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| There are 41 papers published in subject: since this site started. | |||
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| 1. HAS2 Promotes Pancreatic Stellate Cells Activation under TGF-β1/MeCP2 Axis in Chronic Pancreatitis | |||
| LI Ruiping,ZHU Jianwei,PENG Xue,LIU Miaoru,FAN Zijun,CAI Zixuan,SHE Yuanling,GONG Zhenyun,ZHAO Jing,HU Duanmin | |||
Clinical Medicine 14 April 2023
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| Abstract:The pathogenesis of chronic pancreatitis (CP) remains unclear. Few studies have investigated the role of hyaluronic acid synthetase 2 (HAS2) in CP tissue and its effects on pancreatic stellate cells (PSCs). The purpose of this study was to investigate the effect of HAS2 on the occurrence and development of CP fibrosis through the activation of PSCs. Firstly, the effects of up-regulation and down-regulation of HAS2 on α-smooth muscle actin (α-SMA) expression in PSCs were investigated by RT-qPCR and Western blotting. Secondly, the regulatory effects of HAS2 on the fibroblast phenotype of PSCs were investigated by cell wound healing assay, transwell assay and CCK-8 assay. Then, the rescue assay was used to investigate whether HAS2 was regulated by the TGF-β1/MeCP2 axis. Finally, the CP rat model was constructed to explore whether the expression of HAS2 and MeCP2 was increased, and Pearson linear correlation was used to investigate the correlation between the expression level of HAS2 and the degree of pancreatic fibrosis. The results revealed that HAS2 promoted α-SMA expression in PSCs, and the down-regulation of HAS2 inhibited the migration and proliferation of PSCs. Knockdown of HAS2 in PSCs inhibits MeCP2-induced α-SMA expression and HAS2 is regulated by TGF-β1/MeCP2 axis. The expressions of HAS2 and MeCP2 were increased in CP model rats compared with the control group, and the expression levels of HAS2 were positively correlated with degree of pancreatic fibrosis. In conclusion, HAS2 can induce PSCs to activate and maintain the fibrotic phenotype of PSCs, and this effect is regulated by TGF-β1/MeCP2 axis. | |||
| TO cite this article:LI Ruiping,ZHU Jianwei,PENG Xue, et al. HAS2 Promotes Pancreatic Stellate Cells Activation under TGF-β1/MeCP2 Axis in Chronic Pancreatitis[OL].[14 April 2023] http://en.paper.edu.cn/en_releasepaper/content/4760270 | |||
| 2. Measurement and correlation analysis of upper airway and mandible, hyoid in patients with bilateral anterior disc displacement | |||
| Hou Yijun,Pan Xiaojing | |||
| Clinical Medicine 23 March 2022
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| Abstract:Objective: To evaluate the presence of upper airway stenosis in patients with bilateral anterior disc displacement, and to further demonstrate the relationship between temporomandibular joint, airway, and hyoid bone. Methods: 64 patients with bilateral anterior disc displacement shown by CBCT in the joint specialty of Stomatological Hospital of Lanzhou University from June 2020 to August 2021 were selected as the patient group, 65 patients with normal joints diagnosed by arthrologists were selected as the control group. The included patients were 18-44 years old, with normal BMI index and skeletal class I. The number of patients with high angle and low angle in the experimental group was the same as that in the control group. First, Dolphin11.8 was used to measure joint space, airway volume, and cross-sectional area. It also reconstructed lateral cranial radiographs were used to measure the parameters of the mandibular and hyoid bone. last, we analyzed the correlation. Results: There was no difference in segmentation parameters among all patients. In patients with bilateral anterior disc displacement, the airway is narrow, the mandible retracts, and the hyoid bone is lower and more posterior. The linear ratio of condylar sagittal position （LR） was correlated with the airway volume of palatopharynx and glossopharynx, and with the length of the mandibular body and the sagittal position of mandible. Conclusions: Patients with bilateral anterior disc displacement and patients with OSAHS show similar changes in the position of mandible and hyoid bone. When meeting patients with joint problems, stomatologists should pay attention to asking them whether they have problems with airway obstruction. | |||
| TO cite this article:Hou Yijun,Pan Xiaojing. Measurement and correlation analysis of upper airway and mandible, hyoid in patients with bilateral anterior disc displacement[OL].[23 March 2022] http://en.paper.edu.cn/en_releasepaper/content/4757016 | |||
| 3. Derivation of a 17 myocardial segment angiographic scoring system and its validation | |||
| XU Mingxing,HE Yongming | |||
| Clinical Medicine 09 September 2017
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| Abstract:The Syntax Score has been devised to characterize the number of lesions, and their functional impact, location, and complexity in terms of coronary artery trees. An obvious fallacy is that the Syntax Score system over simply divided coronary artery circulation system into right or left dominant coronary artery circulation, which fails to reflect the great variability of coronary artery trees. Furthermore, the Syntax Score is in essence blood vessel-based rather than blood vessel importance-based. Finally, the scores assigned for the lesion characteristics, such as calcification, tortuosity, angulation, and thrombosis, etc, are largely arbitrary in the Syntax score. In the current study, we have aimed to devise a new scoring system, the 17 myocardial segment based coronary scoring system, to accurately describe the anatomical characteristics of the native coronary artery trees, to grade the complexity of the acquired coronary artery diseases according to the importance of a blood vessel, and to collect the treatment information on lesions. We have successfully completed a program to realize the above-mentioned aims based on the following preexisting or initiated classifications or rules: 54 coronary artery circulations; a 17 myocardial segment model; the 3 areas delineated by 3 anatomical landmarks on the left heart surface; law of competitive myocardial blood supply for the 3 areas; and blood flow for parent vessels equals the summation of blood flow for daughter vessels. The utility of the 17 myocardial segment based coronary scoring system for prediction of outcomes will be investigated prospectively in the conduct of the trial: in acute myocardial infarction patients undergoing emergency percutaneous coronary intervention trial (AMI-EPCI trial). Once validated and standardized, the 17 myocardial segment based coronary scoring system will be available online. | |||
| TO cite this article:XU Mingxing,HE Yongming. Derivation of a 17 myocardial segment angiographic scoring system and its validation[OL].[ 9 September 2017] http://en.paper.edu.cn/en_releasepaper/content/4741405 | |||
| 4. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis | |||
| Hou Jinxuan,Zou Kun,Xu Yu | |||
| Clinical Medicine 09 September 2017
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| Abstract:The aim of this meta-analysis was to assess the clinicopathological and prognostic significance of circulating tumor cells (CTCs) in patients with esophageal cancer. We searched PubMed, EMBASE, Science Citation Index Expanded, Cochrane library (from inception to October 2016) with the key words "esophageal cancer", "circulating tumor cells", "prognosis" and "peripheral blood". Hazard ratio, risk ratio, odds ratio and their 95% confidence intervals were set as effect measures. All analyses were performed by STATA 12.0. 17 studies were retrieved, CTCs positive was significant associated with poor progression-free survival (HR = 2.55; 95%CI: 2.12-3.06) and overall survival (HR = 2.46; 95%CI: 1.94-3.11). CTCs positive were also associated with high recurrence (OR=2.66; 95%CI: 1.63-4.35) and poor response of chemoradiotherapy (RR=0.80; 95%CI: 0.66-0.97). For clinicopathological characteristics, CTCs positive was significantly associated with TNM staging, depth of infiltration, regional lymph nodes metastasis, distant metastasis, lymphatic invasion and venous invasion. The meta-analysis has confirmed the significant clinicopathological and prognostic value of CTCs positive for both PFS and OS in patients with esophageal cancer. | |||
| TO cite this article:Hou Jinxuan,Zou Kun,Xu Yu. Clinicopathological and prognostic significance of circulating tumor cells in patients with esophageal cancer : A meta-analysis[OL].[ 9 September 2017] http://en.paper.edu.cn/en_releasepaper/content/4741316 | |||
| 5. the expression and function of the neonatal Fc receptor in thyrocytes of Hashimoto's thyroiditis | |||
| ZHAO Chenxu,GAO Ying,LI Yuan,ZHAO Lanlan,ZHANG Yang,ZHANG Hong,LU Guizhi,WANG Suxia,GUO Xiaohui | |||
| Clinical Medicine 28 April 2017
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| Abstract:Objective: Thyroglobulin (Tg) and thyroid peroxidase (TPO) antibodies (TgAb and TPOAb),which are primarily of the immunoglobulin G (IgG) class, can mediate antibody-dependent cell-mediated cytotoxicity in vitro. However, it is unclear whether any thyrocyte molecules can facilitate the transport and elimination of TgAb and TPOAb. The IgG transport receptor neonatal Fc receptor (FcRn) is a candidate mediator of these processes. In this study, we aimed to evaluate FcRn expression and function in normal and Hashimoto's thyroiditis (HT) thyrocytes. Methods: FcRn expression in primary thyrocyte cultures (four normal and four HT groups) was examined by polymerase chain reaction (PCR) and Western blotting. Localization of FcRn was demonstrated by immunoelectron microscopy. A double immunofluorescence staining method was adopted to detect FcRn and internalized human TgAb IgG. Stimulation experiments were performed to assess the regulation of FcRn expression by T helper cell 1 (Th1) (IFN-γ and TNF-α) and Th2 cytokines (IL-10 and IL-4). Results: FcRn expression was lower in HT thyrocytes than in normal thyrocytes. FcRn was located in the cytoplasm, membranes, mitochondria and transport vesicles of thyrocytes. Both human IgG and TgAb IgGwere internalized by thyrocytes in a pH-dependent manner and co-localized with FcRn in thyrocytes. FcRn expression was downregulated by Th1 and Th2 cytokines in both normal and HT thyrocytes in a dose-dependent manner. Conclusions: Our results suggest that FcRn may be associated with the transport and metabolism of IgG in thyrocytes and that transport is independent of IgG type. FcRn may be involved in HT pathogenesis | |||
| TO cite this article:ZHAO Chenxu,GAO Ying,LI Yuan, et al. the expression and function of the neonatal Fc receptor in thyrocytes of Hashimoto's thyroiditis[OL].[28 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4728936 | |||
| 6. Sarcomatoid carcinoma transformation: a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma | |||
| XU Song,LIU Renwang,LIU Xia,SHI Tao,LI Xiongfei,ZHONG Diansheng,WANG Yan,CHEN Gang,CHEN Jun | |||
| Clinical Medicine 15 April 2017
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| Abstract:Objective: Almost all EGFR-mutant lung cancers develop resistance to EGFR tyrosine kinase inhibitors (EGFR-TKIs). Several mechanisms for this acquired resistance have been identified, including development of an EGFR T790M mutation, MET amplification, hepatocyte growth factor (HGF) overexpression, loss of PTEN expression, epithelial to mesenchymal transition and transformation to small cell lung cancer. Herein, we presented a lung cancer patient with EGFR exon 19 deltion who was resistant to EGFR TKI treatment. Method: To further explore the underlying mechanisms, we performed a gene mutation profiling by next generation sequencing (NGS). Results: The mechanism of drug resistance is very rare. Some adenocarcinoama cells aquired T790M mutation in EGFR exon 20, and other adenocarcinoama cells transformed into sarcomatoid carcinoma. Conclusion: This case inspires us again the importance of tissue re-biopsy once the acquired resistance occurs after TKI consistant pressure. Sarcomatoid carcinoma transformation is a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma. | |||
| TO cite this article:XU Song,LIU Renwang,LIU Xia, et al. Sarcomatoid carcinoma transformation: a rare manifestation of EGFR TKI drug resistance in a patient with lung adenocarcinoma[OL].[15 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4725568 | |||
| 7. Pirfenidone inhibits migration, differentiation, and proliferation of human retinal pigment epithelial cells in vitro | |||
| WANG Jing,YANG Yangfan,XU Jiangang,LIN Xianchai,WU Kaili,YU Minbin | |||
| Clinical Medicine 13 June 2016
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| Abstract:Purpose: To investigate the effects of pirfenidone (PFD) on the migration, differentiation, and proliferation of retinal pigment epithelial (RPE) cells and demonstrate whether the drug induces cytotoxicity. Methods: Human RPE cells (line D407) were treated with various concentrations of PFD. Cell migration was measured by scratch assay. The protein levels of fibronectin (FN), connective tissue growth factor (CTGF), α-smooth muscle actin (α-SMA), transforming growth factor beta (TGFβS), and Smads were assessed by Western blot analyses. Levels of mRNA of TGFβS, FN, and Snail1 were analyzed using reverse transcriptase-polymerase chain reaction (RT-PCR). Cell apoptosis was detected by flow cytometry using Annexin V/PI Apoptosis Kit and the percentages of cells labeled in different apoptotic stage were compared. A trypan blue assay was used to assess cell viability. Results: PFD inhibited RPE cells migration. Western blot analyses showed that PFD inhibited the expression of FN, α-SMA, CTGF, TGFβ1, TGFβ2, Smad2/3, and Smad4. Similarly, PFD also down-regulated mRNA levels of Snail1, FN, TGFβ1, TGFβ2. No significant differences were observed in cell apoptosis or viability between the control and PFD-treated groups. Conclusions: PFD inhibited RPE cell migration, differentiation, and proliferation in vitro and caused no significant cytotoxicity. | |||
| TO cite this article:WANG Jing,YANG Yangfan,XU Jiangang, et al. Pirfenidone inhibits migration, differentiation, and proliferation of human retinal pigment epithelial cells in vitro[OL].[13 June 2016] http://en.paper.edu.cn/en_releasepaper/content/4692614 | |||
| 8. Glibenclamide Improves Survival and Neurological Outcome after Cardiac Arrest in Rats | |||
| Huang Kaibin,Gu Yong,Hu Yafang,Ji Zhong,Wang Shengnan,Lin Zhenzhou,Li Xing,Xie Zuoshan,Pan Suyue | |||
| Clinical Medicine 21 May 2016
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| Abstract: Objectives: Glibenclamide (GBC) confers neuroprotection in animal models as well as retrospective clinical studies. This study determines whether GBC improves outcome after cardiac arrest in rats. Methods and Results: Male Sprague-Dawley rats successfully resuscitated from 8-min asphyxial cardiac arrest were randomized to GBC or Vehicle group. Rats in the GBC group were intraperitoneally administered GBC with a loading dose of 10 μg/kg at 10 mins and a maintenance dose of 1.2 μg at 6, 12, 18, and 24 hrs after return of spontaneous circulation (ROSC), while rats in the Vehicle group received equivalent volume of vehicle solution. Survival was recorded every day and neurologic deficit scores were assessed at 24, 48, 72 hrs and 7 days after ROSC (n = 22 in each group). Results showed that GBC treatment increased 7-day survival rate, reduced neurologic deficit scores and prevented neuronal loss in the hippocampal CA1 region. To investigate the neuroprotective effects of GBC in acute phase, we observed neuronal injury at 24 hrs after ROSC, and found that GBC significantly decreased the rate of neuronal necrosis and apoptosis. In addition, GBC reduced the mRNA expression of tumor necrosis factor α and monocyte chemoattractant protein-1 in the cortex after ROSC. Furthermore, the sulfonylurea receptor 1 and transient receptor potential M4 heteromers, the putative therapeutic targets of GBC, were up-regulated after cardiac arrest and cardiopulmonary resuscitation, indicating that they might be involved in neuroprotective effect of GBC. Conclusions: GBC treatment substantially improved survival and neurological outcome throughout a 7-day period after ROSC. The salutary effects of GBC was associated with suppression of neuronal necrosis and apoptosis, as well as inflammation in the brain. | |||
| TO cite this article:Huang Kaibin,Gu Yong,Hu Yafang, et al. Glibenclamide Improves Survival and Neurological Outcome after Cardiac Arrest in Rats[OL].[21 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693594 | |||
| 9. High expression of c-Fos promotes radioresistance and predicts poor prognosis in malignant glioma | |||
| LIU Zhigang,WANG Hui | |||
| Clinical Medicine 29 December 2015
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| Abstract:c-Fos is a major component of activator protein (AP)-1 complex, which has been implicated in cell differentiation, proliferation, angiogenesis, invasion and metastasis. In this study, we investigated the role of c-Fos gene in glioma radiosensitivity and figured out the involved molecular mechanisms. Following downregulation of c-Fos gene by lenti-virus in glioma cell lines, we analyzed the radiosensitivity, DNA damage repair capacity, and cell cycle distribution of c-Fos. At last, we explored its prognostic value in 41 malignant glioma patients by immunohistochemistry. Our results showed that c-Fos inhibition could sensitize glioma cells to radiation by increasing radiation induced DNA double strand breaks(DSBs), disturbing the DNA damage repair process, promoting G2 cell cycle arrest and apoptosis. c-Fos protein overexpression correlated with poor prognosis in glioma patients who received standard treatment. Our findings provide new insights into the mechanism of radioresistance in malignant glioma. Therefore, c-Fos may hopefully become a novel therapeutic target for malignant glioma patients. | |||
| TO cite this article:LIU Zhigang,WANG Hui. High expression of c-Fos promotes radioresistance and predicts poor prognosis in malignant glioma[OL].[29 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4673825 | |||
| 10. Investigation on the wear behavior of human tooth dentin treated by gamma irradiation | |||
| Ping Qing,Shengbin Huang,Shanshan Gao,Linmao Qian,Haiyang Yu | |||
| Clinical Medicine 08 December 2015
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| Abstract:This study aimed to evaluate the effect of gamma irradiation on the wear behavior of human tooth dentin in terms of alteration in crystallography and composition. Human premolars (n = 19) were collected to obtain perpendicular-sectioned dentin slides and parallel-sectioned dentin slides. Each slab was subjected to 2 Gy radiation dose to a cumulative dose of 60 Gy for 5 d a week, which lasted ix weeks. Nano-scratch tests were conducted on dentin surfaces with progressive loads from 0.1 mN to 80 mN. Scratch traces were observed using a scanning electron microscope and a surface profilometer. The effect of irradiation treatment on crystallography and chemical composition of dentin was investigated through X-ray diffraction and Fourier transform infrared spectroscopy. Changes in surface microhardness (SMH) were also evaluated. Nano-scratch results showed that the coefficient of friction of dentin increased after irradiation was administered; the depths and widths of the scratches were larger than those of dentin before irradiation was administered. Irradiation decreased the crystallinity of dentin and induced the formation of large crystals. The carbonate:mineral (C:M) ratio also increased. SMH significantly decreased after irradiation was administered. The main damage mechanisms involved delamination and crack formation in perpendicular-sectioned slides and parallel-sectioned slides of dentin after irradiation was administered. Therefore, irradiation directly affected the wear behavior of dentin on human tooth; irradiation also altered crystallography, chemical composition, and SMH of dentin. | |||
| TO cite this article:Ping Qing,Shengbin Huang,Shanshan Gao, et al. Investigation on the wear behavior of human tooth dentin treated by gamma irradiation[OL].[ 8 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4670360 | |||
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