Cope's rule in cryptodiran turtles: do the body sizes of extant species reflect a trend of phyletic size increase?

Cope's rule of phyletic size increase is questioned as a general pattern of body size evolution. Most studies of Cope's rule have examined trends in the paleontological record. However, neontological approaches are now possible due to the development of model-based comparative methods, as well as the availability of an abundance of phylogenetic data. I examined whether the phylogenetic distribution of body sizes in extant cryptodiran turtles is consistent with Cope's rule. To do this, I examined body size evolution in each of six major clades of cryptodiran turtles and also across the whole tree of cryptodirans (n = 201 taxa). Extant cryptodiran turtles do not appear to follow Cope's rule, as no clade showed a significant phyletic body size trend. Previous analyses in other extant vertebrates have also found no evidence for phyletic size increase, which is in contrast to the paleontological data that support the rule in a number of extinct vertebrate taxa.     

The Abnormally Phosphorylated Tau Lesion of Early Alzheimer’s Disease

The perirhinal cortex (area 35) is well-known locus for neurofibrillary tangles (NFT) in initial Alzheimer’s disease (AD) and fully developed AD and may contain tau alterations in non-demented elderly. The topography and location of this vulnerable cortex, however, is difficult to appreciate because of its variable architecture and to deviations imposed by temporal sulcal patterns. We have immunostained human brains with a short duration of dementia using antibody AT8, which recognize abnormally hyperphosphorylated tau, calcium binding protein-parvalbumin and other phenotype markers to more fully appreciate the extent of area 35 before it is obscured by pathology. We have observed in the mildly affected AD tau immunoreactive lesion that extends from the temporopolar/insular region anteriorly to the posterior parahippocampal cortex. In its anterior–posterior course, it covers the medial bank of the collateral sulcus. Although the tau lesion encroaches slightly into the temporopolar cortex (area TG) anteriorly and medially and the ectorhinal cortex (area 36) laterally, area 35 is unambiguously defined. Ventromedial temporal pathology as revealed by AT8 suggests the presence of a relatively large lesion early in AD involving all of the perirhinal cortex and other non-isocortical areas. The present study demonstrated that the early stage AD patients exhibited AT8 immunoreactive cells in the temporopolar, hippocampus, perirhinal, entorhinal, and insular cortices. Special issue article in honor of Dr. George DeVries.     

Effect of damming on distribution of rainbow trout in Hokkaido,Japan

Rainbow trout introduced into Hokkaido in 1920 have become widely distributed due to extensive release into many reservoirs and lakes for sport-fishing; their presence often results in reductions of native fish populations. We analyzed and predicted the relationship between the probability of occurrence of rainbow trout and the proximity of dams (or attributed reservoirs), using a database of the presence or absence of rainbow trout collected during 1960–2004 in Hokkaido to clarify the spread patterns of exotic species (e.g., rainbow trout) due to large-scale damming over a long period. Rainbow trout were abundant in streams within approximately 10 km of dams in recent years, regardless of whether the stream was up- or down-stream from the dam and after accounting for the effects of other environmental variables (e.g. elevation, population density, and survey year). A delayed increase in trout occurrence below dams as compared with above dams suggests that the occurrence below dams may be largely due to escapement of stocked populations and a continuously increasing abundance since 1970. The management of dams and reservoirs is necessary to prevent further spread of rainbow trout because they can threaten habitats of native Japanese salmonids through various mechanisms.

Assessing the performance of NDVI as a proxy for plant biomass using non-linear models: a case study on the Kerguelen archipelago

Numerous ecological studies, including of the polar environment, are now using the remotely sensed normalized difference vegetation index (NDVI, e.g. PAL-NDVI or MODIS-NDVI) as a proxy of vegetation productivity rather than performing direct vegetation assessments. Even though previous data strongly suggested a saturation of NDVI at high biomass values, few studies have explicitly included this characteristic in the modelling process. Here, we developed a generalized non-linear model to explicitly model the relationship between temporal variations of NDVI (Pathfinder AVHRR Land 8 km dataset) and empirical field data. We illustrated our approach on the Kerguelen archipelago by using a green biomass index (point-intercept protocol) sampled at a small scale relative to PAL-NDVI data, and in presence of spatial (water) and temporal (cloud contamination, snow) heterogeneity, i.e. field conditions encountered in many ecological studies. We showed a strong relationship (r _pred.obs = 0.89 [0.77; 0.95]_95%) between this index and the seasonal component of NDVI time series (NDVI_comp). Despite the absence of lignified species in the stand, the NDVI_comp reached an asymptote (0.54 ± 0.05) for high values of green biomass index stressing the need to account for non-linearity when relating NDVI and plant measurements. We provided here a new methodological framework to standardize comparisons between studies assessing performance of NDVI as a proxy of vegetation data.

岗田酸诱导大鼠脑神经细胞表达谷氨酸转运体EAAT1

为研究tau蛋白高度磷酸化与谷氨酸转运体功能之间的关系,实验采用免疫组织化学、荧光双标记技术及大鼠额叶皮质定位注射的方法,观察了蛋白磷酸酶抑制剂岗田酸（okadaic acid,OA)所致神经细胞退化对谷氨酸转运体亚型EAAT1表达的影响。结果如下：（1）在OA注射中心区神经元早期出现胞体固缩、肿胀、核移位,在注射3d时细胞破碎,发生坏死,并有大量炎性细胞浸润等病理现象;边周区细胞呈AT8（微管相关蛋白tau磷酸化指标）免疫阳性反应;（2）OA首先诱导神经细胞突起远端tau蛋白磷酸化,并逐渐向胞体发展,形成营养不良的神经细胞突起和神经纤维缠结样病理改变;（3）AT8免疫阳性反应脑区的神经细胞高表达谷氨酸转运体EAAT1,在12h阳性表达细胞数显著增多（P＜0．01）,1d时达峰值（P＜0．001）,3d时明显减少。在OA作用下EAAT1表达于星形胶质细胞和神经元。结果提示,OA致微管相关蛋白tau高度磷酸化时可诱导该区星形胶质细胞和神经元高表达谷氨酸转体EAAT1。EAAT1高表达的病理生理意义有待进一步的阐明。     

含P301L突变的Tau转基因小鼠纯合子品系的建立及鉴定

目的:建立含P301L突变的tau转基因小鼠的纯合子品系。方法:雄原核显微注射法获得含P301L突变的tau转基因阳性首建鼠,通过SYBR Green实时荧光定量PCR法和传统育种方式结合鉴定纯合子和杂合子。结果:共选育出95只纯合子,鉴定出的纯合子具有优于杂合子模拟老年痴呆生物学特性改变的优势。结论:外源性基因tau能稳定遗传,采用的SYBR Green实时荧光定量PCR和传统育种方式结合筛选鉴定纯合子和杂合子快速、经济、可靠。     

The toxicity of tau in Alzheimer disease: turnover, targets and potential therapeutics

It has been almost 25 years since the initial discovery that tau was the primary component of the neurofibrillary tangles (NFTs) in Alzheimer disease (AD) brain. Although AD is defined by both β-amyloid (Aβ) pathology (Aβ plaques) and tau pathology (NFTs), whether or not tau played a critical role in disease pathogenesis was a subject of discussion for many years. However, given the increasing evidence that pathological forms of tau can compromise neuronal function and that tau is likely an important mediator of Aβ toxicity, there is a growing awareness that tau is a central player in AD pathogenesis. In this review we begin with a brief history of tau, then provide an overview of pathological forms of tau, followed by a discussion of the differential degradation of tau by either the proteasome or autophagy and possible mechanisms by which pathological forms of tau may exert their toxicity. We conclude by discussing possible avenues for therapeutic intervention based on these emerging themes of tau's role in AD.     

Tau function and dysfunction in neurons: its role in neurodegenerative disorders

Alzheimer’s disease (AD) is the most usual neurodegenerative disorder leading to dementia in the aged human population. It is characterized by the presence of two main brain pathological hallmarks: senile plaques and neurofibrillary tangles (NFTs). NFTs are composed of fibrillar polymers of the abnormally phosphorylated cytoskeletal protein tau.     

Visualizing the microtubule-associated protein tau in the nucleus

Although tau is mainly known as an axonal microtubule-associated protein,many studies indicate that it is not restricted to this subcellular compartment.Assessing tau’s subcellular distribution,however,is not trivial as is evident from transgenic mouse studies.When human tau is over-expressed,it can be immunohistochemically localized to axons and the somatodendritic domain,modeling what is found in neurodegenerative diseases such as Alzheimer’s disease.Yet,in wild-type mice,despite its abundance,tau is difficult to visualize even in the axon.It is even more challenging to detect this protein in the nucleus,where tau has been proposed to protect DNA from damage.To establish a framework for future studies into tau’s nuclear functions,we compared several methods to visualize endogenous nuclear tau in cell lines and mouse brain.While depending on the fixation and permeabilization protocol,we were able to detect nuclear tau in SH-SY5Y human neuroblastoma cells,we failed to do so in N2a murine neuroblastoma cells.As a second method we used subcellular fractionation of mouse tissue and found that in the nucleus tau is mainly present in a hypophosphorylated form.When either full-length or truncated human tau was expressed,both accumulated in the cytoplasm,but were also found in the nuclear fraction.Because subcellular fractionation methods have their limitations,we finally isolated nuclei to probe for nuclear tau and found that the nuclei were free of cytoplasmic contamination.Together our analysis identifies several protocols for detecting tau in the nucleus where it is found in a less phosphorylated form.