Refined Sea Salt Markers for Coastal Cities Facilitating Quantification of Aerosol Aging and PM2.5 Apportionment.

Sea salt (ss) aerosols in PM2.5 are often quantified through source apportionment by applying sodium (Na+) and chloride (Cl-) as the markers, but both markers can be substantially emitted from anthropogenic sources. In this study, we differentiate ss from nonss (nss) portions of Na+ and Cl- to better apportion PM2.5 in a coastal tropical urban environment. Size-resolved ionic profiles accounting for Cl- depletion of aged ss were applied to 162-day measurements during 2012 and 2018-2019. Results show that the nss (likely anthropogenic) portions, on average, account for 50-80% of total Na+ and Cl- in submicron aerosols (PM1). This corresponds to up to 2.5 µg/m3 of ss in submicron aerosols that can be ∼10 times overestimated if one attributes all Na+ and Cl- in PM1 to ss. Employing the newly speciated ss- and nss-portions of Na+ and Cl- to source apportionment of urban PM2.5 via positive matrix factorization uncovers a new source of transported anthropogenic emissions during the southwest monsoon, contributing to 12-15% of PM2.5. This increases anthropogenic PM2.5 by ≥19% and reduces ss-related PM2.5 by >30%. In addition to demonstrating Cl- depletion (aging) in submicron aerosols and quantifying ssNa+, nssNa+, ssCl-, as well as nssCl- therein, the refined PM2.5 apportionment resolves new insights on PM2.5 of anthropogenic origins in urban environments, useful to facilitate policy making.

Overcoming cancer chemotherapy resistance by the induction of ferroptosis.

Development of resistance to chemotherapy in cancer continues to be a major challenge in cancer management. Ferroptosis, a unique type of cell death, is mechanistically and morphologically different from other forms of cell death. Ferroptosis plays a pivotal role in inhibiting tumour growth and has presented new opportunities for treatment of chemotherapy-insensitive tumours in recent years. Emerging studies have suggested that ferroptosis can regulate the therapeutic responses of tumours. Accumulating evidence supports ferroptosis as a potential target for chemotherapy resistance. Pharmacological induction of ferroptosis could reverse drug resistance in tumours. In this review article, we first discuss the key principles of chemotherapeutic resistance in cancer. We then provide a brief overview of the core mechanisms of ferroptosis in cancer chemotherapeutic drug resistance. Finally, we summarise the emerging data that supports the fact that chemotherapy resistance in different types of cancers could be subdued by pharmacologically inducing ferroptosis. This review article suggests that pharmacological induction of ferroptosis by bioactive compounds (ferroptosis inducers) could overcome chemotherapeutic drug resistance. This article also highlights some promising therapeutic avenues that could be used to overcome chemotherapeutic drug resistance in cancer.

NMT1 Enhances the Stemness of NSCLC Cells by Activating the PI3K/AKT Pathway.

INTRODUCTION: Abundant studies have disclosed that proteins can function as pivotal tumor promoters or suppressors in cancers' progression. This work was planned to investigate the regulatory function of N-myristoyltransferase-1 (NMT1) on non-small cell lung cancer (NSCLC) and the underlying molecular mechanisms. METHODS: The self-renewal abilities were assessed through a spheroid-formation assay. The tumorigenic abilities were examined through nude mice in vivo assay. The proteins' expression was measured through Western blot. The NMT1 protein expression in tumor tissues was measured through an IHC assay. The cell migration and invasion was confirmed through a transwell assay. The IC50 was verified through a CCK-8 assay. The NMT1 mRNA expression in NSCLC tissues was detected through RT-qPCR. RESULTS: It was demonstrated that NMT1 exhibited higher expression in spheroid cells. Additionally, NMT1 facilitated the stemness in NSCLC. It was also found that NMT1 accelerated NSCLC tumor metastasis and the resistance to cisplatin. Moreover, NMT1 activated the PI3K/AKT pathway to facilitate stemness in NSCLC. NMT1 was also higher in tumor tissues of NSCLC patients and resulted in a poor survival rate. CONCLUSION: NMT1 enhanced the stemness of NSCLC cells by activating the PI3K/AKT pathway. This discovery suggested that NMT1 may be a valid therapeutic biomarker for NSCLC.

Integrated proteomic and metabolomic analysis to study the effects of spaceflight on Candida albicans.

BACKGROUND: Candida albicans is an opportunistic pathogenic yeast, which could become pathogenic in various stressful environmental factors including the spaceflight environment. In this study, we aim to explore the phenotypic changes and possible mechanisms of C. albicans after exposure to spaceflight conditions. RESULTS: The effect of C. albicans after carried on the "SJ-10" satellite for 12 days was evaluated by proliferation, morphology, environmental resistance and virulence experiment. The result showed that the proliferation rate, biofilm formation, antioxidant capacity, cytotoxicity and filamentous morphology of C. albicans were increased in the spaceflight group compared to the control group. Proteomics and metabolomics technologies were used to analyze the profiles of proteins and metabolites in C. albicans under spaceflight conditions. Proteomic analysis identified 548 up-regulated proteins involved in the ribosome, DNA replication, base excision repair and sulfur metabolism in the spaceflight group. Moreover, 332 down-regulated proteins related to metabolic processes were observed. The metabolomic analysis found five differentially expressed metabolites. The combined analysis of proteomic and metabolomic revealed the accumulation of cysteine and methionine in C. albicans after spaceflight. CONCLUSIONS: Mechanisms that could explain the results in the phenotypic experiment of C. albicans were found through proteomic and metabolomic analysis. And our data provide an important basis for the assessment of the risk that C. albicans could cause under spaceflight environment.

Hematopoietic stem cells and lineage cells undergo dynamic alterations under microgravity and recovery conditions.

Spaceflight leads to health risks including bone demineralization, skeletal muscle atrophy, cardiovascular dysfunction, and disorders of almost all physiologic systems. However, the impacts of microgravity on blood lineage cells and hematopoietic stem cells (HSCs) in vivo are largely unknown. In this study, we analyzed peripheral blood samples from 6 astronauts who had participated in spaceflight missions and found significant changes in several cell populations at different time points. These dynamic alterations of lineage cells and the role of HSCs were further studied in a mouse model, using hindlimb unloading (HU) to simulate microgravity. Large reductions in the frequency of NK cells, B cells, and erythrocyte precursors in the bone marrow of the HU mice were observed, together with an increased frequency of T cells, neutrophils, and HSCs. T cell levels recovered faster than those of B cells and erythrocyte precursors, whereas the recovery rates of NK cells and granulocytes were slow. In addition, competitive reconstitution experiments demonstrated the impaired function of HSCs, although these changes were reversible. Deep sequencing showed changes in the expression of regulatory molecules important for the differentiation of HSCs. This study provides the first determination of altered HSC function under simulated microgravity in vivo. The impairment of HSC function and differentiation provides an explanation for the immune disorders that occur under simulated microgravity. Thus, our findings demonstrated that spaceflight and simulated microgravity disrupt the homeostasis of immune system and cause dynamic alterations on both HSCs and lineage cells.-Cao, D., Song, J., Ling, S., Niu, S., Lu, L., Cui, Z., Li, Y., Hao, S., Zhong, G., Qi, Z., Sun, W., Yuan, X., Li, H., Zhao, D., Jin, X., Liu, C., Wu, X., Kan, G., Cao, H., Kang, Y., Yu, S., Li, Y. Hematopoietic stem cells and lineage cells undergo dynamic alterations under microgravity and recovery conditions.

CLPREM: A real-time traffic prediction method for 5G mobile network.

Network traffic prediction is an important network monitoring method, which is widely used in network resource optimization and anomaly detection. However, with the increasing scale of networks and the rapid development of 5-th generation mobile networks (5G), traditional traffic forecasting methods are no longer applicable. To solve this problem, this paper applies Long Short-Term Memory (LSTM) network, data augmentation, clustering algorithm, model compression, and other technologies, and proposes a Cluster-based Lightweight PREdiction Model (CLPREM), a method for real-time traffic prediction of 5G mobile networks. We have designed unique data processing and classification methods to make CLPREM more robust than traditional neural network models. To demonstrate the effectiveness of the method, we designed and conducted experiments in a variety of settings. Experimental results confirm that CLPREM can obtain higher accuracy than traditional prediction schemes with less time cost. To address the occasional anomaly prediction issue in CLPREM, we propose a preprocessing method that minimally impacts time overhead. This approach not only enhances the accuracy of CLPREM but also effectively resolves the real-time traffic prediction challenge in 5G mobile networks.

Protective effect of Baoyuan Jieyu formula on long-term spaceflight composite stress-induced depressive-like behavior and memory deficits through regulation of Ca2+ channel currents.

Long-term spaceflight composite stress (LSCS) can cause adverse effects on human systems, especially the central nervous system. This study aimed to identify the underlying mechanisms of the protective effect of Baoyuan Jieyu Formula (BYJYF) on LSCS-induced depressive-like behavior and memory deficits. In this experiment, we simulated the real space station environment for a period of 42 days. Novel object recognition test and forced swimming test were used to assess the memory abilities and depression level of rats as well as test the therapeutic effects of BYJYF treatment. Results showed LSCS could induce depressive-like behavior and damage short-term memory in the behavioral level, and BYJYF could enhance the ability to resist LSCS. Meanwhile, LSCS increased the levels of CRH, ACTH, and CORT and induced HPA axis hyperactivity, which can be relieved by BYJYF. Further, we predicted and verified the potential signaling pathways of BYJYF. Results showed BYJYF may reverse the inhibition of LSCS on Ca2+ channel currents. And we also found that BYJYF may exert its medicinal effects via four main active components including saikosaponin A. Overall, BYJYF exhibited protective effects against LSCS-induced depressive-like behavior and memory deficits, which might be ascribed to the regulation of Ca2+ channel currents and four active components. And it might become a promising candidate medicine for diseases induced by LSCS.

Whole-transcriptome RNA sequencing reveals CeRNA regulatory network under long-term space composite stress in Rats.

To systematically evaluate the effect of simulated long-term spaceflight composite stress (LSCS) in hippocampus and gain more insights into the transcriptomic landscape and molecular mechanism, we performed whole-transcriptome sequencing based on the control group (Ctrl) and the simulated long-term spaceflight composite stress group (LSCS) from six hippocampus of rats. Subsequently, differential expression analysis was performed on the Ctrl and LSCS groups, followed by enrichment analysis and functional interaction prediction analysis to investigate gene-regulatory circuits in LSCS. In addition, competitive endogenous RNA (ceRNA) network was constructed to gain insights into genetic interaction. The result showed that 276 differentially expressed messenger RNAs (DEmRNAs), 139 differentially expressed long non-coding RNAs (DElncRNAs), 103 differentially expressed circular RNAs (DEcircRNAs), and 52 differentially expressed microRNAs (DEmiRNAs) were found in LSCS samples compared with the controls, which were then subjected to enrichment analysis of Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways to find potential functions. PI3K-Akt signaling pathway and MAPK signaling pathway may play fundamental roles in the pathogenesis of LSCS. A ceRNA network was constructed with the predicted 340 DE pairs, which revealed the interaction roles of 220 DEmiRNA-DEmRNA pairs, 76 DEmiRNA-DElncRNA pairs, and 44 DEmiRNA-DEcircRNA pairs. Further, Thrombospondins2 was found to be a key target among those ceRNAs. Overall, we conducted for the first time a full transcriptomic analysis of the response of hippocampus to the LSCS that involved a potential ceRNA network, thus providing a basis to study the underlying mechanism of the LSCS.

Long-term spaceflight composite stress induces depressive behaviors in model rats through disrupting hippocampus synaptic plasticity.

INTRODUCTION: Long-term spaceflight composite stress (LSCS) can cause adverse effects on human systems, including the central nervous system, which could trigger anxiety and depression. AIMS: This study aimed to identify changes in hippocampus synaptic plasticity under LSCS. METHODS: The present study simulated the real long-term space station environment by conducting a 42-day experiment that involved simulating microgravity, isolation, noise, circadian rhythm disruptions, and low pressure. The mood and behavior of the rats were assessed by behavior test. Transmission electron microscopy and patch-clamp were used to detect the changes in synapse morphology and electrophysiology, and finally, the expression of NMDA receptor channel proteins was detected by western blotting. RESULTS: The results showed that significant weight loss, anxiety, and depressive behaviors in rats were observed after being exposed to LSCS environment for 42 days. The synaptic structure was severely damaged, manifested as an obvious decrease in postsynaptic density thickness and synaptic interface curvature (p < 0.05; p < 0.05, respectively). Meanwhile, LTP was significantly impaired (p < 0.0001), and currents in the NMDAR channel were also significantly reduced (p < 0.0001). Further analysis found that LSCS decreased the expression of two key subtype proteins on this channel. CONCLUSION: These results suggested that LSCS-induced depressive behaviors by impairing synaptic plasticity in rat hippocampus.

"Integrative learning" promotes learning but not memory in older rats.

Background: We had previously advanced the concept of "Integrative Learning", that is, "under the role of 'meta-learning self', learners actively integrate learning materials to achieve rapid and in-depth understanding of knowledge", and designed an animal behavioral model to compare the effects of "Integrative Learning" (IL) vs. "Progressive Learning" (PL) in young rats. It was found that IL is more advantageous than PL. Here, we aim to examine whether the same phenomenon persist in older rats. Methods: Fifteen 12-month-old male Sprague-Dawley (SD) rats were selected as subjects and randomly divided into the IL group and the PL group, and a 14-unit integrative T-maze was constructed for the study. Training and testing procedures contained three stages: the learning stage, the memory retention test stage and the Gestalt transfer learning stage. Data on young rats (1-month-old) from the previous study were also drawn here for comparisons on learning performance. Results: (1) The 12-session learning stage can be divided into three sub-stages as each sub-stage represented the new opening of one third of the whole path in the PL group. There were significant interactions in total errors made between groups and sessions: the PL group had significantly fewer errors during Sub-stage One due to a much shorter path to be learned, however, the IL group's errors made sharply dropped as learning progressed into Sub-stage Two and Three, and were maintained at a significantly lower level than the PL group during Sub-stage Three. (2) When compared with young rats, age had a main effect on the number of errors made-the 1-month-old groups learned overall better and faster than the older groups, whereas the pattern of group differences between the IL and PL learning modes remained consistent across young and older groups. (3) Unlike young rats, during the memory retention test stage and the Gestalt transfer learning stage, the IL group did not perform better than the PL group in older rats. Conclusions: (1) "Integrative Learning" promotes learning but not memory in older rats. (2) Higher-order cognitive abilities that support meta-cognition, long-term retention and knowledge transfer might be deteriorating in older rats.

[Big data analysis of coastal illegal fishing from the perspective of compensation of ecological and environmental damage]. / 生态环境损害赔偿视域下的近海非法捕捞大数据分析.

Illegal fishing is one of the sources of marine ecological damage. The implementation of compensation of ecological and environmental damage in this field is poorly understood. In this study, we examined data pertaining to coastal illegal fishing cases during 2018-2022 using the big data publicly made available by China Judgement Online. The main results included: 1) there are numerous types of illegal fishing, and more efforts should focus on the nature and extent of illegal fishing, with electrofishing and trawl being suitable entry points; 2) Special attention should be paid to the variation characteristics of rakes in the range of high illegal catch weight and value. It was suggested to optimize and adjust its management mode to avoid the frequent occurrence of such illegal fishing cases of rake; 3) The varieties of assessment models increased the uncertainty of damages computation, which might be reduced by establishing strong criteria for value quantification and damage assessment; 4) There is limited scientific support for the compensation for releasing the most popular ecological restoration technique for illegal fishing. As a result, the "compensation" design for "restoration" should be implemented, while the potential for additional restoration methods should be investigated.

Long-term spaceflight composite stress induces depression and cognitive impairment in astronauts-insights from neuroplasticity.

The environment on the space station is quite unique compared to Earth, which is a composite of multiple stressors, such as microgravity, isolation, confinement, noise, circadian rhythm disturbance, and so on. During prolonged space missions, astronauts have to stay in such extreme environments for long periods, which could induce adverse effects on both their physical and mental health. In some circumstances, this kind of long-term spaceflight composite stress (LSCS) could also induce depression and cognitive impairment in various ways, including dysregulating the neuroplasticity of the brains of astronauts, which should be attached to great importance. Here, we have comprehensively reviewed the impact of individual and combined stressors on depression and cognitive function during long-term spaceflight, explained the underlying mechanisms of those effects from the perspective of neuroplasticity, and current countermeasures for mitigating these challenges. This review provides insights into LSCS and potential neuroplasticity mechanisms, current with potentially great impact for understanding and mitigating the mental health risks and traumas of career astronauts and space tourists.

Comprehensive analysis of transcriptomics and metabolomics to understand tail-suspension-induced myocardial injury in rat.

Background/Aims: The effect and underlying mechanism of microgravity on myocardium still poorly understood. The present study aims to reveal the effect and underlying mechanism of tail-suspension-induced microgravity on myocardium of rats. Methods: Tail-suspension was conducted to simulate microgravity in rats. Echocardiography assay was used to detect cardiac function. The cardiac weight index was measured. Hematoxylin and eosin (HE) staining and transmission electron microscopy assay were conducted to observe the structure of the tissues. RNA sequencing and non-targeted metabolomics was employed to obtain transcriptome and metabolic signatures of heart from tail-suspension-induced microgravity and control rats. Results: Microgravity induced myocardial atrophy and decreased cardiac function in rats. Structure and ultrastructure changes were observed in myocardium of rats stimulated with microgravity. RNA sequencing for protein coding genes was performed and identified a total of 605 genes were differentially expressed in myocardium of rats with tail suspension, with 250 upregulated and 355 downregulated (P < 0.05 and | log2fold change| > 1). A total of 55 differentially expressed metabolites were identified between the two groups (VIP > 1 and P < 0.05) by the metabolic profiles of heart tissues from microgravity groups and control. Several major pathways altered aberrantly at both transcriptional and metabolic levels, including FoxO signaling pathway, Amyotrophic lateral sclerosis, Histidine metabolism, Arginine and proline metabolism. Conclusion: Microgravity can induce myocardial atrophy and decreases cardiac function in rats and the molecular alterations at the metabolic and transcriptomic levels was observed, which indicated major altered pathways in rats with tail suspension. The differentially expressed genes and metabolites-involved in the pathways maybe potential biomarkers for microgravity-induced myocardial atrophy.

Baoyuan jieyu formula ameliorates depression-like behaviour in rats induced by simulated long-term spaceflight composite stress through regulating MAPK and BDNF pathways.

During space flight, astronauts are exposed to various influences of extreme environments and susceptible to develop depression-like behavior. Thus, this study aims to explore the molecular biological mechanism of the cause of depression-like behavior and reveal the effect of Baoyuan Jieyu Formula (BYJYF) on ameliorating depression-like behavior. Here, rats exposed to simulated long-term spaceflight composite stress (LSCS) reduced the sucrose preference rate (P <0.01), and the time of forced swimming immobility and the number of climbing times were also reduced (P < 0.01, P < 0.001). Moreover, the number of neurons in the CA3 region of the hippocampus decreased ( P< 0.01, P < 0.05, P < 0.001), the staining became weak, and the Nissl body decreased. Antibody chip detected a total of 854 protein molecules in the hippocampus, of which 51 and 37 proteins were significantly different in the LSCS group and LSCS+BYJYF group, respectively, focusing on signaling pathways such as MAPK and neurotrophin. Western blot was used to verify the related proteins of these two pathways. Conclusively, simulated LSCS can induce depression-like behavior and neuronal damage. BYJYF can reduce neuronal apoptosis, and promote neuron survival by regulating the MAPK and the neurotrophin signaling pathway to protect neurons and combat LSCS.

Panax quinquefolium saponin attenuates cardiac remodeling induced by simulated microgravity.

BACKGROUND: Cardiac atrophy and reduced cardiac distensibility have been reported following space flight. Cardiac function is correspondingly regulated in response to changes in loading conditions. Panax quinquefolium saponin (PQS) improves ventricular remodeling after acute myocardial infarction by alleviating endoplasmic reticulum stress and Ca2+overload. However, whether PQS can ameliorate cardiac atrophy following exposure to simulated microgravity remains unknown. PURPOSE: To explore the protective role of PQS in cardiac remodeling under unloading conditions and its underlying mechanisms. METHODS: Hindlimb unloading (HU) model was used to simulate unloading induced cardiac remodeling. Forty-eight male rats were randomly assigned to four groups, including control, PQS, HU and HU + PQS. At 8 weeks after the experiment, cardiac structure and function, serum levels of Creatine Kinase-MB (CK-MB), Cardiactroponin T (cTnT), ischemia modified albumin (IMA), and cardiomyocyte apoptosis were measured. Network pharmacology analysis was used to predict the targets of the six major constituents of PQS, and the signaling pathways they involved in were analyzed by bioinformatics methods. Changes in the key proteins involved in the protective effects of PQS were further confirmed by Western Blot. RESULTS: Simulated microgravity led to increases in serum levels of CK-MB, cTnT and IMA, remodeling of cardiac structure, impairment of cardiac function, and increased cardiomyocyte apoptosis as compared with control. PQS treatment significantly reduced serum levels of CK-MB, cTnT and IMA, improved the impaired cardiac structure and function, and decreased cardiomyocyte apoptosis induced by unloading. The activation of AMPK and inhibition of Erk1/2 and CaMKII/HDAC4 were demonstrated in the cardiocytes of HU rats after PQS treatment. CONCLUSION: PQS provides protection against cardiac remodeling induced by simulated microgravity, partly resulting from changes in the signaling pathways related to energy metabolism reduction, calcium overloading and cell apoptosis.

On-orbit sleep problems of astronauts and countermeasures.

Sufficient sleep duration and good sleep quality are crucial to ensure normal physical and mental health, cognition and work performance for the common people, as well as astronauts. On-orbit sleep problem is very common among astronauts and has potential detrimental influences on the health of crewmembers and the safety of flight missions. Sleep in space is becoming a new medical research frontier. In this review we summarized on-orbit sleep problems of astronauts and six kinds of causes, and we presented the effects of lack of sleep on performance as well as mental and physical health, then we proposed seven kinds of countermeasures for sleep disturbance in spaceflight, including pharmacologic interventions, light treatment, crew selection and training, Traditional Chinese Medicine and so on. Furthermore, we discussed and oriented the prospect of researches on sleep in space.

Myocardial CKIP-1 Overexpression Protects from Simulated Microgravity-Induced Cardiac Remodeling.

Human cardiovascular system has adapted to Earth's gravity of 1G. The microgravity during space flight can induce cardiac remodeling and decline of cardiac function. At present, the mechanism of cardiac remodeling induced by microgravity remains to be disclosed. Casein kinase-2 interacting protein-1 (CKIP-1) is an important inhibitor of pressure-overload induced cardiac remodeling by decreasing the phosphorylation level of HDAC4. However, the role of CKIP-1 in the cardiac remodeling induced by microgravity is unknown. The purpose of this study was to determine whether CKIP-1 was also involved in the regulation of cardiac remodeling induced by microgravity. We first detected the expression of CKIP-1 in the heart from mice and monkey after simulated microgravity using Q-PCR and western blotting. Then, myocardial specific CKIP-1 transgenic (TG) and wild type mice were hindlimb-suspended (HU) to simulate microgravity effect. We estimated the cardiac remodeling in morphology and function by histological analysis and echocardiography. Finally, we detected the phosphorylation of AMPK, ERK1/2, and HDAC4 in the heart from wild type and CKIP-1 transgenic mice after HU. The results revealed the reduced expression of CKIP-1 in the heart both from mice and monkey after simulated microgravity. Myocardial CKIP-1 overexpression protected from simulated microgravity-induced decline of cardiac function and loss of left ventricular mass. Histological analysis demonstrated CKIP-1 TG inhibited the decreases in the size of individual cardiomyocytes of mice after hindlimb unloading. CKIP-1 TG can inhibit the activation of HDAC4 and ERK1/2 and the inactivation of AMPK in heart of mice induced by simulated microgravity. These results demonstrated CKIP-1 was a suppressor of cardiac remodeling induced by simulated microgravity.

Circulating microRNAs Correlated with Bone Loss Induced by 45 Days of Bed Rest.

The purpose of this study was to find the circulating microRNAs (miRNAs) co-related with bone loss induced by bed rest, and testify whether the selected miRNAs could reflect the bone mineral status of human after bed-rest. We analyzed plasma miRNA levels of 16 subjects after 45 days of -6° head-down tilt bed rest, which is a reliable model for the simulation of microgravity. We characterize the circulating miRNA profile in individuals after bed rest and identify circulating miRNAs which can best reflect the level of bone loss induced by bed rest. Expression profiling of circulating miRNA revealed significant downregulation of 37 miRNAs and upregulation of 2 miRNAs, while only 11 of the downregulated miRNAs were further validated in a larger volunteer cohort using qPCR. We found that 10 of these 11 miRNAs (miR-103, 130a, 1234, 1290, 151-5p, 151-3p, 199a-3p, 20a, 363, and 451a) had ROC curve that distinguished the status after bed rest. Importantly, significant positive correlations were identified between bone loss parameters and several miRNAs, eventually miR-1234 showed clinical significance in detecting the bone loss of individuals after 45 days of bed rest.

Dammarane Sapogenins Ameliorates Neurocognitive Functional Impairment Induced by Simulated Long-Duration Spaceflight.

Increasing evidence indicates the occurrence of cognitive impairment in astronauts under spaceflight compound conditions, but the underlying mechanisms and countermeasures need to be explored. In this study, we found that learning and memory abilities were significantly reduced in rats under a simulated long-duration spaceflight environment (SLSE), which includes microgravity, isolation confinement, noises, and altered circadian rhythms. Dammarane sapogenins (DS), alkaline hydrolyzed products of ginsenosides, can enhance cognition function by regulating brain neurotransmitter levels and inhibiting SLSE-induced neuronal injury. Bioinformatics combined with experimental verification identified that the PI3K-Akt-mTOR pathway was inhibited and the MAPK pathway was activated during SLSE-induced cognition dysfunction, whereas DS substantially ameliorated the changes in brain. These findings defined the characteristics of SLSE-induced cognitive decline and the mechanisms by which DS improves it. The results provide an effective candidate for improving cognitive function in spaceflight missions.

The complete mitochondrial genome of the Gray's grenadier anchovy Coilia grayii (Teleostei, Engraulidae).

In this paper, the complete mitochondrial DNA (mtDNA) sequence of Coilia grayii was determined. The mitochondrial genome was 16,851 bp in length, including 13 protein-coding genes, 2 ribosomal RNAs (rRNAs), 22 transfer RNAs (tRNAs) and a non-coding control region as those found in other vertebrates, with the gene identical to that of typical vertebrates. The overall base composition of the heavy strand were 26.09% of A, 31.14% of T, 15.58% of C and 27.19% of G, with a slight AT bias of 57.23%. With the exception of ND6 and eight tRNA genes, all other mitochondrial genes were encoded on the heavy strand.