Lithium extraction from hard rock lithium ores(spodumene,lepidolite,zinnwaldite,petalite):Technology,resources,environment and cost

Lithium production in China mainly depends on hard rock lithium ores,which has a defect in resources,environment,and economy compared with extracting lithium from brine.This paper focuses on the research progress of extracting lithium from spodumene,lepidolite,petalite,and zinnwaldite by acid,alkali,salt roasting,and chlorination methods,and analyzes the resource intensity,environmental impact,and production cost of industrial lithium extraction from spodumene and lepidolite.It is found that the sulfuric acid method has a high lithium recovery rate,but with a complicated process and high energy consumption;alkali and chlorination methods can directly react with lithium ores,reducing energy consumption,but need to optimize reaction conditions and safety of equipment and operation;the salt roasting method has large material flux and high energy consumption,so require adjustment of sulfate ratio to increase the lithium yield and reduce production cost.Compared with extracting lithium from brine,extracting lithium from ores,calcination,roasting,purity,and other processes consume more resources and energy;and its environmental impact mainly comes from the pollutants discharged by fossil energy,9.3-60.4 times that of lithium extracted from brine.The processing cost of lithium extraction from lepidolite by sulfate roasting method is higher than that from spodumene by sulfuric acid due to the consumption of high-value sulfate.However,the production costs of both are mainly affected by the price of lithium ores,which is less competitive than that of extracting lithium from brine.Thus,the process of extracting lithium from ores should develop appropriate technology,shorten the process flow,save resources and energy,and increase the recovery rate of related elements to reduce environmental impact and improve the added value of by-products and the economy of the process.

The growth rate of hepatocellular carcinoma is different with different TNM stages at diagnosis

Background: Hepatocellular carcinoma(HCC) progresses fast and has a poor prognosis, but the growth rate in different TNM stages is not clear. The present study was to estimate the growth rate of HCC with different TNM stages at diagnosis. Methods: Baseline demographics and tumor characteristics were analyzed for 10145 patients in Surveillance, Epidemiology, and End Results(SEER) Program-registered HCC. Multiple linear regression models were used for age adjustment with patient race, sex, marital status, and HCC grade. Results: The age at diagnosis was younger in Caucasians and males. The adjusted average age of patients with stage I HCC was 65.26 years. The adjusted age of patients with stage II, IIIA, IIIB, and IIIC was-0.17,-0.25,-0.29, and-0.55 adjusted-year younger compared with patients with stage I HCC(all P < 0.001). The adjusted average age of patients with T1 was 65.26 years. The age adjustment was-0.17,-0.26, and-0.55 respectively(all P < 0.001) for T2, T3 or T4 tumors without distant metastases. Conclusions: These findings demonstrated that the more advanced the HCC stage at diagnosis, the younger the age at diagnosis and the faster the HCC growth from tumor occurrence.

内侧杏仁核的神经调节素1信号通路调控青春期社会隔离导致 的自闭样行为

Autistic spectrum disorder(ASD),characterized by impairments in social interaction and repetitive behaviors,is a complex neurodevelopmental brain disorder that is reportedly increasing in prevalence globally[1].It is widely accepted that genetic and environmental factors alone or in combination cause ASD[2].

The Memory Orchestra:Contribution of Astrocytes

For decades,memory research has centered on the role of neurons,which do not function in isolation.However,astrocytes play important roles in regulating neuronal recruitment and function at the local and network levels,forming the basis for information processing as well as memory formation and storage.In this review,we discuss the role of astrocytes in memory functions and their cellular underpinnings at multiple time points.We summarize important breakthroughs and controversies in the field as well as potential avenues to further illuminate the role of astrocytes in memory processes.

AICellCounter:A Machine Learning-Based Automated Cell Counting Tool Requiring Only One Image for Training

Dear Editor,To decipher brain functions,brain cells are generally prelabeled and then imaged using a high-resolution confocal system,and manual or automatic counting methods are widely used in the quantitative and semiquantitative analysis of these confocal images.Therefore,cell counting becomes a bottleneck in efficient analysis because manual counting is laborious and time-consuming.Therefore,an accurate and user-friendly automated cell counting tool is needed for biological researchers.

Non-hallucinogenic Psychedelic Analog Design:A Promising Direction for Depression Treatment

Depression is the most common neuropsychiatric disorder,affecting 350million people worldwide;it has been a leading cause of suicide,causing serious harm to family members and consuming a large amount of social resources.The onset time of traditional antidepressants is usually 3-4 weeks,and there is no ameliorating effect in nearly one-third of patients with depression.

Astrocytic GABA_B Receptors in Mouse Hippocampus Control Responses to Behavioral Challenges through Astrocytic BDNF

Major depressive disorder(MDD) is a common mood disorder that affects almost 20% of the global population.In addition,much evidence has implicated altered function of the gamma-aminobutyric acid(GABAergic) system in the pathophysiology of depression.Recent research has indicated that GABA_B receptors(GABA_BRs) are an emerging therapeutic target in the treatment of stress-related disorders such as MDD.However,which cell types with GABA_BRs are involved in this process is unknown.As hippocampal dysfunction is implicated in MDD,we knocked down GABA_BRs in the hippocampus and found that knocking down these receptors in astrocytes,but not in GABAergic or pyramidal neurons,caused a decrease in immobility in the forced swimming test(FST) without affecting other anxiety-and depression-related behaviors.We also generated astrocytespecific GABABR-knockout mice and found decreased immobility in the FST in these mice.Furthermore,the conditional knockout of GABA_BRs in astrocytes selectively increased the levels of brain-derived neurotrophic factor protein in hippocampal astrocytes,which controlled the decrease in immobility in the FST.Taken together,our findings contribute to the current understanding of which cell types expressing GABA_BRs modulate antidepressant activity in the FST,and they may provide new insights into the pathological mechanisms and potential targets for the treatment of depression.

Astrocyte-Derived Lactate Modulates the Passive Coping Response to Behavioral Challenge in Male Mice

Every organism inevitably experiences stress. In the face of acute, intense stress, for example, periods of passivity occur when an organism's actions fail to overcome the challenge. The occurrence of inactive behavior may indicate that struggling would most likely be fruitless.Repeated serious stress has been associated with mood disorders such as depression. The modulation of passive coping response patterns has been explored with a focus on the circuit level. However, the cellular and molecular mechanisms are largely uncharacterized. Here, we report that lactate is a key factor in the astrocytic modulation of the passive coping response to behavioral challenge in adult mice. We found increased extracellular lactate in the medial prefrontal cortex(mPFC) when mice experienced the forced swimming test(FST). Furthermore, we discovered that disturbing astrocytic glycogenolysis, which is a key step for lactate production in the mPFC, decreased the duration of immobility in the FST. Knocking down monocarboxylate transporter 4(MCT4), which is expressed exclusively in astrocytes and transports lactate from astrocytes to the extracellular space, caused similar results in the FST. The behavioral effect of both the pharmacological disturbance of astrocytic glycogenolysis and viral disruption of MCT4 expression was rescued via the administration of L-lactate. Moreover, we found that both pharmacological and viral modulation of astrocytederived lactate in mPFC slices increased the excitability of layer V pyramidal neurons, and this enhancement was reversed by exogenous L-lactate administration. These results highlight astrocyte-derived lactate as a biological mechanism underlying the passive coping response to behavioral challenge and may provide new strategies to prevent mood disorders.

Expression Patterns of Inducible Cre Recombinase Driven by Differential Astrocyte-Specific Promoters in Transgenic Mouse Lines

Astrocytes are the most abundant cell type in the central nervous system(CNS).They provide trophic support for neurons,modulate synaptic transmission and plasticity,and contribute to neuronal dysfunction.Many transgenic mouse lines have been generated to obtain astrocyte-specific expression of inducible Cre recombinase for functional studies;however,the expression patterns of inducible Cre recombinase in these lines have not been systematically characterized.We generated a new astrocyte-specific Aldh1 l1-CreER^(T2)knock-in mouse line and compared the expression pattern of Cre recombinase between this and five widely-used transgenic lines(hGfap-CreER^(T2)from The Jackson Laboratory and The Mutant Mouse Resource and Research Center,Glast-CreER^(T2),Cx30-CreER^(T2),and Fgfr3-iCreER^(T2))by crossing with Ai14 mice,which express tdTomato fluorescence following Cre-mediated recombination.In adult Aldh1 l1-CreER^(T2):Ai 14 transgenic mice,tdTomato was detected throughout the CNS,and five novel morphologicallydefined types of astrocyte were described.Among the six evaluated lines,the specificity of Cre-mediated recombination was highest when driven by Aldh1 l1 and lowest when driven by hGfap;in the latter mice,co-staining between tdTomato and NeuN was observed in the hippocampus and cortex.Notably,evident leakage was noted in Fgfr3-iCreER^(T2)mice,and the expression level of tdTomato was low in the thalamus when Cre recombinase expression was driven by Glast and in the capsular part of the central amygdaloid nucleus when driven by Cx30.Furthermore,tdTomato was clearly expressed in peripheral organs in four of the lines.Our results emphasize that the astrocyte-specific CreER^(T2)transgenic lines used in functional studies should be carefully selected.

The ATP Level in the mPFC Mediates the Antidepressant Effect of Calorie Restriction

Food deprivation can rescue obesity and overweight-induced mood disorders,and promote mood performance in normal subjects.Animal studies and clinical research have revealed the antidepressant-like effect of calorie restriction,but little is known about the mechanism of calorie restriction-induced mood modification.Previous studies have found that astrocytes modulate depressive-like behaviors.Inositol 1,4,5-trisphosphate receptor type 2(IP3R2)is the predominant isoform in mediating astrocyte Ca2+signals and its genetic knockout mice are widely used to study astrocyte function in vivo.In this study,we showed that deletion of IP3R2 blocked the antidepressant-like effect induced by calorie restriction.In vivo microdialysis experiments demonstrated that calorie restriction induced an increase in ATP level in the medial prefrontal cortex(mPFC)in naïve mice but this effect disappeared in IP3R2-knockout mice,suggesting a role of astrocytic ATP in the calorie restriction-induced antidepressant effect.Further experiments showed that systemic administration and local infusion of ATP into the mPFC induced an antidepressant effect,whereas decreasing ATP by Apyrase in the mPFC blocked calorie restriction-induced antidepressant regulation.Together,these findings support a role for astrocytic ATP in the antidepressant–like effect caused by calorie restriction.

Heteromolecular Plasticity in Striatal Astrocytes

Astrocytes,which are at least as abundant as neurons in the central nervous system,are crucial for sustaining nearly all aspects of brain functions,including ion and neurotransmitter homeostasis,neural circuit formation,synaptic plasticity,and function as well as neurovascular coupling[1].Astrocytes are also involved in diseases,including Huntington’s disease(HD)[2].

Epigenetic Mechanism of Depression after Early Life Stress

Major depressive disorder(MDD),etiologically complex and disabling,is a common psychiatric disorder that affects~16%of the world's population[1,2].The interaction of susceptibility genes and environmental factors leads to the development of MDD[3].Early life stress,a major risk factor,increases the risk of adulthood depression by up to 3-fold[4,5].Epigenetic mechanisms are the link between environmental stimuli and disease[6],and previous studies have revealed key roles of epigenetic processes in regulating MDD[7].However,the epigenetic mechanism of MDD after early life stress remains little known.

A Novel Phagocytic Role of Astrocytes in Activity-dependent Elimination of Mature Excitatory Synapses

One of the grand strategies in the development of the nervous system is to overproduce constructive elements and then selectively to prune the excess,for example,by synaptic pruning.Given limited resources,surviving synapses are nurtured and reinforced,while the unsuccessful synapses are eliminated.Synaptic pruning also persists in the mature nervous system via activity-dependent plasticity,which is crucial for learning and memory.To assemble refined mature neuronal circuits and maintain homeostasis,synaptic pruning must proceed in a controlled and timely manner.Aberrant synaptic pruning may lead to neurodevelopmental disorders,such as autism,schizophrenia,and epilepsy[1].

Monitoring the Activity of Astrocytes in Learning and Memory

Introduction Learning and memory are crucial for our ability to perform the activities of daily life and to guide future behavior based on past experience[1].Previous studies have focused extensively on the role of neurons in learning and memory,suggesting that the information is stored in the brain as changes in synaptic efficiency and neuronal excitability within participating neuronal ensembles[2].