High-Performance Low-Iridium Catalyst for Water Oxidation: Breaking Long-Ranged Order of IrO2 by Neodymium Doping.

Exploring efficacious low-Ir electrocatalysts for oxygen evolution reaction (OER) is crucial for large-scale application of proton exchange membrane water electrolysis (PEMWE). Herein, an efficient non-precious lanthanide-metal-doped IrO2 electrocatalyst is presented for OER catalysis by doping large-ionic-radius Nd into IrO2 crystal. The doped Nd breaks the long-ranged order structure by triggering the strain effect and thus inducing an atomic rearrangement of Nd─IrO2 involving the forming of Nd─O─Ir bonds along with an increased amount of oxygen vacancies (Ov), giving rise of a long-ranged disorder but a short-ranged order structure. The formed Nd─O─Ir bonds tailor the electronic structure of Ir, leading to a lowered d-band center that weakens intermediates absorption on Ir sites. Moreover, doping Nd triggers Nd─IrO2 to catalyze OER mainly through lattice oxygen mechanism (LOM) by activating lattice oxygen owing to abundant Ov. The optimal catalyst only requires a relatively low overpotential of 263 mV@10 mA cm-2 with a high mass activity of 216.98 A gIr -1 (at 1.53 V) (eightfold of commercial IrO2), and also shows a superior durability at 50 mA cm-2 (20 h) than commercial IrO2 (3 h) due to the oxidation-suppressing effect induced by Nd doping. This work offers insights into designing high-performance low-Ir electrocatalysts for PEMWE application.

Bisphenol S exposure induces intestinal inflammation via altering gut microbiome.

Bisphenol S (BPS), a substitute for bisphenol A, is widely used in the manufacture of food packaging materials, raising concern over its toxicity. However, evidence is still lacking on whether gut microbiota involved in BPS induced intestinal inflammation in mammals, as well as its underlying mechanism. Using mouse BPS exposure model, we found intestinal inflammation characterized by shortened colon length, crypt distortion, macrophage accumulation and increased apoptosis. As for gut microbiota, 16s rRNA gene amplicon sequencing showed BPS exposure induced gut dysbiosis, including increased pro-inflammatory microbes such as Ileibacterium, and decreased anti-inflammatory genera such as Lactobacillus, Blautia and Romboutsia. Besides, LC-MS/MS-based untargeted metabolomic analysis indicated BPS impaired both bacteria and host metabolism. Additionally, transcriptome analysis of the intestine revealed abnormal gene expression in intestinal mucosal barrier and inflammation. More importantly, treating mice with antibiotics significantly attenuated BPS-induced gut inflammation via the regulation of both bacterial and host metabolites, indicating the role of gut microbiota. Collectively, BPS exposure induces intestinal inflammation via altering gut microbiota in mouse. This study provides the possibility of madecassic acid, an anti-inflammatory metabolite, to prevent BPS-induced intestinal inflammation and also new insights in understanding host-microbiota interaction in BPS toxicity.

NF-κB Inducing Kinase Attenuates Colorectal Cancer by Regulating Noncanonical NF-κB Mediated Colonic Epithelial Cell Regeneration.

BACKGROUND & AIMS: Dysregulated colonic epithelial cell (CEC) proliferation is a critical feature in the development of colorectal cancer. We show that NF-κB-inducing kinase (NIK) attenuates colorectal cancer through coordinating CEC regeneration/differentiation via noncanonical NF-κB signaling that is unique from canonical NF-kB signaling. METHODS: Initial studies evaluated crypt morphology/functionality, organoid generation, transcriptome profiles, and the microbiome. Inflammation and inflammation-induced tumorigenesis were initiated in whole-body NIK knockout mice (Nik-/-) and conditional-knockout mice following administration of azoxymethane and dextran sulfate sodium. RESULTS: Human transcriptomic data revealed dysregulated noncanonical NF-kB signaling. In vitro studies evaluating Nik-/- crypts and organoids derived from mature, nondividing CECs, and colonic stem cells exhibited increased accumulation and stunted growth, respectively. Transcriptomic analysis of Nik-/- cells revealed gene expression signatures associated with altered differentiation-regeneration. When assessed in vivo, Nik-/- mice exhibited more severe colitis with dextran sulfate sodium administration and an altered microbiome characterized by increased colitogenic microbiota. In the inflammation-induced tumorigenesis model, we observed both increased tumor burdens and inflammation in mice where NIK is knocked out in CECs (NikΔCEC). Interestingly, this was not recapitulated when NIK was conditionally knocked out in myeloid cells (NikΔMYE). Surprisingly, conditional knockout of the canonical pathway in myeloid cells (RelAΔMYE) revealed decreased tumor burden and inflammation and no significant changes when conditionally knocked out in CECs (RelAΔCEC). CONCLUSIONS: Dysregulated noncanonical NF-κB signaling is associated with the development of colorectal cancer in a tissue-dependent manner and defines a critical role for NIK in regulating gastrointestinal inflammation and regeneration associated with colorectal cancer.

Hepatic toxicity prediction of bisphenol analogs by machine learning strategy.

Toxicological studies have demonstrated the hepatic toxicity of several bisphenol analogs (BPs), a prevalent type of endocrine disruptor. The development of Adverse Outcome Pathway (AOP) has substantially contributed to the rapid risk assessment for human health. However, the lack of in vitro and in vivo data for the emerging BPs has limited the hazard assessment of these synthetic chemicals. Here, we aimed to develop a new strategy to rapidly predict BPs' hepatotoxicity using network analysis coupled with machine learning models. Considering the structural and functional similarities shared by BPs with Bisphenol A (BPA), we first integrated hepatic disease related genes from multiple databases into BPA-Gene-Phenotype-hepatic toxicity network and subjected it to the computational AOP (cAOP). Through cAOP network and conventional machine learning approaches, we scored the hepatotoxicity of 20 emerging BPs and provided new insights into how BPs' structure features contributed to biologic functions with limited experimental data. Additionally, we assessed the interactions between emerging BPs and ESR1 using molecular docking and proposed an AOP framework wherein ESR1 was a molecular initiating event. Overall, our study provides a computational approach to predict the hepatotoxicity of emerging BPs.

Multi-omics approach characterizes the role of Bisphenol F in disrupting hepatic lipid metabolism.

Bisphenol F (BPF), a substitute for bisphenol A (BPA), is ubiquitous existed in various environmental media. Exposure to BPF may promote non-alcoholic fatty liver disease (NAFLD), while the potential mechanism is still unknown. In current study, we used in vitro and in vivo model to evaluate its hepatotoxicity and molecular mechanism. Using multi-omics approach, we found that BPF exposure led to changes in hepatic transcriptome, metabolome and chromatin accessible regions that were enriched for binding sites of transcription factors in bZIP family. These alterations were enriched with pathways integral to the endoplasmic reticulum stress and NAFLD. These findings suggested that BPF exposure might reprogram the chromatin accessibility and enhancer landscape in the liver, with downstream effects on genes associated with endoplasmic reticulum stress and lipid metabolism, which relied on bZIP family transcription factors. Overall, our study describes comprehensive molecular alterations in hepatocytes after BPF exposure and provides new insights into the understanding of the hepatoxicity of BPF.

Bisphenol S impairs mitochondrial function by targeting Myo19/oxidative phosphorylation pathway contributing to axonal and dendritic injury.

Exposure to bisphenol S (BPS) is known to adversely affect neuronal development. As pivotal components of neuronal polarization, axons and dendrites are indispensable structures within neurons, crucial for the maintenance of nervous system function. Here, we investigated the impact of BPS exposure on axonal and dendritic development both in vivo and in vitro. Our results revealed that exposure to BPS during pregnancy and lactation led to a reduction in the complexity, density, and length of axons and dendrites in the prefrontal cortex (PFC) of offspring. Employing RNA sequencing technology to elucidate the underlying mechanisms of axonal and dendritic damage induced by BPS, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis highlighted a significant alteration in the oxidative phosphorylation (OXPHOS) pathway, essential for mitochondrial function. Subsequent experiments demonstrate BPS-induced impairment in mitochondrial function, including damaged morphology, decreased adenosine triphosphate (ATP) and superoxide dismutase (SOD) levels, and increased reactive oxygen species and malondialdehyde (MDA). These alterations coincided with the downregulated expression of OXPHOS pathway-related genes (ATP6V1B1, ATP5K, NDUFC1, NDUFC2, NDUFA3, COX6B1) and Myosin 19 (Myo19). Notably, Myo19 overexpression restored the BPS-induced mitochondrial dysfunction by alleviating the inhibition of OXPHOS pathway. Consequently, this amelioration was associated with a reduction in BPS-induced axonal and dendritic injury observed in cultured neurons of the PFC.

The Review of Hybridization of Transition Metal-Based Chalcogenides for Lithium-Ion Battery Anodes.

Transition metal chalcogenides as potential anodes for lithium-ion batteries have been widely investigated. For practical application, the drawbacks of low conductivity and volume expansion should be further overcome. Besides the two conventional methods of nanostructure design and the doping of carbon-based materials, the component hybridization of transition metal-based chalcogenides can effectively enhance the electrochemical performance owing to the synergetic effect. Hybridization could promote the advantages of each chalcogenide and suppress the disadvantages of each chalcogenide to some extent. In this review, we focus on the four different types of component hybridization and the excellent electrochemical performance that originated from hybridization. The exciting problems of hybridization and the possibility of studying structural hybridization were also discussed. The binary and ternary transition metal-based chalcogenides are more promising to be used as future anodes of lithium-ion batteries for their excellent electrochemical performance originating from the synergetic effect.

Characteristics of Virulent ST5-SCCmec II Methicillin-Resistant Staphylococcus aureus Prevalent in a Surgery Ward.

Objective: To investigate the transmission pathway of a MRSA prevalence in a pancreatic surgery ward in a Chinese teaching hospital. Methods: Molecular epidemiology investigations were carried out combined PFGE, MLST, SCCmec typing and whole-genome sequencing for 20 successive MRSA isolates (2 isolates from the ward environment). Resistance and virulence genes were detected using specific PCR. Bacterial identification and AST were performed using the Vitek 2 Compact System. Clinical data of enrolled cases were retrieved from electronic case records. Results: From January 2020 to May 2020, successive isolated 20 MRSA strains were clarified to 2 PFGE patterns (A = 19, B = 1) in the ward. Both isolates from environment and patients belonged to sequence type ST5-SCCmec II-spa type t311. MRSA-related resistance genes mecA, blaZ, ermA, ant(4')-Ia and norA were found in each clone. All 20 isolates carried tst, hlg, hla, eta, eap, fnbA and seo virulence genes, other virulence genes such as sea, sec, seb, seg, sei, sem, sen, ebpS and fnbB were also found in partial stains. All patients had fever symptom, 27.8% were accompanied by diarrhea, 88.9% had undergone surgery or invasive procedures within 30 days. Finally, 94.4% of these patients recovered. Conclusion: This study confirmed a prevalence of ST5-MRSA-II-t311 clone in a surgery ward, indicated MRSA is a risk factor for post-surgery nosocomial infection and hand hygiene and environmental surveillance should not be ignored.

Maternal BPAF exposure impaired synaptic development and caused behavior abnormality in offspring.

Bisphenol A (BPA) has been widely restricted, leading to a significant increase in the production of bisphenol AF (BPAF), one of the most common bisphenol analogs use as a substitute for BPA. However, there is limit evidence on the neurotoxicity of BPAF, especially the potential effects of maternal exposed to BPAF on offspring. A maternal BPAF exposure model was used to evaluate its effects on long-term neurobehaviors in offspring. We found that maternal BPAF exposure resulted in immune disorders, characterized by abnormal CD4+T cell subsets, and their offspring exhibited anxiety- and depression-like behaviors, as well as impairments in learning-memory, sociability and social novelty. Further, brain bulk RNA-sequencing (RNA-seq) and hippocampus single-nucleus RNA-sequencing (snRNA-seq) of offspring showed that differentially expressed genes (DEGs) were enriched in pathways related to synaptic and neurodevelopment. Synaptic ultra-structure of offspring was damaged after maternal BPAF exposure. In conclusion, maternal BPAF exposure induced behavior abnormality in adult offspring, together with synaptic and neurodevelopment defects, which might be related to maternal immune dysfunction. Our results provide a comprehensive insight into the neurotoxicity mechanism of maternal BPAF exposure during gestation. Given the increasing and ubiquitous exposure to BPAF, especially during sensitive periods of growth and development, the safety of BPAF requires urgent attention.

Caloric restriction remodels the hepatic chromatin landscape and bile acid metabolism by modulating the gut microbiota.

BACKGROUND: Caloric restriction (CR) has been known to promote health by reprogramming metabolism, yet little is known about how the epigenome and microbiome respond during metabolic adaptation to CR. RESULTS: We investigate chromatin modifications, gene expression, as well as alterations in microbiota in a CR mouse model. Collectively, short-term CR leads to altered gut microbial diversity and bile acid metabolism, improving energy expenditure. CR remodels the hepatic enhancer landscape at genomic loci that are enriched for binding sites for signal-responsive transcription factors, including HNF4α. These alterations reflect a dramatic reprogramming of the liver transcriptional network, including genes involved in bile acid metabolism. Transferring CR gut microbiota into mice fed with an obesogenic diet recapitulates the features of CR-related bile acid metabolism along with attenuated fatty liver. CONCLUSIONS: These findings suggest that CR-induced microbiota shapes the hepatic epigenome followed by altered expression of genes responsible for bile acid metabolism.

Association of Endocrine-Disrupting Chemicals with All-Cause and Cause-Specific Mortality in the U.S.: A Prospective Cohort Study.

Wide exposure to endocrine-disrupting chemicals (EDCs) poses a great risk on human health. However, few large-scale cohort studies have comprehensively estimated the association between EDCs exposure and mortality risk. This study aimed to investigate the association of urinary EDCs exposure with mortality risk and quantify attributable mortality and economic loss. Multivariable Cox proportional hazards regression models were performed to investigate the association of 38 representative EDCs exposure with mortality risk in the National Health and Nutrition Examination Survey (NHANES). During a median follow-up of 7.7 years, 47,279 individuals were enrolled. All-cause mortality was positively associated with 1-hydroxynaphthalene, 2-hydroxynaphthalene, cadmium, antimony, cobalt, and monobenzyl phthalate. Cancer mortality was positively associated with cadmium. Cardiovascular disease (CVD) mortality was positively associated with 1-hydroxynaphthalene, 2-hydroxynaphthalene, and 2-hydroxyfluorene. Nonlinear U-shaped relationships were found between all-cause mortality and cadmium and cobalt, which was also identified between 2-hydroxyfluorene and CVD mortality. J-shaped association of cadmium exposure with cancer mortality was also determined. EDCs exposure may cause 56.52% of total deaths (1,528,500 deaths) and around 1,897 billion USD in economic costs. Exposure to certain phthalates, polycyclic aromatic hydrocarbons, phytoestrogens, or toxic metals, even at substantially low levels, is significantly associated with mortality and induces high economic costs.

Early-life bisphenol AP exposure impacted neurobehaviors in adulthood through microglial activation in mice.

Bisphenol AP (BPAP), a structural analog of bisphenol A (BPA), has been widely detected in environment and biota. BPAP was reported to interfere with hormone and metabolism, while limited data were available about its effects on neurobehavior, especially exposure to it during early-life time. A mouse model of early-life BPAP exposure was established to evaluate the long-term neurobehaviors in offspring. Collectively, early-life BPAP exposure caused anxiety-like behaviors and impaired learning and memory in adult offspring. Through brain bulk RNA-sequencing (RNA-seq), we found differential expressed genes were enriched in pathways related to behaviors and neurodevelopment, which were consistent with the observed phenotype. Besides, single-nucleus RNA-sequencing (snRNA-seq) showed BPAP exposure altered the transcriptome of microglia in hippocampus. Mechanistically, BPAP exposure induced inflammations in hippocampus through upregulating Iba-1 and activating the microglia. In addition, we observed that BPAP exposure could activate peripheral immunity and promote proportion of macrophages and activation of dendritic cells in the offspring. In conclusion, early-life exposure to BPAP impaired neurobehaviors in adult offspring accompanied with excessive activation of hippocampal microglia. Our findings provide new clues to the underlying mechanisms of BPAP's neurotoxic effects and therefore more cautions should be taken about BPAP.

Draft genome of the medicinal tea tree Melaleuca alternifolia.

BACKGROUND: Melaleuca alternifolia is a commercially important medicinal tea tree native to Australia. Tea tree oil, the essential oil distilled from its branches and leaves, has broad-spectrum germicidal activity and is highly valued in the pharmaceutical and cosmetic industries. Thus, the study of genome, which can provide reference for the investigation of genes involved in terpinen-4-ol biosynthesis, is quite crucial for improving the productivity of Tea tree oil. METHODS AND RESULTS: In our study, the next-generation sequencing was used to investigate the whole genome of Melaleuca alternifolia. About 114 Gb high quality sequence data were obtained and assembled into 1,838,159 scafolds with an N50 length of 1021 bp. The assembled genome size is about 595 Mb, twice of that predicted by flow cytometer (300 Mb) and k-mer analysis (345 Mb). Benchmarking Universal Single-Copy Orthologs analyses indicated that only 11.3% of the conserved single-copy genes were miss. Repetitive regions cover over 40.43% of the genome. A total of 44,369 protein-coding genes were predicted and annotated against Nr, Swissprot, Refseq, COG, KOG, and KEGG database. Among these genes, 32,909 and 16,241 genes were functionally annotated in Nr and KEGG, respectively. Moreover, 29,411 and 14,435 genes were functionally annotated in COG and KOG. Additionally, 457,661 simple sequence repeats and 1109 transcription factors (TFs) form 67 TF families were identified in the assembled genome. CONCLUSION: Our findings provide a draft genome sequencing of M. alternifolia which can act as a reference for the deep sequencing strategies, and are useful for future functional and comparative genomics analyses.

Intriguing H2S Tolerance of the PtRu Alloy for Hydrogen Oxidation Catalysis in PEMFCs: Weakened Pt-S Binding with Slower Adsorption Kinetics.

High quality of hydrogen is the key to the long lifetime of proton-exchange membrane fuel cell (PEMFC) vehicles, while trace H2S impurities in hydrogen significantly affect their durability and fuel expense. Herein, we demonstrate a robust PtRu alloy catalyst with an intriguing H2S tolerance as the PEMFC anode, showing a stronger antipoisoning capability toward hydrogen oxidation reaction compared with the Pt/C anode. The PtRu/C-based single PEMFC shows approximately 14.3% loss of cell voltage after 3 h operation with 1 ppm of H2S in hydrogen, significantly lower than that of Pt/C-based PEMFCs (65%). By adopting PtRu/C as the anode, the H2S limit in hydrogen can be increased to 1.7 times that of the Pt/C anode, assuming that the PEMFC runs for 5000 h, which is conductive for the cost reduction of hydrogen purification. The three-electrode electrochemical test indicates that PtRu/C exhibits a slower adsorption kinetics toward S2- species with poisoning rates of 0.02782, 0.02982, and 0.03682 min-1 at temperatures of 25, 35, and 45 °C, respectively, all lower than those of Pt/C. X-ray absorption fine structure spectra indicate the weakened Pt-S binding for PtRu/C in comparison to Pt/C with a longer Pt-S bond length. Density functional theory calculation analyses reveal that adsorption energy of sulfur on the Pt surface was reduced for PtRu/C, showing 1-10% decrease at different Pt sites for (111), (110), and (100) planes, which is ascribed to the downshifted Pt d-band center caused by the ligand and strain effects due to the introduction of second metallic Ru. This work provides a valuable guide for the development of the H2S-tolerant catalysts for long-term application of PEMFCs.

Association between exposure to cadmium and risk of all-cause and cause-specific mortality in the general US adults: A prospective cohort study.

BACKGROUND: Cadmium has been suggested to accumulate in the body over a lifetime, posing a great threat to human health. So far, few studies have studied the association between cadmium exposure and long-term health outcomes in adults. OBJECTIVES: To investigate the risk of mortality with blood cadmium level in adults (participants of NHANES, 1999-2014). METHODS: We evaluated the associations between cadmium and risk of mortality. Data on mortality and cadmium exposure were collected in NHANES database including 39,865 participants. Multivariate Cox regression models were established for calculating hazard ratios (HRs) and 95%CI between cadmium exposure and all-cause and specific-cause mortality outcomes. RESULTS: Totally, 39,865 individuals with 19,260 males (48.3%) and 20,605 females (51.7%) were included in the study. During a total of 341,017 person-years of follow-up 5,094 deaths were documented, including 1,067 cardiovascular disease (CVD) and 890 cancers. Compared with the lowest quantile of cadmium exposure level group, the adjusted HRs in the highest quantile cadmium exposure level group were 1.73 (95%CI: 1.52-1.97) for all-cause mortality, 1.72 (95%CI: 1.28-2.30) for CVD mortality and 1.87 (95%CI: 1.49-2.36) for cancer mortality, respectively (P for trend: <0.001). Additionally, significant interactions with smoking status in the stratified analyses of all-cause mortality and cancer mortality, age in the stratified analyses of cancer mortality were found (P for interaction: 0.002, <0.001 and 0.012). CONCLUSIONS: In this nationwide representative sample of the population, we found that higher blood cadmium concentration was associated with increased risks of all-cause and specific-cause mortality. These data further evidence the link between mortality and cadmium concentration. It is of great importance for both policy makers and the public to minimize cadmium exposure, and to reduce long-term adverse health effects.

A comparative study of electrochemical and electrostatic doping modulation of magnetism in Fe3O4via ultracapacitor structure.

Electric field control of magnetism can boost energy efficiency and have brought revolutionary breakthroughs in the development of widespread applications in spintronics. Electrolyte gating plays an important role in magnetism modulation. In this work, reversible room-temperature electric field control of saturation magnetization in Fe3O4via a supercapacitor structure is demonstrated with three types of traditional gate electrolytes for comparison. Different magnetization response and responsible mechanisms are revealed by Operando magnetometry PPMS/VSM and XPS characterization. The main mechanism in Na2SO4, KOH aqueous electrolytes is electrochemical effect, while both electrochemical and electrostatic effects were found in LiPF6organic electrolyte. This work offers a kind of reference basis for selecting appropriate electrolyte in magnetism modulation by electrolyte-gating in the future, meanwhile, paves its way towards practical use in magneto-electric actuation, voltage-assisted magnetic storage, facilitating the development of high-performance spintronic devices.

Preimplantation triclosan exposure alters uterine receptivity through affecting tight junction protein†.

Triclosan is a broad-spectrum antibacterial agent and widely exists in environmental media and organisms. Triclosan exposure has been reported to have adverse effects on reproduction including embryo implantation disorder. During the embryo implantation window, it is vital that the endometrium develops into a receptive state under the influence of ovarian hormones. However, the effect of triclosan on embryo implantation and endometrial receptivity remains unclear. In the current study, we found a decreased embryo implantation rate, serum estrogen, and progesterone levels in mice exposed to triclosan from gestation days 0.5 to 5.5. Through RNA sequencing (RNA-seq), we identified nearly 800 differentially expressed genes, which were enriched in various pathways, including uterus development, inflammatory response, and immune system processes. Among those enriched pathways, the tight junction pathway is essential for the establishment of the receptive state of the endometrium. Then, genes involved in the tight junction pathway, including Cldn7, Cldn10, and Crb3, were validated by quantitative real-time polymerase chain reaction and the results were consistent with those from RNA-seq. Through immunofluorescence staining and western blotting, we confirmed that the tight junction protein levels of CLDN7 and CRB3 were increased. All these findings suggest that preimplantation triclosan exposure reduces the rate of embryo implantation through upregulating the expression of the tight junction genes and affecting the receptivity of the endometrium. Our data could be used to determine the sensitive time frame for triclosan exposure and offer a new strategy to prevent implantation failure.

High-fat diet aggravates prenatal low-dose DEHP exposure induced spermatogenesis disorder: Characterization of testicular metabolic patterns in mouse offspring.

Di-(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer and has been identified as a male prenatal reproductive toxicant. A high fat diet (HFD) has also been suggested as another potential disruptor of male reproductive function. Despite this potential synergism between DEHP exposure and HFD, little is known about the concomitant effects of prenatal DEHP and a subsequent HFD exposure on male offspring reproductive injury. Here we established a mouse model of prenatal exposure to DEHP (0.2 mg/kg/day) to assess the testicular development and spermatogenesis in offspring subjected to obesogenic diet during the pubertal period. Gross phenotype, hormone profiles and the testicular metabolome were analyzed to determine the underlying mechanism. We found that prenatal exposure to low-dose DEHP resulted in decreased sperm density, decreased testosterone (T) levels, increased luteinizing hormone (LH) levels and testicular germ cell apoptosis. Furthermore, these injury phenotypes were aggravated by pubertal HFD treatment. Testicular riboflavin and biotin metabolites were enriched implying their roles in contributing HFD to exacerbate offspring spermatogenesis disorders due to prenatal low-dose DEHP exposure. Our findings suggest that pubertal HFD exacerbates reproductive dysfunction associated with prenatal exposure to low-dose DEHP in male adult offspring.

High Cycle Stability of Hybridized Co(OH)2 Nanomaterial Structures Synthesized by the Water Bath Method as Anodes for Lithium-Ion Batteries.

Cobalt oxides have been intensely explored as anodes of lithium-ion batteries to resolve the intrinsic disadvantages of low electrical conductivity and volume change. However, as a precursor of preparing cobalt oxides, Co(OH)2 has rarely been investigated as the anode material of lithium-ion batteries, perhaps because of the complexity of hydroxides. Hybridized Co(OH)2 nanomaterial structures were synthesized by the water bath method and exhibited high electrochemical performance. The initial discharge and charge capacities were 1703.2 and 1262.9 mAh/g at 200 mA/g, respectively. The reversible capacity was 1050 mAh/g after 150 cycles. The reversible capability was 1015 mAh/g at 800 mA/g and increased to 1630 mAh/g when driven back to 100 mA/g. The electrochemical reaction kinetics study shows that the lithium-ion diffusion-controlled contribution is dominant in the energy storage mechanism. The superior electrochemical performance could result from the water bath method and the hybridization of nanosheets and nanoparticles structures. These hybridized Co(OH)2 nanomaterial structures with high electrochemical performance are promising anodes for lithium-ion batteries.