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| There are 45 papers published in subject: since this site started. | |||
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| 1. Asparagine linked glycosylation 8 alpha 13 glucosyltransferase homolog (S. cerevisiae) (ALG8) inhibited TGF beta receptor cognition mechanism | |||
| HONG Tao,WANG Lin | |||
Basic Medicine 12 June 2022
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| Abstract:Asparagine linked glycosylation 8 alpha 13 glucosyltransferase homolog (S. cerevisiae) (ALG8) feedback-inhibited beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) and ALG8 downstream-inhibited karyopherin subunit beta 1 (KPNB1) of TGF beta receptor knowledge and molecular subnetworks were constructed from ALG8 feedback-inhibited and downstream-inhibited networks based on integrating microarray significance analysis (SAM), SPSS correlation coefficient Pearson, gene (protein) reconstruction network (GRNInfer) and the Database for Annotation, Visualization and Integrated Discovery (DAVID). ALG8 feedback-inhibited BTRC of TGF beta receptor mechanism was identified upstream inositol 1 4 5-trisphosphate receptor type 1(ITPR1) of BM CD105+Endothelial_3rd, endoplasmic reticulum membrane, fetalbrain_3rd; microtubule associated protein 1B(MAP1B_2) of structural molecule activity; feedback calmodulin binding transcription activator 1(CAMTA1) of ovarian tumor_disease_3rd, ovary_normal_3rd; F-box and leucine-rich repeat protein 5(FBXL5) of protein ubiquitination, ubiquitin protein transferase activity; KIF3A of ATP binding; downstream C1D nuclear receptor corepressor(C1D) of ovarian tumor_disease_3rd, RNA binding; microtubule associated protein 1B(MAP1B_1) of structural molecule activity. ALG8 downstream-inhibited TGF beta receptor mechanism was identified upstream cyclin-dependent kinase 17(PCTK2) of ATP binding; feedback no result; downstream DAZ interacting zinc finger protein 3(DZIP3) of BM CD105+Endothelial_3rd, fetalbrain_3rd, ovarian tumor_disease_3rd, ovary_normal_3rd, ubiquitin protein transferase activity, RNA binding; iron-sulfur cluster assembly 1(ISCA1) of structural molecule activity; SEL1L ERAD E3 ligase adaptor subunit (SEL1L) of endoplasmic reticulum membrane; DDB1 and CUL4 associated factor 7(WDR68) of protein ubiquitination. We put forward ALG8 inhibited TGF beta receptor and cognition mechanism through activation of ATP binding or RE structural molecule or RNA binding or protein ubiquitination effect on fetalbrain, ovarian tumor_disease and normal, BM CD105+Endothelial. | |||
| TO cite this article:HONG Tao,WANG Lin. Asparagine linked glycosylation 8 alpha 13 glucosyltransferase homolog (S. cerevisiae) (ALG8) inhibited TGF beta receptor cognition mechanism[OL].[12 June 2022] http://en.paper.edu.cn/en_releasepaper/content/4757972 | |||
| 2. Preparation of keratin/chitosan sponge and its application performance evaluation | |||
| YAN Rongrong,SHI Jinsong | |||
| Basic Medicine 13 May 2022
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| Abstract:Uncontrolled bleeding leads to a higher fatality rate in the situation of surgery, traffic accidents and warfare. Traditional hemostatic materials such as bandages are not ideal for uncontrolled or incompressible bleeding. Therefore, it is of great significance to develop a new medical biomaterial with excellent rapid hemostatic effect. As a potential biomedical material, keratin has been developed and paid attention in tissue engineering fields such as promoting wound healing and nerve repair. Herein, a novel keratin/chitosan (K/C) sponge was prepared to achieve rapid hemostasis. The characterizations of K/C sponge were investigated, including SEM, TGA, liquid absorption and porosity, showing that the high porosity up to 90.12 ± 2.17% resulted in an excellent blood absorption. The cytotoxicity test and implantation experiment proved that the K/C sponge was biocompatible and biodegradable. Moreover, the prepared K/C sponge showed better hemostatic performance than chitosan sponge (CS) and the commercially available gelatin sponge in both rat tail amputation and liver trauma bleeding models. Further experiments showed that K/C sponge plays a hemostatic role through the endogenous coagulation pathway, thus shortening the activated partial thromboplastin time (APTT) effectively. Therefore, this study provided a novel K/C sponge which can be served as a promising biomedical hemostatic material. | |||
| TO cite this article:YAN Rongrong,SHI Jinsong. Preparation of keratin/chitosan sponge and its application performance evaluation[OL].[13 May 2022] http://en.paper.edu.cn/en_releasepaper/content/4757746 | |||
| 3. Reduced Nicotinamide Adenine Dinucleotide Phosphate Inhibits Platelet Function | |||
| Gu Yi,Qin Zhenghong | |||
| Basic Medicine 07 March 2018
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| Abstract:Background-In previous studies, the protection of reduced nicotinamide adenine dinucleotide phosphate (NADPH) on neurons against ischemia/reperfusion-induced injury was determined and its inhibition on platelet aggregation was found by accident. Here, the function of NADPH on platelet is explored deeply. Methods and Results-In vitro studies, the effects of different concentrations of NADPH on platelet aggregation induced by ADP (10 μM), thrombin (0.05 U/mL) or AA (0.5 mM) were determined and we found that NADPH could concentration-dependently inhibit platelet aggregation induced by ADP or thrombin. When the inhibitory effects of NAD+, NADH, NADP+ and NADPH on platelet aggregation were compared, NADPH showed the best effect. In vivo studies, the effects between NADPH and aspirin on tail bleeding time, clotting time and ferric chloride-induced thrombosis model were compared in mice or rats. NADPH could prolong the tail bleeding times in mice, especially at 30 min after the injection of NADPH (7.5 mg/kg), while bleeding times in mice given aspirin (15 mg/kg) were significantly longer at any time point in 6 h. As we detected the influence of NADPH or aspirin on clotting times in rats, we found that both of them had no effect. Using a FeCl3-induced abdominal aorta injury thrombosis model, we found that the injection of NADPH provoked a significant time delay of vessel occlusion, while aspirin almost completely prevented the vessel occlusion. After we observed the injured vessel sections under the microscope, we discovered that the thrombi in injured vessel sections of rats injected NADPH were much looser than rats injected normal saline and the thrombi in injured vessel sections of rats given aspirin were fewest. Conclusions-The current results suggest that NADPH can inhibit platelet aggregation and prevent hemostasis and thrombosis. To our knowledge, this is the first study on the effect of NADPH on platelet function. | |||
| TO cite this article:Gu Yi,Qin Zhenghong. Reduced Nicotinamide Adenine Dinucleotide Phosphate Inhibits Platelet Function[OL].[ 7 March 2018] http://en.paper.edu.cn/en_releasepaper/content/4743750 | |||
| 4. Fetal exposure to angiotensin II type 1 autoantibody induces hepatic insulin resistance in the adolescent offspring of rats | |||
| WEI Mingming,ZHANG Suli,YANG Xiaoli,WANG Li,ZHAO Chengrui,LEI Jinghui,WANG Pengli,LIU Huirong | |||
| Basic Medicine 09 February 2017
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| Abstract:Fetal origin of adult disease has gained lots of attention in relation to the occurrence of insulin resistance. Studys found offspring of pregnant rats tested positive for angiotensin II type 1 receptor autoantibody (AT1-AA) exhibited both liver damage and systemic insulin resistance during adulthood. But the mechanism and time-course associated with symptom remain unclear. Normal pregnant rats were administered with preeclampsia serum-derived AT1-AA in the second trimester to establish AT1-AA positive pregnant rat models. Compared to saline group, fasting serum glucose and insulin levels, insulin resistance index values were higher, and impaired glucose tolerance, abnormal insulin tolerance, islet compensatory hypertrophy were observed in adolescent and middle-aged offspring of AT1-AA group. Triglyceride and systolic blood pressure levels were elevated in adolescence. Hepatic glycogen synthetase reduced in the third trimester, adolescence and middle age. Expression of insulin receptor subunit, insulin receptor substrate 1/2, and their phosphoprotein decreased in hepatic insulin signaling pathway of adolescent and middle-aged offspring of AT1-AA group. We found the offspring of AT1-AA positive pregnant rats exist insulin resistance in adolescence. Meanwhile, hepatic insulin receptor and downstream receptor pathway disorder may be an important mechanism of insulin resistance in AT1-AA positive pregnant rat offspring. | |||
| TO cite this article:WEI Mingming,ZHANG Suli,YANG Xiaoli, et al. Fetal exposure to angiotensin II type 1 autoantibody induces hepatic insulin resistance in the adolescent offspring of rats[OL].[ 9 February 2017] http://en.paper.edu.cn/en_releasepaper/content/4718781 | |||
| 5. Association Analyses of TBX5 Gene Polymorphisms with Congenital Heart Disease in Tibetan Population of China | |||
| Zhaobing Su,Qiuhong Chen,Shinan Wu,Xi Wang,Hong Pan,Jianmin Xiao,Jing Wang | |||
| Basic Medicine 19 January 2017
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| Abstract:Objective: TBX5 gene is a member of T-box transcriptional factors that mainly expressed in cardiovascular system and play a significant role in the development of embryonic cardiovascular. The aim of this study is to investigate the association of TBX5 gene polymorphisms with the risk of congenital heart disease (CHD) in the Tibetan population in China. Methods: One hundred and twenty Chinese Tibetan patients with CHD as well as one hundred and twelve matched healthy controls were recruited for this study. And the tagging SNPs were genotyped using Illumina GoldenGate chips. Potential association was evaluated with the chi-square (Χ2) test. Results: The selected tagging SNPs were well genotyped and we found significant differences in allele frequencies and genotype distributions of rs55646156 as well as rs4533090 between CHD patients and controls. The AA genotype of rs55656156 may be am increased risk factor of CHD, while the TT genotype of rs4533090 might be the protective factor against CHD development in Chinese Tibetan population. Conclusions: We have firstly established the association between the tagging SNPs of TBX5 and CHD in the Tibetan population of China in the present study. | |||
| TO cite this article:Zhaobing Su,Qiuhong Chen,Shinan Wu, et al. Association Analyses of TBX5 Gene Polymorphisms with Congenital Heart Disease in Tibetan Population of China[OL].[19 January 2017] http://en.paper.edu.cn/en_releasepaper/content/4717734 | |||
| 6. Mutations in Growth Differentiation Factor 1 (GDF1) are Associated with Ventricular Septal Defect in a Chinese Population | |||
| Wang Jing,Bai Tingting,Yan Jinting,Wang Binbin,Liu Shiming,Chen Qiuhong,Xie Xiaodong,Wang Xi,Wu Shinan,Zhang Wei,Pan Hong | |||
| Basic Medicine 18 August 2016
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| Abstract:Ventricular septal defect (VSD) is the largest subtype of congenital heart defect (CHD). Previous studies have suggested that mutations of growth/differentiation factor 1 (GDF1) contribute to CHD. This study explored the role of GDF1 in the etiology of VSD. A total of 312 VSD Chinese patients and 250 healthy controls were screened for mutations in the GDF1 gene. Compared with the controls and the public database, one 25-bp deletion (truncation mutation), five point non-synonymous mutations (two located in the protein coding region), and one variant in the 5′-UTR were found in 312 VSD Chinese patients. The dual luciferase assays showed that the c.-47G>C mutation in the 5′-UTR affected the capacity of GDF1 promoter to activate transcription. In the meanwhile, the p.A266T and p.P312T mutations in the mature peptide region repressed the activation of the CAGA-Luc reporter which was the responsive reporter of TGFβ signaling pathway. Our study provides important evidence that GDF1 gene mutations might be associated with VSD. | |||
| TO cite this article:Wang Jing,Bai Tingting,Yan Jinting, et al. Mutations in Growth Differentiation Factor 1 (GDF1) are Associated with Ventricular Septal Defect in a Chinese Population[OL].[18 August 2016] http://en.paper.edu.cn/en_releasepaper/content/4701172 | |||
| 7. Simultaneous assay of platelet adhesion at multiple shear rates within a single microfluidic channel | |||
| Zeng Lisha,Yang Jun | |||
| Basic Medicine 01 April 2016
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| Abstract:Cardiovascular diseases are currently the major causes of mortality in the world, especially in developed nations. As a predominant one, thrombosis is the platelet aggregation induced by a high shear rate. Platelet aggregation assay can clarify the occurrence mechanism of thrombosis, as well as used as an important tool in the clinical diagnosis, personalized treatment, and screening of anticoagulants. Thus, relevant studies attracted considerable attention. As an important step in platelet aggregation, platelet adhesion and its detection are also attracted intensive concern. Thus, some analytical methods have been developed for platelet adhesion assay, and the impact of shear rate is one of the focuses. Compared with other devices, biosensors can give a more accurate result within a shorter time. Furthermore, some biosensors can achieve real-time analysis. However, only one or several shear rates can be tested at the same time, which may decrease the analytical efficiency. Meanwhile, in most cases, only the average platelet-adhesion effect within a reactor is detection, and the impact of the distribution of shear rates is improperly neglected. In this study, a microfluidic device with a single channel is designed and fabricated for platelet adhesion assay. When the platelet-rich plasma flows through the collagen-modified sensing surface of the channel bottom, the interaction between platelets and collagen molecules on the entire surface can be simultaneously monitored by using a surface plasmon resonance imaging (SPRi) system. A gradient of the shear rate (0-546) could be formed within the channel by choosing a suitable depth-to-width ratio (1:5), so platelet adhesion at multiple shear rates could be monitored simultaneously. This method enables the measurement of the adhesion process of unlabeled platelets on the entire sensing surface, in vitro, at multiple shear rates. Such a system can obtain more accurate platelet adhesion result at a given shear rate than traditional methods. Furthermore, in an individual operation, platelet adhesion can be repeatedly tested at multiple points with an equal shear rate, so a much higher analytical efficiency can also be achieved. | |||
| TO cite this article:Zeng Lisha,Yang Jun. Simultaneous assay of platelet adhesion at multiple shear rates within a single microfluidic channel[OL].[ 1 April 2016] http://en.paper.edu.cn/en_releasepaper/content/4682815 | |||
| 8. The involvement of sirtuins during optic nerve injury of rats | |||
| MENG Pei,WEI Jiacong,LIANG Jiajian,WANG Jingying,ZHI Ye,CUI Qi,GENG Yiqun | |||
| Basic Medicine 04 January 2016
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| Abstract:Sirtuins protects cells from injury while 7 members may have different roles. In this study, we applied young rat optic nerve injury model to analyze the change of Sirt1-7 at different time point to better understand the role of Sirtuins during optic nerve injury. 12 week old adult male F344 rats were used (total n=36). Rats were divided into two groups randomly. One group underwent optic nerve cut and the other group underwent peripheral nerve-optic nerve graft (PN-ON graft) on the left eye. At the time point of 1 day, 3 day, 1 week, 2 week and 4 week, the rats were sacrificed. Retinas of both eyes were removed. Total RNA was extracted and first-strand cDNA was synthesized. Sirt1-7 and housekeeping β-actin quantitative real-time PCR was performed. The quantitative real time PCR profile showed that 7 members of Sirtuins of both groups had time period after surgery. Sirtuin family mRNA transcript levels increased following optic nerve injury with and without peripheral nerve grafting. Sirt1 showed a quite different transcription pattern from the rest of the members. Our data indicated that Sirt1 and Sirts 2-7, or just Sirt2, played opposing roles in optic nerve injury. Sirts 4 and 6 were the only Sirts higher in the PN-graft group, where neuronal survival should be higher, these results suggested that Sirts 4 and 6 played the predominant role for Sirts in neuroprotection or axon regeneration. | |||
| TO cite this article:MENG Pei,WEI Jiacong,LIANG Jiajian, et al. The involvement of sirtuins during optic nerve injury of rats[J]. | |||
| 9. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats | |||
| Song Zhenyuan,Hu Ji,Zhang Honghong,Xu Guangyin | |||
| Basic Medicine 18 May 2015
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| Abstract:Background: Patients with long-standing diabetes often demonstrate intestinal dysfunction and abdominal pain. However, the pathophysiology of abdominal pain in diabetic patients remains elusive. This study was designed to determine roles of voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) in colonic hypersensitivity of diabetic rats. Methods: Diabetic models were induced by a single intraperitoneal injection of Streptozotocin (STZ; 65 mg/kg i.p.) in adult female rats. Behavioral responses to colorectal distention (CRD) were used to determine colonic sensitivity in rats. Colon-specific DRG neurons labeled with DiI were acutely dissociated for measuring excitability and sodium channel currents by whole-cell patch clamp recordings. Western blot analysis was employed to measure the expression of NaV1.7 and NaV1.8 of colon DRGs. Results: STZ injection produced a significantly lower distention threshold than control rats in responding to CRD. STZ injection also depolarized the resting membrane potentials, hyperpolarized action potential threshold, decreased rheobase and increased number of action potentials evoked by 2 and 3 times rheobase stimulation and ramp current stimulation. Furthermore, STZ injection enhanced neuronal sodium current densities of DRG neurons innervating the colon. STZ injection also led to a significant upregulation of NaV1.7 and NaV1.8 expression in colon DRGs compared with age and sex-matched control rats. Conclusion: Our results suggest that enhanced neuronal excitability following STZ injection, which might be mediated by upregulation of NaV1.7 and NaV1.8 expression in primary sensory neurons, may play an important role in diabetic colonic hypersensitivity. | |||
| TO cite this article:Song Zhenyuan,Hu Ji,Zhang Honghong, et al. Enhanced Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channel in Primary Sensory Neurons in Diabetic Rats[OL].[18 May 2015] http://en.paper.edu.cn/en_releasepaper/content/4644279 | |||
| 10. Discussion on the Calculation of Absolute Bioavailability | |||
| Jiang Wei,Yang Juan-juan,Cao Lei,Shi Xiao-lian,Cao Yong-xiao* | |||
| Basic Medicine 18 April 2015
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| Abstract:The absolute bioavailability (F) is defined as the ratio of drug amounts between being absorbed and the total amount of drug being administrated one after extravascular administration. It is calculated as the ratio of area under plasma drug concentration-time curve (AUC) between the extravascular administration and the intravenous injection. However, the distribution of a drug after intravenous administration does not reach balance in the body when the plasma drug concentration declines sharp at the distribution phase. Therefore, at this phase plasma drug concentration can't reflect the total drug amount in body. The goal of the present investigation was to analyze its insufficient and give a modification. The literatures about absolute bioavailability were searched by the keyword "absolute bioavailability" in "Pubmed" from 1983 to 2014. The data on plasma drug concentration were obtained from literatures directly or recovered from the concentration-time curve by Microsoft Paint. The plasma drug concentrations were calculated at each time point at the distribution phase according to the plasma drug concentration-time relationship at elimination phase, which represent the drug amount in body. The AUC basing on the drug concentrations in distribution balance after intravenous injection was 75%±11% of the one basing on actual measured drug concentrations in literatures. The absolute bioavailability from the literatures was 76%±12% of the actual one basing on the AUC from distribution balanced drug concentrations. Therefore, the present method underestimating absolute bioavailability should be corrected. | |||
| TO cite this article:Jiang Wei,Yang Juan-juan,Cao Lei, et al. Discussion on the Calculation of Absolute Bioavailability[OL].[18 April 2015] http://en.paper.edu.cn/en_releasepaper/content/4638715 | |||
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