Neural stem cell-conditioned medium upregulated the PCMT1 expression and inhibited the phosphorylation of MST1 in SHSY5Y cells induced by Aβ_(25-35)

A progressive neurodegenerative disease,Alzheimer’s disease(AD).Studies suggest that highly expressed protein isoaspartate methyltransferase 1(PCMT1)in brain tissue.In the current study,we explored the effects of neural stem cell-conditioned medium(NSC-CDM)on the PCMT1/MST1 pathway to alleviate Aβ_(25-35)-induced damage in SH-SY5Y cells.Our data suggested that Aβ_(25-35) markedly inhibited cell viability.NSC-CDM or Neural stem cell-complete medium(NSC-CPM)had a suppression effect on toxicity when treatment with Aβ_(25-35),with a greater effect observed with NSC-CDM.Aβ_(25-35)+NSC-CDM group exhibited an increase in PCMT1 expression.sh-PCMT1 markedly decreased cell proliferation and suppressed the protective role of NSC-CDM through the induction of apoptosis and improved p-MST1 expression.Overexpression of PCMT1 reversed the Aβ_(25-35)-induced decrease in cell proliferation and apoptosis.In summary,our findings suggest that NSC-CDM corrects the Aβ_(25-35)-induced damage to cells by improving PCMT1 expressions,which in turn reduces phosphorylation of MST1.

Distributed Scheduling Problems in Intelligent Manufacturing Systems

Currently,manufacturing enterprises face increasingly fierce market competition due to the various demands of customers and the rapid development of economic globalization.Hence,they have to extend their production mode into distributed environments and establish multiple factories in various geographical locations.Nowadays,distributed manufacturing systems have been widely adopted in industrial production processes.In recent years,many studies have been done on the modeling and optimization of distributed scheduling problems.This work provides a literature review on distributed scheduling problems in intelligent manufacturing systems.By summarizing and evaluating existing studies on distributed scheduling problems,we analyze the achievements and current research status in this field and discuss ongoing studies.Insights regarding prior works are discussed to uncover future research directions,particularly swarm intelligence and evolutionary algorithms,which are used for managing distributed scheduling problems in manufacturing systems.This work focuses on journal papers discovered using Google Scholar.After reviewing the papers,in this work,we discuss the research trends of distributed scheduling problems and point out some directions for future studies.

Loss of CREST leads to neuroinflammatory responses and ALS-like motor defects in mice

Background:Amyotrophic lateral sclerosis(ALS)is a late onset neurodegenerative disease with fast progression.ALS has heavy genetic components in which a series of genetic mutations have been identified.In 2013,Mutations of the CREST gene(also known as SS18L1),which functions as a calcium-regulated transcriptional activator,were found in sporadic ALS patients.However,the pathogenic causality and mechanisms of ALS-associated mutations of CREST remain to be determined.Methods:In this study,we constructed CREST knockout and Q394X knock-in mice with CRISPR/Cas9 system.Using biochemical and imaging tools,we illustrated core pathological phenotypes in CREST mutant mice and claimed the possible pathogenic mechanisms.Furthermore,we also observed locomotion defects in CREST mutant mice with behavioural tests.Results:We demonstrate that ALS-related CREST-Q388X mutation exhibits loss-of-function effects.Importantly,the microglial activation was prevalent in CREST haploinsufficiency mice and Q394X mice mimicking the human CREST Q388X mutation.Furthermore,we showed that both CREST haploinsufficiency and Q394X mice displayed deficits in motor coordination.Finally,we identified the critical role of CREST-BRG1 complex in repressing the expression of immune-related cytokines including Ccl2 and Cxcl10 in neurons,via histone deacetylation,providing the molecular mechanisms underlying inflammatory responses within mice lack of CREST.Conclusion:Our findings indicate that elevated inflammatory responses in a subset of ALS may be caused by neuron-derived factors,suggesting potential therapeutic methods through inflammation pathways.

Interspecific interactions between burrowing dung beetles and earthworms on yak dung removal and herbage growth in an alpine meadow

Interspecific interactions between two spatiotemporally co-occurred species sharing a single resource are considered to be either competitive or facilitative.This study examined the possible interspecific interactions between a dung-tunneling beetle species(Onthophagus yubarinus)and an earthworm species(Aporrectodea noctuma),two major detritivores responsible for dung removal in a Tibetan alpine meadow.We conducted a two-way,factorial field experiment using replicated chambers,and measured the performances of beetles and earthworms,as well as yak dung removal,soil properties and aboveground plant biomass over two months.Earthworm presence significantly decreased the body size of beetle larvae and the weight of tunnel dung that beetle larvae live on.In contrast,beetle presence did not affect the performance of earthworms.Beetles,earthworms and their interaction significantly increased dung removal and soil organic carbon concentration at the end of the experiment.Beetles alone significantly increased soil total N and P,soluble N and P concentrations,but earthworms alone had nonsignificant effects on these nutrient variables.Beetles and earthworms additively enhanced soluble N and P concentrations,and aboveground plant biomass at the end of the experiment.These results indicate 1)there was a one-sided negative relationship between dung-tunneling beetles and earthworms,resulting from the consumption of earthworms on food resource of beetle larvae;and 2)the coexistence of beetles and earthworms facilitated dung removal interactively and plant growth additively by increasing nutrient availability.