Soil microbiomes divergently respond to heavy metals and polycyclic aromatic hydrocarbons in contaminated industrial sites

Contaminated sites from electronic waste(e-waste)dismantling and coking plants feature high concentrations of heavy metals(HMs)and/or polycyclic aromatic hydrocarbons(PAHs)in soil.Mixed contamination(HMsþPAHs)hinders land reclamation and affects the microbial diversity and function of soil microbiomes.In this study,we analyzed HM and PAH contamination from an e-waste dismantling plant and a coking plant and evaluated the influences of HM and PAH contamination on soil microbiomes.It was noticed that HMs and PAHs were found in all sites,although the major contaminants of the e-waste dismantling plant site were HMs(such as Cu at 5,947.58±433.44 mg kg^(-1),Zn at 4,961.38±436.51 mg kg^(-1),and Mn at 2,379.07±227.46 mg kg^(-1)),and the major contaminants of the coking plant site were PAHs(such as fluorene at 11,740.06±620.1 mg kg^(-1),acenaphthylene at 211.69±7.04 mg kg^(-1),and pyrene at 183.14±18.89 mg kg^(-1)).The microbiomes(diversity and abundance)of all sites were determined via high-throughput sequencing of 16S rRNA genes,and redundancy analysis was conducted to investigate the relations between soil microbiomes and contaminants.The results showed that the microbiomes of the contaminated sites divergently responded to HMs and PAHs.The abundances of the bacterial genera Sulfuritalea,Pseudomonas,and Sphingobium were positively related to PAHs,while the abundances of the bacterial genera Bryobacter,Nitrospira,and Steroidobacter were positively related to HMs.This study promotes an understanding of how soil microbiomes respond to single and mixed contamination with HMs and PAHs.

STAT3 ameliorates cognitive deficits by positively regulating the expression of NMDARs in a mouse model of FTDP-17

In tauopathies,memory impairment positively strongly correlates with the amount of abnormal tau aggregates;however,how tau accumulation induces synapse impairment is unclear.Recently,we found that human tau accumulation activated Signal Transduction and Activator of Transcription-1(STAT1)to inhibit the transcription of synaptic N-methyl-D-aspartate receptors(NMDARs).Here,overexpressing human P301L mutant tau(P301L-hTau)increased the phosphorylated level of Signal Transduction and Activator of Transcription-3(STAT3)at Tyr705 by JAK2,which would promote STAT3 translocate into the nucleus and activate STAT3.However,STAT3 was found mainly located in the cytoplasm.Further study found that P301L-htau acetylated STAT1 to bind with STAT3 in the cytoplasm,and thus inhibited the nuclear translocation and inactivation of STAT3.Knockdown of STAT3 in STAT3flox/flox mice mimicked P301L-hTau-induced suppression of NMDARs expression,synaptic and memory impairments.Overexpressing STAT3 rescued P301L-hTau-induced synaptic and cognitive deficits by increasing NMDARs expression.Further study proved that STAT3 positively regulated NMDARs transcription through direct binding to the specific GAS element of NMDARs promoters.These findings indicate that accumulated P301L-hTau inactivating STAT3 to suppress NMDARs expression,revealed a novel mechanism for tau-associated synapse and cognition deficits,and STAT3 will hopefully serve as a potential pharmacological target for tauopathies treatment.

Recombinant human erythropoietin ameliorates cognitive dysfunction of APP/PS1 mice by attenuating neuron apoptosis via HSP90β

Dear Editor,Recently,lower hemoglobin/anemia in the elderly is found to be associated with cognitive impairment and Alzheimer’s disease(AD),1 implying that erythropoietin(EPO)may be of benefit for AD.As a clinically safe-to-use drug,besides its hematopoietic function,recombinant human EPO(rhEPO)is reported to present multifaceted neuroprotective effects.2 Unfortunately,few clinical studies investigated the effect of rhEPO in AD patients.

STAT3 ameliorates cognitive deficits by positively regulatingthe expression of NMDARs in a mouse model of FTDP-17

In tauopathies,memory impairment positively strongly correlates with the amount of abnormal tau aggregates;however,how tau accumulation induces synapse impairment is unclear.Recently,we found that human tau accumulation activated Signal Transduction and Activator of Transcription-1(STAT1)to inhibit the transcription of synaptic N-methyl-D-aspartate receptors(NMDARs).Here,overexpressing human P301L mutant tau(P301L-hTau)increased the phosphorylated level of Signal Transduction and Activator of Transcription-3(STAT3)at Tyr705 by JAK2,which would promote STAT3 translocate into the nucleus and activate STAT3.However,STAT3 was found mainly located in the cytoplasm.Further study found that P301L-htau acetylated STAT1 to bind with STAT3 in the cytoplasm,and thus inhibited the nuclear translocation and inactivation of STAT3.Knockdown of STAT3 in STAT3^(flox/flox) mice mimicked P301L-hTau-induced suppression of NMDARs expression,synaptic and memory impairments.Overexpressing STAT3 rescued P301L-hTau-induced synaptic and cognitive deficits by increasing NMDARs expression.Further study proved that STAT3 positively regulated NMDARs transcription through direct binding to the specific GAS element of NMDARs promoters.These findings indicate that accumulated P301L-hTau inactivating STAT3 to suppress NMDARs expression,revealed a novel mechanism for tau-associated synapse and cognition deficits,and STAT3 will hopefully serve as a potential pharmacological target for tauopathies treatment.