Attraction of ambrosia and bark beetles to coast live oaks infected by Phytophthora ramorum

1 Sudden oak death is caused by the apparently introduced oomycete, Phytophthora ramorum. We investigated the role of bark and ambrosia beetles in disease progression in coast live oaks Quercus agrifolia. 2 In two Marin County, California sites, 80 trees were inoculated in July 2002 with P. ramorum and 40 were wounded without inoculation. Half of the trees in each group were sprayed with the insecticide permethrin [cyclopropanecarboxylic acid, 3‐(2,2‐dichloroethenyl)‐2,2‐dimethyl‐(3‐phenoxyphenyl) methyl ester] to prevent ambrosia and bark beetle attacks, and then were sprayed twice per year thereafter. After each treatment, sticky traps were placed on only the permethrin‐treated trees. Beetles were collected periodically in 2003. 3 Inoculated trees accounted for 95% of all beetles trapped. The ambrosia beetles Monarthrum scutellare and Xyleborinus saxeseni and the western oak bark beetle Pseudopityophthorus pubipennis were the most abundant of the seven species trapped. 4 Permethrin treatment delayed initiation of beetle attacks and significantly reduced the mean number of attacks per tree. Beetles did not attack any wounded or noncankered inoculated trees. 5 Trees with larger cankers trapped more beetles early in the disease. Once permethrin lost effectiveness, the number of beetle entrance tunnels was a more reliable predictor of subsequent trap catch than was canker size. 6 Beetles were initially attracted to P. ramorum cankers in response to kairomones generated in the host‐pathogen interaction. After beetles attacked the permethrin‐treated trees, aggregation pheromones most probably were the principal factor in beetle colonization behaviour.     

AFLPs detect low genetic diversity for Phytophthora nemorosa and P. pseudosyringae in the US and Europe

In California and Oregon, two recently described oomycete forest pathogens, Phytophthora nemorosa and P. pseudosyringae, overlap in their host and geographic ranges with the virulent P. ramorum, causal agent of “sudden oak death.” Epidemiological observations, namely broader geographic distribution and lack of landscape-level mortality, led to the hypothesis they are native to this region, whereas multiple lines of evidence indicate P. ramorum is exotic to North America. We used AFLP analysis to measure genetic variability in the homothallic P. nemorosa and P. pseudosyringae and to evaluate the hypothesis of endemism. We analysed 39 P. nemorosa and 48 P. pseudosyringae isolates (29 American and 19 European) from throughout their geographic and host ranges. In the US, both P. nemorosa and P. pseudosyringae have a dominant AFLP clone with several closely related variants. There is no evidence that genetic diversity is partitioned by host or location in P. nemorosa, but the US P. pseudosyringae clonal lineage is largely nested within a more genetically variable European group. Though the absence of highly variable sampled source populations does not allow us to determine whether each species is native or introduced in the western US with certainty, the results are most consistent with the hypothesis that both are introduced — P. pseudosyringae perhaps from Europe. Invasive Phytophthora species are increasingly being implicated in emergent forest diseases, highlighting the need to identify and characterize both native and previously unknown introduced forest Phytophthoras.     

干细胞治疗感音神经性耳聋

治疗内耳疾病的主要困难之一是找到耳蜗毛细胞或者螺旋神经元丢失所导致的听力损失的治疗方法。本文讨论使用干细胞替代感觉细胞丢失为目的的几个治疗策略。作者最近在成年内耳中发现了可以分化为毛细胞的干细胞,发现了胚胎干细胞可在体外转化为毛细胞并表达毛细胞标记物。在动物模型中,成年内耳干细胞、神经干细胞和胚胎干细胞来源的前体细胞可分化成为毛细胞和神经细胞。本文将讨论使用干细胞再生损伤毛细胞的不同方法,介绍几种可行的动物模型,并讨论发展基于干细胞的细胞替代疗法治疗内耳损伤中存在的困难。     

The A1555G mitochondrial DNA mutation in Greek patients with non-syndromic, sensorineural hearing loss

Mitochondrial DNA mutations are undoubtedly a factor that contributes to sensorineural, non-syndromic deafness. One specific mutation, the A1555G, is associated with both aminoglycoside-induced and non-syndromic hearing impairment. The mutation is considered to be the most common of all mitochondrial DNA deafness-causing mutations but its frequency varies between different populations. Here we report on the first large screening of the A1555G mitochondrial DNA mutation in the Greek population. The aim of this study was to determine the frequency of the A1555G mutation in Greek sensorineural, non-syndromic deafness patients, with childhood onset. We screened 478 unrelated Greek patients with hearing loss of any degree and found two individuals harboring the A1555G mutation (0.42%). Both cases had been subjected to aminoglycosides. They were prelingual, familial and homoplasmic for the A1555G mutation. One of the cases was also found heterozygous for the frequent GJB2 35delG mutation, while the other case was negative. The A1555G mutation seems to be less common than in other European populations.     

Mitochondria and arrhythmias

Mitochondria are essential to providing ATP, thereby satisfying the energy demand of the incessant electrical activity and contractile action of cardiac muscle. Emerging evidence indicates that mitochondrial dysfunction can adversely affect cardiac electrical functioning by impairing the intracellular ion homeostasis and membrane excitability through reduced ATP production and excessive reactive oxygen species (ROS) generation, resulting in increased propensity to cardiac arrhythmias. In this review, the molecular mechanisms linking mitochondrial dysfunction to cardiac arrhythmias are discussed with an emphasis on the impact of increased mitochondrial ROS on the cardiac ion channels and transporters that are critical to maintaining normal electromechanical functioning of the cardiomyocytes. The potential of using mitochondria-targeted antioxidants as a novel antiarrhythmia therapy is highlighted.     

Neuromuscular response of the trunk to inertial based sudden perturbations following whole body vibration exposure

The effects of whole body vibration exposure on the neuromuscular responses following inertial-based trunk perturbations were examined. Kinematic and surface EMG (sEMG) data were collected while subjects were securely seated on a robotic platform. Participants were either exposed to 10 min of vibration or not, which was followed by sudden inertial trunk perturbations with and without timing and direction knowledge. Amplitude of sEMG was analyzed for data collected during the vibration protocol, whereas the onset of sEMG activity and lumbar spine angle were analyzed for the perturbation protocol. Data from the vibration protocol did not show a difference in amplitude of sEMG for participants exposed to vibration and those not. The perturbation protocol data showed that those not exposed to vibration had a 14% faster muscle onset, despite data showing no difference in fatigue level.     

非综合征型遗传性耳聋基因的研究进展及相关网络资源

耳聋是一种最常见的人类感觉系统缺陷,70%的遗传性耳聋属于非综合征型听力缺损。据估计非综合征型遗传性耳聋基因总数在100个以上,迄今已经有大约80个基因座被绘制于人类染色体上,至少23个基因得鉴定。本文系统地介绍了已鉴定的23个非综合征型耳聋基因,并列举了与遗传性耳聋相关的部分网络资源以供参考。 Abstract:Deafness is the most prevalent sensory system impairment of human,and 70% of genetic deafness belongs to nonsyndromic hearing impairment.The total number of genes involved in nonsyndromic hereditary deafness has been estimated to above 100.So far,approximate 80 loci have been mapped to human chromosome,and 23 genes have been identified.In this article,these 23 genes were summarized systematically and some databases about hereditary deafness were provided for reference.     

Animal models used to test the interactions between infectious agents and products of cigarette smoked implicated in sudden infant death syndrome

Animal test systems are reviewed that have relevance to sudden infant death syndrome (SIDS) are reviewed. These test interactions between infectious agents (or their toxins) and products of cigarette smoke. Infectious agents implicated in SIDS include members of the enterobacteria and clostridia, Staphylococcus aureus and Streptococcus pyogenes. Smoking is thought to be the single most preventable cause of SIDS. Tobacco smoke contains many extremely toxic products including cyanide and nicotine. Many animal test systems are available to examine the potency of bacterial toxins and smoke-derived components. These include mice, hamsters, rats and chick embryos. Such systems reveal synergy between bacterial toxins, especially endotoxin and superantigens. They have also demonstrated potentiation of low levels of bacterial toxin by low levels of both nicotine and its primary metabolite, cotinine. These findings suggest a possible causal explanation for the fact that passive exposure to cigarette smoke is a risk factor in sudden infant death syndrome.