Pollination syndromes predict brood-site deceptive pollination by female hoverflies in Paphiopedilum dianthum (Orchidaceae)

In order to explore the relationship between the pollinator and pollination syndromes, and to evaluate the possibility of predicting likely pollinators based on pollination syndromes, the pollination biology of Paphiopedilum dianthum was examined. This species shares a close phylogenetic relationship, similar habit, and a recognizable syndrome of floral features (including helmet-shaped labellum, big dorsal sepal, and black warts or hairs on petals) with other brood-site deceptive Paphiopedilum species. According to the pollination syndrome concept, P. dianthum would be pollinated by hoverflies and attract pollinators with brood-site deception. Results were consistent with this prediction. Paphiopedilum dianthum was mainly pollinated by female hoverflies (Episyrphus balteatus), and these flies were indeed lured by the false brood-site on the orchid flower. It is suggested that the pollination syndrome may be correlated with pollination selective pressure, but not simply with pollinator species, and that accurate prediction requires consideration of all factors influencing floral characters, including habit and evolutionary history.     

Landscape dynamics and evolution of colonizer syndromes: interactions between reproductive effortand dispersal in a metapopulation

The evolutionary consequences of changes in landscape dynamics for the evolution of life history syndromes are studied using a metapopulation model. We consider in turn the long-term effects of a change in the local disturbance rate, in the maximal local population persistence, in habitat productivity, and in habitat fragmentation. We examine the consequences of selective interactions between dispersal and reproductive effort by comparing the outcome of joint evolution to a situation where the species has lost the potential to evolve either its reproductive effort or its dispersal rate. We relax the classical assumption that any occupied site in the metapopulation reaches its carrying capacity immediately after recolonization. Our main conclusions are the following: (1) genetic diversity modifies the range of landscape parameters for which the metapopulation is viable, but it alters very little the qualitative evolutionary trends observed for each trait within this range. Although they are both part of a competition/colonization axis, reproductive effort and dispersal are not substitutable traits: their evolution reflects more directly the change in the landscape dynamics, than a selective interaction among them. (2) no general syndrome of covariation between reproductive effort and dispersal can be predicted: the pattern of association between the two traits depends on the type of change in landscape dynamics and on the saturation level. We review empirical evidence on colonizer syndromes and suggest lines for further empirical work. This revised version was published online in July 2006 with corrections to the Cover Date.     

原位杂交研究对虾白斑杆状病毒在虾体内感染过程

应用地高辛标记的对虾白斑杆状病毒（ｗｈｉｔｅ ｓｐｏｔ ｓｙｎｄｒｏｍｅ ｂａｃｕｌｏｖｉｒｕｓ,ＷＳＳＶ）核酸探针,与人工感染后不同时间采集的对虾组织样品进行原位杂交,以动态研究病毒从侵染至对虾以病死亡的过程。将典型感染ＷＳＳＶ的病虾组织投喂健康对虾,结果显示：ＷＳＳＶ道德通过侵染消化道上皮进入虾体内增殖,此后随着细胞裂解、病毒粒子释放,游离的粒子伴随血淋巴循环进而杂其它靶组织,直至对虾发病死亡     

Peroxisome biogenesis and molecular defects in peroxisome assembly disorders

Peroxisome assembly in mammals requires more than 14 genes. So far, we have isolated seven complementation groups (CGs) of peroxisome biogenesis-defective Chinese hamster ovary (CHO) cell mutants, Z65, Z24/ZP107, ZP92, ZP105/ZP139, ZP109, ZP110, ZP114. Two peroxin cDNAs, PEX2 and PEX6, were first cloned by genetic phenotype-complementation assay using Z65 and ZP92, respectively, and were shown to be responsible for peroxisome biogenesis disorders (PBD) such as Zellweger syndrome, of CG-F (the same as CG-X in U.S.A.) and CG-C (the same as CG-IV), respectively. Pex2p is a RING zinc finger membrane protein of peroxisomes and Pex6p is a member of the AAA ATPase family. We likewise isolated PEX12 encoding a peroxisomal integral membrane protein in the RING family, by functional complementation of ZP109, demonstrating PEX12 to be responsible for CG-III PBD. We also cloned PEX1 by screening of human liver cDNA library, using ZP107. PEX1 mutation was delineated to be the genetic cause of PBD in the most highest incidence group, CG-E (the same a CG-I). Moreover, we recently found that Pex5p, using PEX5-defective ZP105 and ZP139. Thus, CHO cell mutants defective in peroxisome biogenesis are indeed shown to be very useful for the studies of peroxisome assembly and delineating pathogenic genes in PBD. Furthermore, we have isolated novel CGs of CHO mutants, ZP119 and ZP126.     

Prevalence of Sleep Apnea and Electrocardiographic Disturbances in Morbidly Obese Patients

Objective: To determine the prevalence of sleep apnea in morbidly obese patients and its relationship with cardiac arrhythmias. Research Methods and Procedures: Fifty‐two consecutive morbidly obese (body mass index ≥ 40 kg/m²) outpatients from the Obesity Clinic of the National Institute of Nutrition Salvador Zubirán underwent two nights of polysomnography with standard laboratory techniques. Electrocardiographic polysomnography signals (Lead II) were evaluated by two experienced cardiologists, and sleep complaints were measured with a standard sleep questionnaire (Sleep Disorders Questionnaire). In order to make comparisons between groups with different severities of sleep‐disordered breathing, we classified the patients in four groups using the apnea‐hypopnea index (AHI): Group 1, AHI 5 < 15 (n = 10); Group 2, AHI 15 < 30 (n = 10); Group 3, AHI 30 < 65 (n = 14); Group 4, AHI ≥ 65 (n = 17). Results: A wide range of sleep‐disordered breathing, ranging from AHI of 2.5 to 128.9 was found. Ninety‐eight percent of the sample (n = 51) had an AHI ≥ 5 (mean = 51 ± 37), and 33% had severe sleep apnea with AHI ≥ 65 with a mean nocturnal desaturation time of <65% over 135 minutes. Electrocardiographic abnormalities were present in 31% of the patients. Cardiac rhythm alterations showed an association with the level of sleep‐disordered breathing and oxygen desaturation. Discussion: We conclude that there is a high prevalence of sleep apnea in morbidly obese patients and that the risk for cardiac arrhythmias increases in this population in the presence of a severe sleep apnea (AHI ≥ 65) with severe oxygen desaturation (Sao ₂ ≤ 65%).     

A Glucocorticoid Receptor Gene Marker Is Associated with Abdominal Obesity,Leptin, and Dysregulation of the Hypothalamic‐Pituitary‐Adrenal Axis

Objective: Abdominal obesity has a key role in the pathogenesis of prevalent and serious diseases and has been shown to be associated with an altered hypothalamic‐pituitary‐adrenal (HPA) axis function, which is regulated by endocrine feedback mediated via hippocampal glucocorticoid receptors (GR). Research Methods and Procedures: We examined the HPA axis function by repeated salivary samples for the assessment of cortisol, as well as other endocrine, anthropometric, metabolic, and circulatory variables in middle‐aged Swedish men (n = 284). With the restriction enzyme BclI, variants of the GR gene (GRL) locus were identified and two alleles with fragment lengths of 4.5 and 2.3 kilobases (kb) were detected. Results: The observed frequencies were 40.1% for the 2.3‐ and 2.3‐kb, 46.2% for the 4.5‐ and 2.3‐kb, and 13.7% for the 4.5‐ and 4.5‐kb genotypes. The larger allele (4.5 and 4.5 kb) was associated with elevated body mass index (BMI; p < 0.001), waist‐to‐hip circumference ratio (p = 0.015), abdominal sagittal diameter (p = 0.002), leptin (p < 0.001), and systolic blood pressure (borderline, p = 0.058). The 4.5‐ and 4.5‐kb allele was associated with leptin after adjustment for BMI. Moreover, salivary cortisol values, particularly after stimulation by a standardized lunch (p = 0.040 to 0.086), were elevated in the men with the larger allele. Discussion: These results indicate that there is an association between a deficient GR function, defined as a poor feedback regulation of the HPA axis activity, and a polymorphic restriction site at the GR gene locus. An abnormal control of HPA axis function due to genetic alterations may contribute to the pathogenesis of abdominal obesity.     

不同寄主来源的根虫瘟霉菌株对小菜蛾幼虫的毒力比较

在不同寄主来源的4株根虫瘟霉Zoophthora radicans对小菜蛾 Plutella xylostella 2龄幼虫的生物测定中,发现源于小菜蛾的菌株ARSEF1100毒力最强,在0.53～319.32/mm²的孢子剂量下,接种后第8 天累计死亡率为2.38%～97.44%,虫尸全部表现典型的虫瘟霉症状;源于叶蝉的ARSEF2699和F99101菌株的同日累计死亡率分别为2.38%～50.00% (剂量为1.56～314.84/mm²孢子)和2.38%～57.89% (剂量为1.84～484.08/mm²的孢子);而源于菜粉蝶的ARSEF1342菌株在3.54～633.0/mm²的孢子剂量下只引发6.52%～13.63%的累计死亡率,后3个菌株致死的小菜蛾幼虫仅部分表现典型症状。所获数据经时间剂量-死亡率模型模拟分析,剂量效应参数依次为ARSEF1100 (1.89) > F99101 (1.48) > ARSEF2699 (1.23) > ARSEF1342 (0.37),相互间差异均达极显著水平。接种后4～8 天内,ARSEF1100的LD₅₀值分别为231.68、113.08、71.41、40.87和35.30/mm²的孢子,其毒力远高于其余3个菌株;ARSEF2699的相应LD₅₀值为1344.43、922.39、555.58、410.06和397.07/mm²的孢子;F99101的LD₅₀值为666.86、451.64、413.82、350.65和332.57/mm²的孢子,而ARSEF1342的毒力太弱难以估计。这些结果表明,ARSEF1100菌株最有希望用于小菜蛾的微生物防治。     

猪繁殖与呼吸综合征病毒N基因的克隆及高效表达*

本试验参照GenBank公布的Porcine reproductive and respiratory syndrome virus(PRRSV)VR2332株的核苷酸序列,设计并合成了一对引物,应用RT-PCR方法扩增出了PRRSV的核衣壳蛋白基因(N基因).在对N基因及pET32a载体双酶切后进行连接,构建了高效原核表达载体pETN.将pETN重组质粒转化BL21(DE3)宿主菌后,对培养条件及诱导表达条件(IPTG最佳浓度、作用时间)等影响表达的因素进行优化,实现了PRRSV核衣壳蛋白基因的高效表达.     

SARS-CoV Sars7a和EGFP融合蛋白真核表达载体构建及其表达

根据SARS-CoV sars7a基因设计并化学合成部分重叠引物,经二轮PCR获得sars7a基因片段,以此片段为模板并利用一对带有Kozak序列及删除终止密码的引物进行PCR,获得产物与pEGFP-N1载体连接,使sars7a基因位于EGFP的基因上游,得到含编码Sars7a-EGFP融合蛋白基因的哺乳动物细胞表达载体.采用细胞核转染技术将重组表达载体转染K562细胞,以流式细胞仪和共聚焦显微镜分析,可检测到EGFP的绿色荧光,表明Sars7a-EGFP得到表达,该蛋白分布于整个细胞,提示Sars7a并非膜蛋白,更可能是胞浆蛋白.此外,该蛋白的表达对K562细胞凋亡无明显影响.     

The Effect of a Monoclonal Antibody Coupled to Ricin A Chain-Derived Peptides on Endothelial Cells in Vitro: Insights into Toxin-Mediated Vascular Damage

Immunotoxins (ITs) containing plant or bacterial toxins have a dose-limiting toxicity of vascular leak syndrome (VLS) in humans. The active A chain of ricin toxin (RTA), other toxins, ribosome-inactivating proteins, and the VLS-inducing cytokine IL-2 contain the conserved sequence motif (x)D(y) where X = L, I, G, or V and Y = V, L, or S. RTA-derived LDV-containing peptides attached to a monoclonal antibody, RFB4, induce endothelial cell (EC) damage in vitro and vascular leak in two animal models in vivo. We have now investigated the mechanism(s) by which this occurs and have found that (1) the exposed D75 in the LDV sequence in RTA and the C-terminal flanking threonine play critical roles in the ability of RFB4-conjugated RTA peptide to bind to and damage ECs and (2) the LDV sequence in RTA induces early manifestations of apoptosis in HUVECs by activating caspase-3. These data suggest that RTA-mediated inhibition of protein synthesis (due to its active site) and apoptosis (due to LDV) may be mediated by different portions of the RTA molecule. These results suggest that ITs prepared with RTA mutants containing alterations in LDVT may kill tumor cells in vivo in the absence of EC-mediated VLS.