Output Cycles Research Articles

Analysis of the Relationship between Fiscal Policy Shocks and Monetary Stability in Iraq's Economy for the Period 1990-2018

The research aims to measure the impact of positive and negative fiscal policy shocks on monetary stability in Iraq, which represents monetary stability as an indicator of real and price stability. Fiscal policy shocks are quantitative changes in public spending and public revenue affecting the output and price cycle, and fiscal policy despite the accompanying time gaps, but it remains a policy Influential and has a significant degree of impact on economic growth and development in developing countries. The fiscal policy represents a numerical translation of the economic and social objectives planned in the state's general budget tool consistent with the GDP cycle. The economic and social goals stem from the core of the functions and the main objectives of the fiscal policy, namely the allocation of resources, stability and restoration Distribution and these functions, as we know, free market techniques may fail to achieve them, which interferes with the financial policy to address the failure of the market to reach the set goals, and that coordination between fiscal and monetary policies does not mean a loss of independence as much as it means correcting fiscal and monetary policies without causing undesirable adverse effects upon the necessary correction. For local courses Opposing this coordination, and we have touched on the monetary stability index adopted by the International Monetary Fund (IMF) to discuss the impact of financial shocks on the monetary stability index in Iraq, where the Iraqi economy witnessed positive fiscal and revenue policy shocks with limited negative financial shocks in spending. Public and public revenue and the impact was studied through the existence of long-term relationships that link fiscal policy shocks, i.e. quantitative changes in public spending and public revenue on monetary stability. The boundary test within the Autoregression techniques of distributed Lag demonstrated the existence of a long-term relationship between fiscal policy shocks and monetary stability in Iraq.

Express and Purify Human CRY2 for Functional Analyses

The circadian rhythm is a biological clock responsible for regulating the daily cycles of essential physiological and metabolic processes, such as sleep wake cycles, by responding to light and dark changes. Every cell has its own circadian rhythm that is synchronized by a master clock in the brain. At the cellular level, circadian rhythms are controlled by a time‐delayed transcriptional‐translational feed‐back loop (TTFL), which consists of several core proteins. These proteins include circadian locomotor output cycles protein kaput (CLOCK), brain and muscle ARNT‐like 1 (BMAL1), cryptochrome (CRY), and period (PER). CLOCK and BMAL1 initiate the TTFL by activating the transcription of several circadian genes including CRYs and PERs that will be translated in the cytosol. With accumulation after a certain time, CRYs/PERs complexes will translocate back to the nucleus to negatively inhibit CLOCK/BMAL1 activities to finish the TTFL. There are two paralogs of CRY within the human genome: CRY1 and CRY2, both of which have essential roles in the negative feedback. The purpose of this project is to study the structure and function of human CRY2. Regardless of many advances in this field including available structure of CRYs, the detailed interaction between CRY2 to other circadian core proteins are still limited. Through this research we would be able to express and purify large quantities of hCRY2 that will be used for the future interaction studies. The results will deepen our understanding of the mechanisms behind circadian rhythm and its associated diseases, facilitating the development of prevention and treatment strategies.

Data‐driven battery degradation prediction: Forecasting voltage‐capacity curves using one‐cycle data

AbstractWith the wide deployment of rechargeable batteries, battery degradation prediction has emerged as a challenging issue. However, battery life defined by capacity loss provides limited information regarding battery degradation. In this article, we explore the prediction of voltage‐capacity curves over battery lifetime based on a sequence to sequence (seq2seq) model. We demonstrate that the data of one present voltage‐capacity curve can be used as the input of the seq2seq model to accurately predict the voltage‐capacity curves at 100, 200, and 300 cycles ahead. This offers an opportunity to update battery management strategies in response to the predicted consequences. Besides, the model avoids feature engineering and is flexible to incorporate different numbers of input and output cycles. Therefore, it can be easily transplanted to other battery systems or electrochemical components. Furthermore, the model features data generation, that is, we can use the data of only one cycle to generate a large spectrum of aging data at the future cycles for developing other battery diagnosis or prognosis methods. In this way, the time and energy consuming battery degradation tests can be sharply reduced.image

No significant association between SNPs in the CLOCK and ADH4 genes and susceptibility to cluster headaches: A systematic review and meta-analysis.

The circadian locomotor output cycles kaput (CLOCK) gene and the alcohol dehydrogenase 4 (ADH4) gene are promising candidates for susceptibility to cluster headaches (CH). Associations of the three single nucleotide polymorphisms (SNPs)-CLOCK SNP rs1801260 and ADH4 SNPs rs1800759, and rs1126671-with CH were studied previously, but the results were inconsistent. Associations between the three SNPs (rs1801260, rs1126671, and rs1800759) and CH risk were separately assessed by pooled odds ratios (ORs) along with 95% confidence intervals (95% CIs) based on five different genetic models. Methodological quality was assessed using the Newcastle-Ottawa Quality Assessment Scale (NOS). All statistical analyses were carried out with RevMan 5.3 software. Eight studies involving 1437 CH patients and 2541 healthy controls were selected for quantitative synthesis, from five studies on CLOCK rs1801260, five on ADH4 rs1800759, and three on ADH4 rs1126671. Our pooled data did not support associations between the three SNPs (rs1801260 in the CLOCK gene, rs1800759 and rs1126671 in the ADH4 gene) and susceptibility to CH (rs1801260: OR 1.10, 95% CI: 0.95-1.28; p=0.19; rs1800759: OR 1.06, 95% CI: 0.93-1.22; p=0.37; and rs1126671: OR 1.09, 95% CI: 0.92-1.28; p=0.32). We found no significant associations between the three SNPs (rs1801260 in the CLOCK gene and rs1800759 and rs1126671 in the ADH4 gene) and the susceptibility to CH across both Caucasian and Asian ethnicities in our meta-analysis.

Circadian Regulator CLOCK Drives Immunosuppression in Glioblastoma.

The symbiotic interactions between cancer stem cells and the tumor microenvironment (TME) are critical for tumor progression. However, the molecular mechanism underlying this symbiosis in glioblastoma (GBM) remains enigmatic. Here, we show that circadian locomotor output cycles kaput (CLOCK) and its heterodimeric partner brain and muscle ARNT-like 1 (BMAL1) in glioma stem cells (GSC) drive immunosuppression in GBM. Integrated analyses of the data from transcriptome profiling, single-cell RNA sequencing, and TCGA datasets, coupled with functional studies, identified legumain (LGMN) as a direct transcriptional target of the CLOCK-BMAL1 complex in GSCs. Moreover, CLOCK-directed olfactomedin-like 3 (OLFML3) upregulates LGMN in GSCs via hypoxia-inducible factor 1-alpha (HIF1α) signaling. Consequently, LGMN promotes microglial infiltration into the GBM TME via upregulating CD162 and polarizes infiltrating microglia toward an immune-suppressive phenotype. In GBM mouse models, inhibition of the CLOCK-OLFML3-HIF1α-LGMN-CD162 axis reduces intratumoral immune-suppressive microglia, increases CD8+ T-cell infiltration, activation, and cytotoxicity, and synergizes with anti-programmed cell death protein 1 (anti-PD-1 therapy). In human GBM, the CLOCK-regulated LGMN signaling correlates positively with microglial abundance and poor prognosis. Together, these findings uncover the CLOCK-OLFML3-HIF1α-LGMN axis as a molecular switch that controls microglial biology and immunosuppression, thus revealing potential new therapeutic targets for patients with GBM.

Credit, output and financial stress: A non‐linear LVSTAR application to Brazil

AbstractWe estimate a bi‐variate LVSTAR model to investigate the non‐linear interplay between Brazil’s credit, output and financial cycles between 1999 and 2017. We use financial stress as the regime‐switching variable to assess how it impacts economic performance. We find evidence of a lengthy transition between regimes. Moreover, Granger Causality tests indicate statistical precedence of credit growth through financial intermediaries. After credit shocks, we find non‐mean‐reverting trajectories and that financial stress worsens the economic downturn. Counterintuitively, total credit growth increases after adverse output shocks. This appears to be caused by elevated public credit provision relative to private credit flows, triggered by anticyclical policy.

MTOR-AKT Signaling in Cellular Clock Resetting Triggered by Osmotic Stress.

Aims: The circadian clock oscillates in a cell-autonomous manner with a period of ∼24 h, and the phase is regulated by various time cues such as light and temperature through multiple clock input pathways. We previously found that osmotic and oxidative stress strongly affected the circadian period and phase of cellular rhythms, and triple knockout of apoptosis signal-regulating kinase (ASK) family members, Ask1, Ask2, and Ask3, abolished the phase shift (clock resetting) induced by hyperosmotic pulse treatment. We aimed at exploring a key molecule(s) and signaling events in the clock input pathway dependent on ASK kinases. Results: The phase shift of the cellular clock induced by the hyperosmotic pulse treatment was significantly reduced by combined deficiencies of the clock(-related) genes, Dec1, Dec2, and E4 promoter-binding protein 4 (also known as Nfil3) (E4bp4). In addition, liquid chromatography mass/mass spectrometry (LC-MS/MS)-based proteomic analysis identified hyperosmotic pulse-induced phosphorylation of circadian locomotor output cycles caput (CLOCK) Ser845 in an AKT-dependent manner. We found that AKT kinase was phosphorylated at Ser473 (i.e., activated) in response to the hyperosmotic pulse experiments. Inhibition of mechanistic target of rapamycin (mTOR) kinase by Torin 1 treatment completely abolished the AKT activation, suppressed the phosphorylation of CLOCK Ser845, and blocked the clock resetting induced by the hyperosmotic pulse treatment. Innovation and Conclusions: We conclude that mTOR-AKT signaling is indispensable for the CLOCK Ser845 phosphorylation, which correlates with the clock resetting induced by the hyperosmotic pulse treatment. Immediate early induction of the clock(-related) genes and CLOCK carboxyl-terminal (C-terminal) region containing Ser845 also play important roles in the clock input pathway through redox-sensitive ASK kinases. Antioxid. Redox Signal. 37, 631-646.

The effects of financial integration during crises

We investigate the role of financial integration in the spread of the 2008 global financial crisis. Using a rich dataset covering 31 countries between 1978 and 2018, we find that during the 2008 financial crisis, when two countries have a higher level of financial integration, their consumption cycles are more synchronized. Similar patterns are found for investment and output. However, we also find that during times outside of the 2008 financial crisis, higher financial integration leads to more divergent consumption and output cycles. We build a two-country model with global banks and variable capital utilization to illustrate that the impact of financial integration on business cycle synchronization depends on the type of shock and that variable capital utilization is the key to accounting for the relationship between financial integration and investment synchronization. The calibrated model replicates our empirical findings reasonably well. Finally, our welfare analysis indicates that financial integration leads to welfare losses during financial crises but to welfare gains outside of financial crises.

Circadian Control of Mitochondria in Reactive Oxygen Species Homeostasis.

Significance: Mitochondria produce most of the cellular ATP through the process of oxidative phosphorylation. Energy metabolism in the mitochondria is associated with the production of reactive oxygen species (ROS). Excessive ROS production leads to oxidative stress and compromises cellular physiology. Energy metabolism in the mitochondria depends on nutrient flux and cellular metabolic needs, which are in turn connected with the feeding/fasting cycle. In animals, the feeding/fasting cycle is controlled by the circadian clock that generates 24-h rhythms in behavior, metabolism, and signaling. Recent Advances: Here, we discuss the role of the circadian clock and rhythms in mitochondria on ROS homeostasis. The circadian clock is involved in mitochondrial ROS production and detoxification through the control of nutrient flux and oxidation, uncoupling, antioxidant defense, and mitochondrial dynamics. Critical Issues: Little is known on the molecular mechanisms of circadian control of mitochondrial functions. The circadian clock regulates the expression and activity of mitochondrial metabolic and antioxidant enzymes. The regulation involves a direct transcriptional control by Circadian Locomotor Output Cycles Kaput/brain and muscle ARNT-like 1(CLOCK/BMAL1), nuclear factor erythroid-2-related factor 2 (NRF2) transcriptional network, and sirtuin-dependent posttranslational protein modifications. Future Perspectives: We hypothesize that the circadian clock orchestrates mitochondrial physiology to synchronize it with the feeding/fasting cycle. Circadian coordination of mitochondrial function couples energy metabolism with diets and contributes to antioxidant defense to prevent metabolic diseases and delay aging. Antioxid. Redox Signal. 37, 647-663.

Caffeine Therapy for Apnea of Prematurity: Role of the Circadian CLOCK Gene Polymorphism.

Standard-dose caffeine citrate has been routinely prescribed for apnea of prematurity (AOP) management; however, some preterm infants respond well to the therapy while others do not. The AOP phenotype has been attributed solely to the immature control of the respiratory system consequent to preterm birth, but there are also important genetic influences. Based on our previous report, we tested the hypothesis that the human circadian locomotor output cycles kaput (CLOCK) gene polymorphisms play a role in the response to caffeine citrate therapy in preterm infants. We also studied the interactions of the circadian clock with aryl hydrocarbon receptor (AHR) signaling pathways in preterm babies who received caffeine citrate. This single-center study collected data from 112 preterm infants (<35 weeks gestational age) between July 2017 and July 2018, including apnea-free (n = 48) and apneic (n = 64) groups. Eighty-eight candidate single nucleotide polymorphisms (SNPs) were tested using the MassARRAY system. Association analysis was performed using the PLINK Whole Genome Data Analysis Toolset and SNPStats software. Linkage disequilibrium (LD) and haplotype analyses were performed using Hapview software. No significant intergroup differences in allele distributions or genotype frequencies of CYP1A2, CYP3A4, CYP3A5, and CYP3A7 were detected in our study on preterm babies. Two more SNPs in AHR were found to be associated with determining the response to caffeine citrate therapy in our pediatric patients. Of the 46 candidate SNPs in the CLOCK gene, 26 were found to be associated with determining the response to caffeine treatment in these babies. Interestingly, a significant association was retained for 18 SNPs in the CLOCK gene after false discovery rate correction. Moreover, strong LD formed in those variants in AHR, ADORA2A, and CLOCK genes was confirmed to be significantly associated with a better response to standard-dose caffeine therapy. In summary, CLOCK gene polymorphisms play a role in determining the response to caffeine therapy in premature neonates with AOP. However, whether the AHR and CLOCK signaling pathways crosstalk with each other during caffeine treatment remains largely unclear. Future clinical studies including more immature babies and basic research are needed to explore the mechanism by which circadian rhythms affect the response to caffeine therapy.

TRITHORAX-dependent arginine methylation of HSP68 mediates circadian repression by PERIOD in the monarch butterfly

Transcriptional repression drives feedback loops that are central to the generation of circadian (∼24-h) rhythms. In mammals, circadian repression of circadian locomotor output cycles kaput, and brain and muscle ARNT-like 1 (CLOCK:BMAL1)-mediated transcription is provided by a complex formed by PERIOD (PER) and CRYPTOCHROME (CRY) proteins. PER initiates transcriptional repression by binding CLK:BMAL1, which ultimately results in their removal from DNA. Although PER's ability to repress transcription is widely recognized, how PER binding triggers repression by removing CLK:BMAL1 from DNA is not known. Here, we use the monarch butterfly as a model system to address this problem because it harbors a simplified version of the CLK:BMAL1-activated circadian clock present in mammals. We report that an intact CLOCK mouse exon 19 homologous region (CLKe19r) and the histone methyltransferase TRITHORAX (TRX) are both necessary for monarch CLK:BMAL1-mediated transcriptional activation, CLK-PER interaction, and PER repression. Our results show that TRX catalytic activity is essential for CLK-PER interaction and PER repression via the methylation of a single arginine methylation site (R45) on heat shock protein 68 (HSP68). Our study reveals TRX and HSP68 as essential links between circadian activation and PER-mediated repression and suggests a potential conserved clock function for HSPs in eukaryotes.

Design and Implementation of Journal Recommendation Model Based on L-BERT

The output cycle and quantity of academic achievements of researchers can promote academic exchanges and integration to a certain extent. Therefore, it is particularly important to design a journal recommendation model for scientific researchers that is fast and relatively suitable for producing scientific research results. Based on this, focusing on the information knowledge of papers and the characteristics of journal topics, combined with deep learning technology, this paper proposes a journal-oriented recommendation model based on L-BERT (LDA-BERT), which realizes the purpose of recommending journals for scholars. Firstly, topic extraction is performed on papers in a specific journal, and the number of topic words is determined by perplexity. Secondly, the vectorized representation of the topic words is carried out by using the BERT model, and the fixed representation value is obtained through the mean value idea. Finally, Euclidean distance is used to determine the similarity between papers and journals. In order to verify the effect of L-BERT model, it is compared with Word2Vec model on the real data set. The results show that the recommended results of L-BERT model are improved by 17%, 10% and 13% respectively in Precision, Recall, and F1-Score, which fully shows that this research has a certain application value, and the research results can help researchers shorten the cycle of looking for journals.

Association of Circadian Locomotor Output Cycles Kaput Rs1801260 and Hypocretin Receptor 1 Rs2271933 Polymorphisms in Patients with Chronic Migraine and Sleep Disorder

Background: Insomnia and excessive daytime sleepiness (EDS) are frequently reported as sleep disorders, especially in patients with chronic migraine (CM). The main drive of conducting a study on the relationship of genes that regulate circadian rhythm is that migraine contains a robust genetic background, and it is known that migraine attacks have circadian characteristics. This study aims to evaluate the relationship of circadian locomotor output cycles kaput (CLOCK) rs1801260 and hypocretin receptor 1 (HCRTR1) rs2271933 gene-related circadian rhythm of patients with CM and sleep disorders. Methods: The present study was designed prospectively in the Mersin University Neurology Clinic. Volunteer individuals aged 18–75 were included in the study in three groups. Each group was made up of 100 individuals. The first group was created among the patients diagnosed with CM. The sleep disorders of patients were evaluated by Epworth Sleep Scale and Pittsburgh Sleep Quality Scale. The second group healthy first-degree relatives of patients. Finally, the third group was formed by the other healthy volunteers who did not have blood relations with the patients. Genotyping was performed for the CLOCK rs1801260 and HCRTR1 rs2271933 genes. Results: Eighty-seven (87%) of the patients, 56 (56%) of the control group 1, and 50 (50%) of the control group 2 consisted of female patients. Their mean ages were 41.1 ± 11.5, 45.7 ± 15.2, and 35.9 ± 10. EDS was detected in 27% of the patients, and poor sleep quality was detected in 67%. About 21% of the patients were found to be suffering from both EDS and poor sleep quality. The CLOCK rs1801260 AG genotype was 6.71 times higher than the AA genotype in the migraine patient group with EDS compared to the second control group (odds ratio [OR]: 6.71, 95% confidence interval [CI]: 0.819–54.992, P = 0.076). The GG genotype, according to the AA genotype, also was found 2.87 times higher in this group (OR = 2.87, 95% CI: 0.336–24.566, P = 0.335). In the group of patients with CM and insomnia, the CLOCK rs1801260 AG genotype was 17.763 times higher than the AA genotype compared to the second control (OR = 17.763, 95% CI: 2.242–140.740, P = 0.006). Conclusion: When CM patients were compared with control groups, CLOCK rs1801260 gene AG genotype was associated with both insomnia and EDS. However, there was no significant relationship between patients and control groups regarding the HCRTR1 rs2271933 gene.

Financial Cycles in Euro Area Economies: A Cross‐Country Perspective Using Wavelet Analysis*

AbstractWe study the cross‐country dimension of financial cycles for six euro area countries using wavelet analysis. Estimated wavelet cohesions show that cycles in equity prices and interest rates display stronger synchronization across countries than real output cycles, whereas credit variables and house prices show lower cross‐country synchronization. We propose a wavelet‐based extension to the spectral envelope that is similar to a frequency‐based time‐varying principal component analysis. The country loadings show that, contrary to all other variables, cycles in loans to households and house prices in Germany and the Netherlands are negatively or less strongly correlated with the common cycles.

CLOCK Genetic Variations Are Associated With Age-Related Changes in Sleep Duration and Brain Volume.

Although a connection between sleep disruption and brain aging has been documented, biological mechanisms need to be further clarified. Intriguingly, aging is associated with circadian rhythm and/or sleep dysfunction in a key gene regulating circadian rhythm, Circadian Locomotor Output Cycles Kaput (CLOCK), has been linked to both aging-related sleep disturbances and neurodegenerative diseases. This study aims to investigate how CLOCK genetic variation associates with sleep duration changes and/or volumetric brain alteration. This population-based cross-sectional study used data from the Korean Genome Epidemiology Study and analyzed sleep characteristics and genetic and brain imaging data in 2 221 participants (mean 58.8 ± 6.8 years, 50.2% male). Eleven single-nucleotide polymorphisms (SNPs) in CLOCK were analyzed using PLINK software v1.09 to test for their association with sleep duration and brain volume. Haplotype analysis was performed by using pair-wise linkage disequilibrium of CLOCK polymorphisms, and multivariate analysis of covariance was for statistical analysis. Decreased sleep duration was associated with several SNPs in CLOCK intronic regions, with the highest significance for rs10002541 (p = 1.58 × 10-5). Five SNPs with the highest significance (rs10002541, rs6850524, rs4580704, rs3805151, rs3749474) revealed that CGTCT was the most prevalent. In the major CGTCT haplotype, decreased sleep duration over time was associated with lower cortical volumes predominantly in frontal and parietal regions. Less common haplotypes (GCCTC/CGTTC) had shorter sleep duration and more decreases in sleep duration over 8 years, which revealed smaller total and gray matter volumes, especially in frontal and temporal regions of the left hemisphere. CLOCK genetic variations could be involved in age-related sleep and brain volume changes.

Hibernation with rhythmicity: the circadian clock and hormonal adaptations of the hibernating Asiatic toads (Bufo gargarizans).

Hibernation is one of the fundamental strategies in response to cold environmental temperatures. During hibernation, the endocrine and circadian systems ensure minimal expenditure of energy for survival. The circadian rhythms of key hormones, melatonin (MT), corticosterone (CORT), triiodothyronine (T3 ), and thyroxine (T4 ), and the underlying molecular regulatory mechanisms of hibernation have been well determined in mammals but not in ectotherms. Here, a terrestrial hibernating species, Asiatic toad (Bufo gargarizans), was employed to investigate the plasma CORT, MT, T3 , and T4 ; and the retina, brain, and liver mRNA expression of the core clock genes, including circadian locomotor output cycles kaput (Clock), brain and muscle ARNT-like 1 (Bmal1), cryptochrome (Cry) 1 and 2, and period (Per) 1 and 2, at 7-time points over a 24-h period under acute cold (1 day at 4°C), and hibernation (45 days at 4°C). Our results showed that the circadian rhythms of the core clock genes were rather unaffected by acute cold exposure in the retina, unlike the brain and liver. In contrast, during hibernation, the liver clock genes displayed significant circadian oscillations, while those in the retina and brain stopped ticking. Furthermore, plasma CORT expressed circadian oscillations in both groups, and T3 in acute cold exposure group, whereas T4 and MT did not. Our results reveal that the plasma CORT and the liver sustain rhythmicity when the brain was not, indicating that the liver clock along with the adrenal clock synergistically maintains the metabolic requirements to ensure basic survival in hibernating Asiatic toads.

The CLOCK protein regulates insulin secretion related with L-type calcium channels in rat pancreatic beta cells

BackgroundCircadian locomotor output cycles kaput protein (CLOCK) plays a crucial role in glucose homeostasis and controlling insulin secretion. However, the mechanism of the CLOCK regulating rhythmic insulin secretion has not been fully understood. MethodsRhythmic expression of the CLOCK in rat pancreatic beta cell was detected. INS-1 cells were transfected with siRNAs to knockdown the CLOCK before the cells were incubated with different concentrations of glucose. Insulin secretion was analyzed by ELISA method. Expression of the L-type calcium channel protein (Cav1.2, Cacna1c) was determined both in the CLOCK-knockdown cells and the control cells. Calcium influx was probed by fluorescent. Chromatin immunoprecipitation (ChIP) test and dual-luciferase reporter gene experiments were applied to verify the relationship between the CLOCK and Cav1.2. ResultsThe CLOCK is abundantly expressed in rat pancreatic beta cells. Transcription level of the CLOCK showed rhythmicity in the beta cells. Compared to the control group, insulin release was significantly impaired with 25 mM glucose incubation in the CLOCK-knockdown group, but not showed with 2.5 mM glucose incubation. The expression of Cav1.2 and the influx of calcium were significantly decreased in the CLOCK-knockdown group with 25 mM glucose incubation. ChIP test indicted that the CLOCK bound to −444∼-454 region of the Cacna1c promoter of the INS-1 cells, but the binding was significantly reduced following the CLOCK-knockdown. Luciferase experiment was in accordance with the finding of ChIP. ConclusionsThe CLOCK mediating Cav1.2 expression may point out a potential pathway of circadian rhythm affecting insulin secretion.

Organic Cathode Materials for Sodium‐Ion Batteries: From Fundamental Research to Potential Commercial Application

AbstractOrganic electroactive compounds hold great potential to act as cathode material for organic sodium‐ion batteries (OSIBs) because of their environmental friendliness, sustainability, and high theoretical capacity. Although some organic electrodes have been developed with good performance, their practical application is still obstructed by some inherent drawbacks such as low conductivity and solubility in organic electrolytes. In addition, research on OSIBs has been mainly focused on the performance of electrodes on the material level and neglected the trade‐off relationship between the high redox potentials and specific capacities. Almost all organic cathodes used in OSIBs lack the ability to be charged first in half‐cells because of the absence of detachable sodium ions, resulting in low attractiveness when assembling full cells with hard carbon as anode. Here, this review presents several existing reaction mechanisms in OSIBs and designs of organic cathode materials. Furthermore, strategies are proposed in order to provide guidelines for improving their performance according to some critical parameters (output voltage, specific capacity, and cycle life) in potential practical OSIBs, and some accounts of organic materials assembled in full cells are summarized. Finally, the challenges and prospects of organic electrodes for OSIBs are also discussed in this review.

Understanding the Associations of Prenatal Androgen Exposure on Sleep Physiology, Circadian Proteins, Anthropometric Parameters, Hormonal Factors, Quality of Life, and Sex Among Healthy Young Adults: Protocol for an International, Multicenter Study.

BackgroundThe ratio of the second finger length to the fourth finger length (2D:4D ratio) is considered to be negatively correlated with prenatal androgen exposure (PAE) and positively correlated with prenatal estrogen. Coincidentally, various brain regions are sensitive to PAE, and their functions in adults may be influenced by the prenatal actions of sex hormones.ObjectiveThis study aims to assess the relationship between PAE (indicated by the 2D:4D ratio) and various physiological (sex hormone levels and sleep-wake parameters), psychological (mental health), and sexual parameters in healthy young adults.MethodsThis study consists of two phases. In phase 1, we will conduct a survey-based study and anthropometric assessments (including 2D:4D ratio and BMI) in healthy young adults. Using validated questionnaires, we will collect self-reported data on sleep quality, sexual function, sleep chronotype, anxiety, and depressive symptoms. In phase 2, a subsample of phase 1 will undergo polysomnography and physiological and genetic assessments. Sleep architecture data will be obtained using portable polysomnography. The levels of testosterone, estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, prolactin, melatonin, and circadian regulatory proteins (circadian locomotor output cycles kaput [CLOCK], timeless [TIM], and period [PER]) and the expression levels of some miRNAs will be measured using blood samples. The rest and activity cycle will be monitored using actigraphy for a 7-day period.ResultsIn Poland, 720 participants were recruited for phase 1. Among these, 140 completed anthropometric measurements. In addition, 25 participants joined and completed phase 2 data collection. Recruitment from other sites will follow.ConclusionsFindings from our study may help to better understand the plausible role of PAE in sleep physiology, mental health, and sexual quality of life in young adults.International Registered Report Identifier (IRRID)DERR1-10.2196/29199

The potential remedy of melatonin on osteoarthritis.

Osteoarthritis (OA), the most common arthritis worldwide, is a degenerative joint disease characterized by progressive cartilage breakdown, subchondral remodeling, and synovial inflammation. Although conventional pharmaceutical therapies aimed to prevent further cartilage loss and joint dysfunction, there are no ideal strategies that target the pathogenesis of OA. Melatonin exhibits a variety of regulatory properties by binding to specific receptors and downstream molecules and exerts a myriad of receptor-independent actions via intracellular targets as a chondrocyte protector, an anti-inflammation modulator, and a free radical scavenger. Melatonin also modulates cartilage regeneration and degradation by directly/indirectly regulating the expression of main circadian clock genes, such as transcriptional activators [brain and muscle aryl hydrocarbon receptor nuclear translocator-like protein (Bmal) and circadian locomotor output cycles kaput (Clock)], transcriptional repressors [period circadian regulator (Per)1/2, cryptochrome (Cry)1/2, and Dec2], and nuclear hormone receptors [Rev-Erbs and retinoid acid-related orphan receptors (Rors)]. Owing to its effects on cartilage homeostasis, we propose a potential role for melatonin in the prevention and therapy of OA via the modulation of circadian clock genes, mitigation of chondrocyte apoptosis, anti-inflammatory activity, and scavenging of free radicals.