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1. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein | |||
ZHAO Dan,ZHAO Jie,LI Shao | |||
Basic Medicine 27 May 2016 | |||
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Abstract:The loss of synapses between neurons as well as progressive neuronal degeneration and apoptosis is the basis of pathological Alzheimer's disease (AD), which directly induces progressive memorial and cognitive impairment of AD patients. Beta amyloid precursor protein (β-APP,APP) is commonly associated with senile plaques formation which is best known for the pathogenesis of AD. More and more studies have shown that the structure and the hydrolysic way of APP play very important roles in neuronal degeneration and apoptosis of AD by many ways. In this paper, we will overview the update progress for the pathophysiological mechanism of neuronal degeneration and apoptosis induced by APP, from the perspective of APP structure and its hydrolysis. | |||
TO cite this article:ZHAO Dan,ZHAO Jie,LI Shao. Update on Alzheimer's neurodegeneration induced by amyloid precursor protein[OL].[27 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693086 |
2. Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication | |||
Wenting Qu,Yongjian Wu,Dandan Li,Yi Wang,Minhao Wu | |||
Basic Medicine 26 May 2016 | |||
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Abstract:Objectives: To explore the role of autophagy on macrophage-mediated phagocytosis and intracellular killing of Pseudomonas aeruginosa (PA), a common extracellular bacterium which often causes various opportunistic infections. Methods: Macrophages were infected with PA or stimulated with zymosan bioparticles. Autophagy was tested by fluorescent microscopy and Western blot for LC3. Phagocytosis and killing efficiency were assessed by plate count assay, flow cytometry or immunofluorescent staining. Phagocytic receptor expression, ROS generation and NO production were examined by PCR, flow cytometry and Griess reaction, respectively. Results: PA infection induced autophagy activation in both mouse and human macrophages. Induction of autophagy by rapamycin or starvation significantly inhibited PA internalization by downregulating phagocytosis receptor expression, and suppressed intracellular killing of PA via reducing ROS and NO production in macrophages. While knockdown of autophagy molecules ATG7 or Beclin1 enhanced macrophage-mediated phagocytosis and intracellular killing of PA. Conclusions: Our study suggested that PA promotes autophagy to suppress macrophage-mediated bacterial phagocytosis and intracellular killing. These insights demonstrated a novel immune evasion mechanism employed by PA, which may provide potential therapeutic strategies of PA infectious diseases. | |||
TO cite this article:Wenting Qu,Yongjian Wu,Dandan Li, et al. Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication[OL].[26 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4692951 |
3. Cryptotanshinone sensitizes Arsenic trioxide-induced Bel-7404 liver cancer cell apoptosis by downregulating phosphorylated-STAT3 in vitro and in vivo | |||
Li Shen,Guangshun Zhang,Zhaohuan Lou,Guanhua Xu,Guangji Zhang | |||
Basic Medicine 25 May 2016 | |||
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Abstract:Background: Arsenic trioxide (ATO) is approved for treating terminal-stage liver cancer in China. Cryptotanshinone (CT), a STAT3 inhibitor, has exhibited certain anti-tumor potency; however, the use of ATO with CT for treating liver cancer has not been reported. Here we try to elucidate how CT could sensitize ATO-induced liver cancer cell apoptosis and examine its correlation with STAT3 in vitro and in vivo. Methods: Cell viabilityof ATO combined with CT was assessed by MTT assay. Cell apoptosis induced by ATO combined with CT was detected by Annexin V/PI staining and apoptosis-related proteins were detected by western blotting. STAT3-related proteins were analysis by western blotting analysis and Immunofluorescence assays. Efficacy evaluation of ATO combined with CT on xenograft was carried in nude mice and related proteins were analysis by Immunohistochemistry assays. Results: First we evaluated cell vitality, and our data indicated that the ATO combined with CT showed obvious growth inhibition of Bel-7404 cells compared to ATO or CT alone. Next we found that ATO combined with CT induced cell apoptosis in Bel-7404 cells and upregulated the activation of apoptosis-related proteins cleaved-caspase-3, cleaved-caspase-9, and cleaved-poly(ADP-ribose) polymerase in a time-dependent manner. Next, we found that ATO combined with CT not only inhibited the constitutive levels of phosphorylated-JAK2 and phosphorylated-STAT3Tyr705 but did so in a time-dependent manner. We also found that ATO combined with CT reversed the upregulated expression of phosphorylated-STAT3Tyr705 stimulated by interleukin-6 and downregulated STAT3 direct target genes and the anti-apoptotic proteins Bcl-2, XIAP, and survivin but obviously upregulated the promoting apoptosis proteins Bax, Bak, and Mcl-1. In vivo studies showed that ATO combined with CT decreased tumor growth. Tumors from ATO combined with CT-treated mice showed decreased levels of phosphorylated-STAT3Tyr705 and the anti-apoptotic protein Bcl-2 but an increased level of pro-apoptotic protein Bax. Conclusions: Our study provides strong evidence of the anti-tumor growth potency of ATO combined with CT and that phosphorylated-STAT3 played a key role in ATO combined with CT-induced liver cancer cell apoptosis. | |||
TO cite this article:Li Shen,Guangshun Zhang,Zhaohuan Lou, et al. Cryptotanshinone sensitizes Arsenic trioxide-induced Bel-7404 liver cancer cell apoptosis by downregulating phosphorylated-STAT3 in vitro and in vivo[OL].[25 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4693550 |
4. Chinese Herbal Medicine and Alzheimer Disease | |||
TAN Yan,LI Jiao,LIANG Mi,HUA Qian | |||
Basic Medicine 24 May 2016 | |||
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Abstract:Chinese herbal medicine (CHM) has a long history in oriental countries. Its characteristics refer to four properties, five flavors, and meridian tropisms. The medical practice of CHM is based on the principles of traditional Chinese medicine (TCM), such as holism, yin-yang theory, Zang-fu system and the five elements, so called Zheng in total. For its therapeutic benefits with relation to brain diseases, such as stroke, Alzheimer's disease (AD), CHM can be dated from 2,500 years ago. In addition, under the guidance of Zheng, there are two mainly causes leading to the on-set of Alzheimer disease (AD) - the deficiency of kidney qi and phlegm-dampness blocking cystitis. Therefore, driven by Zheng, we list two typical Chinese herbal formulae in the treatment of AD, and its mechanisms. | |||
TO cite this article:TAN Yan,LI Jiao,LIANG Mi, et al. Chinese Herbal Medicine and Alzheimer Disease[OL].[24 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4691222 |
5. The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury | |||
ZHOU Beiqun,ZHU Jiangtao | |||
Basic Medicine 17 May 2016 | |||
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Abstract:Mixed lineage kinase domain-like protein (MLKL) was recently identified to play a critical role in necrotic cell death. To examine its role in ischemia injury, we examined its expression and the degradation of MLKL on neuroprotective effects in a middle cerebral artery occlusion (MCAO) model. We found that MLKL expression was significantly increased at 6 h after reperfusion and reached peak at 48 h after I/R injury. Our findings further demonstrated that a small chemical Necrosulfonamide (NSA) decreased MLKL level after I/R injury by increasing the degradation of MLKL through the ubiquitination proteasome pathway. The degradation of MLKL by NSA also increased cleaved PARP-1 level, a marker of apoptosis. The reduction of MLKL by NSA markedly improved neurological deficits compared with vehicle-treated mice after MCAO. NSA pre-treatment and post-treatment reduced infarct volume even when NSA was administrated at 4 h after I/R injury, indicating a long therapeutic window of NSA treatment. These findings suggest that MLKL plays a critical role in ischemic injury and is a new therapeutic target for stroke. Therefore, Promoting the degradation of MLKL may represent a novel avenue for reducing necrotic cell death after ischemic brain injury. | |||
TO cite this article:ZHOU Beiqun,ZHU Jiangtao. The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury[OL].[17 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4690231 |
6. MicroRNAs : New Regulators of IL-22 | |||
Zhou Lu,Ronghua Liu,Enyu Huang,Yiwei Chu | |||
Basic Medicine 16 May 2016 | |||
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Abstract:Interleukin-22 (IL-22) is a cytokine which belongs to IL-10 family. It is produced by T helper 22 (Th22) cells, T helper 1 (Th1) cells, T helper 17 (Th17) cells, natural killer 22 (NK22) cells, natural killer T (NKT) cells, innate lymphoid cells (ILCs) and γδ T cells. IL-22 exerts its functions via binding to a heterodimeric transmembrane receptor complex consisting of IL-22R1 and IL-10R2. IL-22 mainly contributes to tissue repair and host defense. Transcription factors such as retinoid orphan receptor γt (RORγt) and signal transducer and activator of transcription 3 (STAT3) have been reported to play important roles in the regulation of IL-22. Recently, several studies have reported that microRNAs (miRNAs) emerged as powerful regulators of interleukins including IL-22. Here, we introduce the regulators of IL-22, particularly emphasized the miRNAs. ????? | |||
TO cite this article:Zhou Lu,Ronghua Liu,Enyu Huang, et al. MicroRNAs : New Regulators of IL-22[OL].[16 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4689180 |
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. Oncogenetic natural antisense transcript, PTB-AS, promotes glioma cancer by elevating the expression of PTB | |||
Zhu liyuan,Ruan Xiangbin,Wu Fan,Qi Yingjiao,Zhou junjie,Liu Wei,Li liang,Zhang jing,Yin Bin,Jiang Tao,Yuan Jiangang,Qiang Boqin,Han Wei,Peng Xiaozhong | |||
Basic Medicine 12 March 2016 | |||
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Abstract:Glioma is the most common primary malignancy in the brain, which has the high recurrence and lethality rate, and it's imminent to explore the molecular mechanism of this incurable disease. Poly-pyrimidine tract binding protein (PTB, also known as PTBP1) is a kind of RNA-binding protein with various molecular functions and plays an indispensable role in glioma. Since research about the regulation of PTB is limited in microRNAs and transcription factors, here we want to explore the new lncRNA regulators of PTB in order to consummate the principle of controlling the PTB expression and further reveal the molecular mechanism of accommodating glioma tumorigenesis. We identify a novel natural antisense transcript of PTB named PTB-AS and find that the expression of PTB-AS in glioma is significantly directly correlated with PTB-mRNA. Naturally, knocking down the abundance of PTB-AS in glioma can remarkably reduce the expression of PTB mRNA and protein. Then we validate the important function of PTB-AS in glioma for the first time and discover the original fact that PTB-AS influence the stability of PTB-mRNA by directly binding to PTB-3'UTR, what's more, it's the latest finding to demonstrate that miR-9 can negatively regulate PTB in human cancer and in practice PTB-AS could elevate the expression of PTB by masking the binding site of miR-9 in PTB-3'UTR so as to maintain the high expression level of PTB, miR-9 and itself in glioma. | |||
TO cite this article:Zhu liyuan,Ruan Xiangbin,Wu Fan, et al. Oncogenetic natural antisense transcript, PTB-AS, promotes glioma cancer by elevating the expression of PTB[OL].[12 March 2016] http://en.paper.edu.cn/en_releasepaper/content/4680311 |
9. 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]. |
10. Nanomaterials in Bone Regeneration | |||
TIAN Taoran,CAI Xiaoxiao | |||
Basic Medicine 05 December 2015 | |||
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Abstract:Regenerative medicine is gathering more and more interests as it circumvents limitations and imperfections of traditional graft therapies such as autograft and xenograft. As for the part and parcel of regenerative medicine, the prosperous development in material science boost reciprocal approaches in bone regeneration. Nowadays, the refinement of materials leads our sights into a scale of nano. Nanomaterials, owing to their unique biomimic properties and unsurpassed surface merits, brought profound innovations to various fields, including bone tissue engineering. Studies have been designed to reveal interactions between bone tissues and nanomaterials, and thereby explore the potential applications in the same front. In this review, we summarized recent literatures, coming up with the basic characteristics of nanomaterials and their superiorities to traditional materials, and following with their unique features and applications in the process of bone regeneration. By the comparison and analyzing, we hope to purpose a comprehensive understanding over nanomaterials applied in bone regeneration. | |||
TO cite this article:TIAN Taoran,CAI Xiaoxiao. Nanomaterials in Bone Regeneration[OL].[ 5 December 2015] http://en.paper.edu.cn/en_releasepaper/content/4669279 |
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