动物鸣叫声计算机分析

动物鸣叫声计算机分析姜仕仁,丁平,施青松诸葛阳（杭州大学生物科学与技术系３１００１２）ＣｏｍｐｕｔｅｒＡｎａｌｙｓｉｓｏｆＡｎｉｍａｌ’ｓＣａｌｌｉｎｇＳｏｕｎｄ￥ＪｉａｎｇＳｈｉｒｅｎ,Ｄｉｎｇ,Ｐｉｎｇ,ＳｈｉＱｉｎｇｓｏｎｇ,ＺｈｕｇｅＹａｎｇ...     

Deciphering the SUMO code in the kidney

SUMOylation of proteins is an important regulatory element in modulating protein function and has been implicated in the pathogenesis of numerous human diseases such as cancers, neurodegenerative diseases, brain injuries, diabetes, and familial dilated cardiomyopathy. Growing evidence has pointed to a significant role of SUMO in kidney diseases such as DN, RCC, nephritis, AKI, hypertonic stress and nephrolithiasis. Recently, emerging studies in podocytes demonstrated that SUMO might have a protective role against podocyte apoptosis. However, the SUMO code responsible for beneficial outcome in the kidney remains to be decrypted. Our recent experiments have revealed that the expression of both SUMO and SUMOylated proteins is appreciably elevated in hypoxia‐induced tubular epithelial cells (TECs) as well as in the unilateral ureteric obstruction (UUO) mouse model, suggesting a role of SUMO in TECs injury and renal fibrosis. In this review, we attempt to decipher the SUMO code in the development of kidney diseases by summarizing the defined function of SUMO and looking forward to the potential role of SUMO in kidney diseases, especially in the pathology of renal fibrosis and CKD, with the goal of developing strategies that maximize correct interpretation in clinical therapy and prognosis.     

URG11 promotes gastric cancer growth and invasion by activation of β‐catenin signalling pathway

Upregulated gene 11 (URG11), a new gene upregulated by Heptatitis B Virus X protein (HBx), was previously shown to activate β‐catenin and promote hepatocellular growth and tumourigenesis. Although the oncogenic role of URG11 in the development of hepatocellular carcinoma has been well documented, its relevance to other human malignancies and the underlying molecular mechanisms remain largely unknown. Here we reported a novel function of URG11 to promote gastric cancer growth and metastasis. URG11 was found to be highly expressed in gastric cancer tissues compared with adjacent nontumourous ones by immunohistochemical staining and western blot. Knockdown of URG11 expression by small interfering RNA (siRNA) effectively attenuated the proliferation, anchorage‐independent growth, invasiveness and metastatic potential of gastric cancer cells. URG11 inhibition led to decreased expression of β‐catenin and its nuclear accumulation in gastric cancer cells and extensive costaining between URG11 and β‐catenin was observed in gastric cancer tissues. Transient transfection assays with the β‐catenin promoter showed that it was inhibited by URG11‐specific small inhibitory RNA. Moreover, suppression of endogenous URG11 expression results in decreased activation of β‐catenin/TCF and its downstream effector genes, cyclinD1 and membrane type 1 matrix metallopeptidase (MT1‐MMP), which are known to be involved in cell proliferation and invasion, respectively. Taken together, our data suggest that URG11 contributes to gastric cancer growth and metastasis at least partially through activation of β‐catenin signalling pathway. These findings also propose a promising target for gene therapy in gastric cancer.     

便携多路环境数据采集系统

便携多路环境数据采集系统姜仕仁，常杰，葛滢（杭州大学生物科学与技术系，３１００１２）ＡＰｏｒｔａｂｌｅＭｕｌｔｉ－ＰａｓｓａｇｅＥｎｖｉｒｏｎｍｅｎｔａｌＤａｔａＡｕｔｏ－ＳａｍｐｌｉｎｇＳｙｓｔｅｍ．￥ＪｉａｎｇＳｈｉｒｅｎ；ＣｈａｎｇＪｉｅ；Ｇｅ...     

山鶺鴒繁殖期的领域鸣唱特征分析

山(Ｄｅｎｄｒｏｎａｎｔｈｕｓｉｎｄｉｃｕｓ)为雀形目科的小型鸟类,在杭州地区为夏候鸟。4月中、下旬抵达,5～7月为其繁殖季节。多活动于林地及林间空旷地。主食多种农林害虫[1],为著名的益鸟,但数量很少。以往对其生态学和行为方面的研究也不多。在繁殖初期,山为了占领域,往往站立于屋脊或高树上,头左右顾盼,不时地发出尖细的“ｚｈｉｊ敶,ｚｈｉｊ敶,…”如拉锯似的鸣声,因而在野外极易识别。1996年5月上旬至6月中旬,我们对栖息于本校园内的山的占区鸣叫行为进行了观察,同时记录其鸣声,对其鸣声的特征进行了分析。并根…     

春季鸟类晨鸣时序现象的初步研究

对春季鸟类群落始鸣现象的观察和研究表明,各种群之间在一定的时期具有一定的时序,而时序的变化与各个种群的繁殖行为有关。另外也表明鸟类每天的始鸣时间与天气状况有关。     

Expression, purification, and functional characterization of recombinant PTD-SARA

The Smad anchor for receptor activation (SARA) protein is a binding partner for Smad2/3 that plays an important role in the fibrotic promoting signaling pathway initiated by transforming growth factor-β1 (TGF-β1). The C-terminal 665-750 aa of SARA comprises the Smad-binding domain (SBD). By direct interaction through the SBD, SARA inhibits Smad2/3 phosphorylation and blocks the interaction between Smad2/3 and Smad4, thereby restrains the process of fibrosis. In this study, we constructed a SARA peptide aptamer based on the SBD sequence. The recombinant SARA aptamer, fused with a protein transduction domain (PTD-SARA), was cloned, purified from E. coli, and characterized for the first time. The full-length PTD-SARA coding sequence, created with E. coli favored codons, was cloned into a pQE-30 vector, and the recombinant plasmid was transformed into an M15 strain. After Isopropyl β-D-1-Thiogalactopyranoside (IPTG) induction and Ni(2+) affinity purification, recombinant PTD-SARA was further identified by immunoblotting and protein N-terminal sequencing. Epifluorescence microscopy revealed that the recombinant PTD-SARA was transferred into the cytoplasm and nucleus more efficiently than SARA. Moreover, the recombinant PTD-SARA was found to up-regulate the level of E-cadherin and down-regulate the levels of α-SMA and phospho-Smad3 more efficiently than SARA (P < 0.05). Our work explored a method to obtain recombinant PTD-SARA protein. The recombinant PTD-SARA fusion protein could enter HK2 cells (an immortalized proximal tubule epithelial cell line) more efficiently than the SARA protein and reverse the renal epithelial-to-mesenchymal transdifferentiation process that was induced by TGF-β1 more effectively than the SARA protein. Recombinant PDT-SARA is likely to be a potential candidate for clinical prevention and treatment of renal fibrosis.