamine (m/z of 178). The majority intermediates were hydroxylated derivatives and the minority was hydroxyl phenylamine. The degradation pathways were proposed to involve hydroxylation, decarboxylation, dehydrogenation and CN bond cleavage., (Copyright © 2017 Elsevier B.V. All rights reserved.)- Published
- 2017
- Full Text
- View/download PDF
18. Zusanli (ST36) acupoint injection for preventing postoperative ileus: A systematic review and meta-analysis of randomized clinical trials.
- Author
-
Wang M, Gao YH, Xu J, Chi Y, Wei XB, Lewith G, and Liu JP
- Subjects
- Adult, Aged, Aged, 80 and over, Female, Humans, Ileus epidemiology, Male, Middle Aged, Postoperative Complications epidemiology, Young Adult, Acupuncture Points, Acupuncture Therapy, Ileus prevention & control, Ileus therapy, Postoperative Complications prevention & control, Postoperative Complications therapy
- Abstract
Objective: To evaluate the preventive effect of Zusanli (ST36) acupoint injections with various agents, for postoperative ileus (POI)., Methods: We searched electronic databases for randomized controlled trials from inception to 1st February 2015 evaluating ST36 acupoint injection for preventing POI. Revman 5.2.0 was used for data analysis with effect estimates presented as mean difference (MD) with 95% confidence interval (CI). Statistical heterogeneity was tested using I(2) (defined as significant if I(2)>75%). We used a random effects model (REM) for pooling data with significant heterogeneity., Results: Thirty trials involving 2967 participants were included. All trials were assessed as high risk of bias (poor methodological quality). For time to first flatus, meta-analysis favored ST36 acupoint injection of neostigmine (MD -20.70h, 95% CI -25.53 to -15.87, 15 trials, I(2)=98%, REM), vitamin B1 (MD -11.22h, 95% CI -17.01 to -5.43, 5 trials, I(2)=98%, REM), and metoclopramide (MD -15.65h, 95% CI -24.77 to -6.53, 3 trials, I(2)=94%, REM) compared to usual care alone. Meta-analysis of vitamin B1 favored ST36 acupoint injection compared to intra-muscular injection (MD -17.21h, 95% CI -21.05 to -13.36, 4 trials, I(2)=89%, REM). Similarly, for time to bowel sounds recovery and first defecation, ST36 acupoint injection also showed positive effects., Conclusions: ST36 acupoint injections with various agents may have a preventive effect for POI. Safety is inconclusive as few of included trials reported adverse events. Due to the poor methodological quality and likely publication bias further robust clinical trials are required to arrive at a definitive conclusion., (Copyright © 2015 Elsevier Ltd. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.