喷施不同生长调节剂对‘milliongolds’文心兰开花的影响

以文心兰‘milliongolds’品种分株苗为试验材料,研究不同种类和不同浓度的植物生长调节剂喷施对其开花的影响。结果表明:与不喷施生长调节剂(对照)相比,200 mg/L GA3和GA3(200 mg/L)+6-BA(25 mg/L)处理能使文心兰的花期显著提前;单一的6-BA处理使花朵变小,但花芽分化率提高;GA3+6-BA处理使花朵变大,花葶长度增加;喷施200 mg/L和250 mg/L PP333可使文心兰花期推迟,不同浓度PP333可以使花葶矮化;在假鳞茎形成期喷施生长调节剂对花梗第一间距粗度无显著影响。     

多药耐药鲍曼不动杆菌老年患者分离株发现ADC型β-内酰胺酶基因新的变异型

目的调查多药耐药鲍曼不动杆菌老年患者分离株(MDR-ABA-5077)β-内酰胺酶基因分布情况。方法 MDR-ABA-5077株分离自宁波市医疗中心李惠利医院2009年7月住院老年患者,采用聚合酶联反应(PCR)及序列分析的方法分析21种β-内酰胺酶基因。结果本株MDR-ABA共检出3种β-内酰胺酶基因:TEM、SHV、ADC,其余18种β-内酰胺酶基因未检出。ADC阳性基因测得序列经BLAST比对与已在GenBank登录的ADC型AmpC均不相同,经与GenBank登录的ADC型序列分子进化分析,确认为ADC型β-内酰胺酶新的变异型。结论本株MDR-ABA多种β-内酰胺类药物耐药与产TEM、SHV、ADC等3种β-内酰胺酶相关。     

Plexin-B1 activates NF-κB and IL-8 to promote a pro-angiogenic response in endothelial cells

Background

The semaphorins and their receptors, the plexins, are proteins related to c-Met and the scatter factors that have been implicated in an expanding signal transduction network involving co-receptors, RhoA and Ras activation and deactivation, and phosphorylation events. Our previous work has demonstrated that Semaphorin 4D (Sema4D) acts through its receptor, Plexin-B1, on endothelial cells to promote angiogenesis in a RhoA and Akt-dependent manner. Since NF-κB has been linked to promotion of angiogenesis and can be activated by Akt in some contexts, we wanted to examine NF-κB in Sema4D treated cells to determine if there was biological significance for the pro-angiogenic phenotype observed in endothelium.

Methods/Principal Findings

Using RNA interference techniques, gel shifts and NF-κB reporter assays, we demonstrated NF-κB translocation to the nucleus in Sema4D treated endothelial cells occurring downstream of Plexin-B1. This response was necessary for endothelial cell migration and capillary tube formation and protected endothelial cells against apoptosis as well, but had no effect on cell proliferation. We dissected Plexin-B1 signaling with chimeric receptor constructs and discovered that the ability to activate NF-κB was dependent upon Plexin-B1 acting through Rho and Akt, but did not involve its role as a Ras inhibitor. Indeed, inhibition of Rho by C3 toxin and Akt by {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002 blocked Sema4D-mediated endothelial cell migration and tubulogenesis. We also observed that Sema4D treatment of endothelial cells induced production of the NF-κB downstream target IL-8, a response necessary for angiogenesis. Finally, we could show through co-immunofluorescence for p65 and CD31 that Sema4D produced by tumor xenografts in nude mice activated NF-κB in vessels of the tumor stroma.

Conclusion/Significance

These findings provide evidence that Sema4D/Plexin-B1-mediated NF-κB activation and IL-8 production is critical in the generation a pro-angiogenic phenotype in endothelial cells and suggests a new therapeutic target for the anti-angiogenic treatment of some cancers.     

Activin B promotes epithelial wound healing in vivo through RhoA-JNK signaling pathway

Background

Activin B has been reported to promote the proliferation and migration of keratinocytes in vitro via the RhoA-JNK signaling pathway, whereas its in vivo role and mechanism in wound healing process has not yet been elucidated.

Principal Findings

In this study, we explored the potential mechanism by which activin B induces epithelial wound healing in mice. Recombinant lentiviral plasmids, with RhoA (N19) and RhoA (L63) were used to infect wounded KM mice. The wound healing process was monitored after different treatments. Activin B-induced cell proliferation on the wounded skin was visualized by electron microscopy and analyzed by 5′-bromodeoxyuridine (BrdU) incorporation assay. Protein expression of p-JNK or p-cJun was determined by immunohistochemical staining and immunoblotting analysis. Activin B efficiently stimulated the proliferation of keratinocytes and hair follicle cells at the wound area and promoted wound closure. RhoA positively regulated activin B-induced wound healing by up-regulating the expression of p-JNK and p-cJun. Moreover, suppression of RhoA activation delayed activin B-induced wound healing, while JNK inhibition recapitulated phenotypes of RhoA inhibition on wound healing.

Conclusion

These results demonstrate that activin B promotes epithelial wound closure in vivo through the RhoA-Rock-JNK-cJun signaling pathway, providing novel insight into the essential role of activin B in the therapy of wound repair.     

Sequence comparison between the extracellular domain of M2 protein human and avian influenza A virus provides new information for bivalent influenza vaccine design

To prevent the human and economic losses caused by human and avian influenza viruses, it is necessary to prepare safe bivalent influenza vaccines. Recent studies found that human influenza vaccines based on the extracellular domain of influenza M2 protein (M2e) induced broad-spectrum protective immunity in various antigen constructs. A prerequisite for using the M2e protein as a bivalent influenza vaccine component was to find out the sequence differences between human and non-human (avian or swine) influenza M2e proteins. Here, we completed such a comparison using 716 influenza M2e sequences available in Genbank. The results found one region on M2e protein consistent with host restriction specificities: PIRNEWGCRCN, PTRNGWECKCS and PIRNGWECRCN (aa10-20; the human, avian and swine specific M2e sequence, respectively). Interestingly, the comparison result was then validated by immunoblotting and enzyme-linked immunosorbent assay. The monoclonal antibody against the EVETPIRN sequence (aa6-13) of human M2e protein could weakly recognize avian M2e proteins bearing the EVETPTRN sequence (aa6-13) but failed to recognize avian M2e proteins bearing the EVETLTRN sequence (aa6-13). The data in this study provided useful information in the race to develop bivalent influenza vaccines against avian and human influenza A virus infection in human beings.     

Expression of bioactive human M-CSF soluble receptor in transgenic tobacco plants

The cDNA encoding N-terminal three immunoglobin-like domains of human M-CSFR was linked to His-tag and endoplasmic reticulum retention sequence (KDEL) before being inserted into the genome of tobacco plant, Nicotiana tabacum cv. NC-89, by Agrobacterium tumefaciens-mediated transformation. The insertion and expression of target gene were confirmed by PCR, ELISA, and Western blot. The recombinant M-CSFsR reached a maximum expression level of 1.92% of total soluble protein in transgenic tobacco plant leaf tissues. The recombinant M-CSFsR could be purified through a one-step IMAC process and its bioactivity was confirmed by the inhibition of colony formation of J6-1 cells. The results suggested that we successfully expressed a high level of bioactive human M-CSFsR in tobacco plants.     

灰飞虱发育起点温度及有效积温的探讨

利用培养箱在恒温条件下饲养灰飞虱Laodelphax striatellus Fallén,测定了卵、若虫、成虫繁殖前和全世代发育历期,用直线回归法计算了灰飞虱各虫态和全世代的发育起点温度和有效积温分别为10.06、6.43、10.29、8.08℃和102.3、365.2、87.5、552.1日·度。并根据有效积温法则预测了该虫在济宁市1年完成的代数为4～5代。     

广州市景观湖微囊藻的分类学研究

于2008年3月至2009年4月,对广州市区若干景观湖水体的微囊藻属(Microcystis)进行分类学研究。共观察到11种微囊藻,分别是铜绿微囊藻(M. aeruginosa Kützing)、放射微囊藻(M. botrys Teiling)、坚实微囊藻(M. firma Kützing)、水华微囊藻(M. flosaquae Wittrock)、鱼害微囊藻(M. ichthyoblabe Kützing)、挪氏微囊藻(M. novacekii Komárek)、苍白微囊藻(M. pallida (Farlow) Lemm.)、假丝微囊藻(M. pseudofilamentosa Crow)、史密斯微囊藻(M. smithii Komárek & Anagnostidis)、绿色微囊藻(M. viridis A. Braun)和惠氏微囊藻(M. wesenbergii Komárek),对它们的形态学特征进行描述,并比较这些种类间的形态区别。     

钻形紫菀开花期种群构件的生物量分配

在野外用样方法,选取60株钻形紫菀(Aster subulatus Michx.)开花植株,进行根、茎、叶及花等构件的生物量及其物质分配关系的研究.结果表明:钻形紫菀开花期构件生物量为茎>花>根>叶,其变异系数分别为57.15%、64.66%、57.65%和55.2%,具有较大表型可塑性;在各构件物质分配变异系数中,花生物量分配的变异系数相对较大,说明其调节生殖分配的能力较强;植株高度与各构件生物量呈显著的正相关性,随着各构件生物量的增加均呈幂函数形式增加;花生物量分配与总生物量呈显著的正相关性,其余构件生物量分配均与总生物量及花生物量分配呈负相关性,物质分配由营养构件、支持构件、光合构件向生殖构件转移.反映出钻形紫菀具有自我调节生长力的分配策略,对异质环境具有较强适应能力.     

应用基因芯片技术检测非综合征型耳聋基因突变

目的:应用遗传性耳聋基因芯片对散发性聋患者进行分子病因学检测,评估其在遗传性耳聋快速基因诊断中的可靠性。方法:门诊收集散发性聋患者10例,取外周血,提取基因组DNA,用遗传性耳聋基因芯片检测4个中国人中常见的耳聋相关基因中的9个热点突变,包括GJB2(35delG、176del16bp、235delC及299delAT)、GJB3(C538T)、SLC26A4(IVS7-2AG、A2168G)和线粒体DNA 12S rRNA(A1555G、C1494T)。同时,PCR扩增GJB2、线粒体12S rRNA基因全序列,DNA测序,以验证基因芯片检测结果的准确性。结果:在10名耳聋患者中,基因芯片方法检出1例携带线粒体DNA 12S rRNA C1494T突变;2例GJB2基因235delC纯合突变;2例235delC杂合突变;SLC26A4基因和GJB3基因未检出突变。基因芯片的结果与测序结果完全一致。结论:遗传性耳聋基因芯片技术对中国人常见耳聋相关基因热点突变的检出率高,结果准确、可靠,具有快速、高通量、高准确性、低成本等特点,能够满足临床耳聋基因检测的要求,同时结合产前诊断技术能有效预防耳聋患儿的出生,因而具有广阔的临床应用前景。