Background:Tropical forests are repositories of much of the world’s biodiversity and are critical for mitigation of climate ***,the drivers of forest dynamics are poorly *** is in large part due to the lack of long-t...
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Background:Tropical forests are repositories of much of the world’s biodiversity and are critical for mitigation of climate ***,the drivers of forest dynamics are poorly *** is in large part due to the lack of long-term data on forest change and changes in ***:We quantify changes in tree abundance,diversity,and stand structure along transects first enumerated in 1978 and resampled 2019 in Kibale National Park,*** tested five ***,based on the purported role of seed dispersal and herbivory and our quantification of changes in the abundance of frugivores and herbivores,we tested two predictions of how faunal change could have influenced forest ***,based on an evaluation of life history strategies,we tested two predictions concerning how the forest could have changed following disturbance that happened prior to written ***,based on a 50-year climate record,we evaluate the possible influence of climate change on forest ***:More trees were present on the assessed transects in 2019(508)than in 1978(436),species richness remained similar,but diversity declined as the number of dominant species *** increased by only 3 mm over the 50 years but this had not significant effect on forest changes measured *** average monthly maximum temperature increased significantly by 1.05℃ over 50 *** abundance of frugivorous and folivorous primates and elephants increased over the 50 years of *** the prediction that an increase in abundance of seed dispersing frugivores increases the abundance of their preferred fruiting tree species,nor that as an increase in folivore abundance causes a decline in their preferred species were *** predicted,light-demanding species decreased in abundance while shade-tolerant species increased as expected from Kibale being disturbed prior to historical ***,while temperature increased over the 50 years,w
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by senile plaques and neurofibrillary tangles. Senile plaques are deposits of amyloid ?-peptide (A?) produced by the cleavage of a transmembrane p...
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Alzheimer’s disease (AD) is a neurodegenerative disease characterized by senile plaques and neurofibrillary tangles. Senile plaques are deposits of amyloid ?-peptide (A?) produced by the cleavage of a transmembrane protein termed Amyloid Precursor Protein (APP). The amyloidogenic cleavage of APP is performed by γ-secretase complex and ?-site APP cleaving enzyme 1 (BACE1), a key enzyme in AD that can be activated by different noxious stimuli. Interestingly, some viruses could activate double-stranded RNA-activated protein kinase (PKR), which phosphorylates Eukaryotic Initiation Factor 2 alpha (eIF2α). This phosphorylation stops global translation to avoid any synthesis of viral infective proteins, but paradoxically up-regulates BACE1 translation. One of the viral mechanisms to circumvent eIF2α phosphorylation is the recruitment of protein phosphatase 1 (PP1), to fully dephosphorylate eIF2α and allow viral protein synthesis. Due to the functional relationship between BACE1, PKR, PP1 and AD we have performed a large (1122 cases and 1191 control individuals) case-control genetic analysis using two biallelic polymorphisms rs2254958 and rs7480390, located within the genes coding for PKR and the catalytic unit A of PP1, respectively. Although a trend to association of the rs2254958 TT genotype with AD risk was found, our results show that neither rs7480390 nor rs2254958 are associated with AD susceptibility.
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