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Controlling the coherence of chaotic soliton bunch holds the promise to explore novel light-matter interactions and manipulate dynamic events such as rogue waves. However, the coherence control of chaotic soliton bunch remains challenging, as there is a lack of dynamic equilibrium mechanism for stochastic soliton interactions. Here, we develop a strategy to effectively control the coherence of chaotic soliton bunch in a laser. We show that by introducing a lumped fourth-order-dispersion (FOD), the soliton oscillating tails can be formed and generate the potential barriers among the chaotic solitons. The repulsive force between neighboring solitons enabled by the potential barriers gives rise to an alleviation of the soliton fusion/annihilation from stochastic interactions, endowing the capability to control the coherence in chaotic soliton bunch. We envision that this result provides a promising test-bed for a variety of dynamical complexity science and brings new insights into the nonlinear behavior of chaotic laser sources. Controlling the coherence of chaotic waveforms holds the promise to explore novel light‐matter interactions. Here, the authors demonstrate a fourth‐order‐dispersion driven laser that delivers the coherence‐controlled chaotic soliton bunch.

Summary Aims Anesthesia and surgery can cause delirium‐like symptoms postoperatively. Increasing evidence suggests that gut microbiota is a physiological regulator of the brain. Herein, we investigated whether gut microbiota plays a role in postoperative delirium (POD). Methods Mice were separated into non‐POD and POD phenotypes after abdominal surgery by applying hierarchical clustering analysis to behavioral tests. Fecal samples were collected, and 16S ribosomal RNA gene sequencing was performed to detect differences in gut microbiota composition among sham, non‐POD, and POD mice. Fecal bacteria from non‐POD and POD mice were transplanted into antibiotics‐induced pseudo‐germ‐free mice to investigate the effects on behaviors. Results α‐diversity and β‐diversity indicated differences in gut microbiota composition between the non‐POD and POD mice. At the phylum level, the non‐POD mice had significantly higher levels of Tenericutes, which were not detected in the POD mice. At the class level, levels of Gammaproteobacteria were higher in the POD mice, whereas the non‐POD mice had significantly higher levels of Mollicutes, which were not detected in the POD mice. A total of 20 gut bacteria differed significantly between the POD and non‐POD mice. Interestingly, the pseudo‐germ‐free mice showed abnormal behaviors prior to transplant. The pseudo‐germ‐free mice that received fecal bacteria transplants from non‐POD mice but not from POD mice showed improvements in behaviors. Conclusions Abnormal gut microbiota composition after abdominal surgery may contribute to the development of POD. A therapeutic strategy that targets gut microbiota could provide a novel alterative for POD treatment.

RationaleApproximately 20–40% of patients with cancer will experience brain metastasis (BM), which has a great impact on the quality of life and survival rates of patients. Whole brain radiotherapy (WBRT) is an effective method for the treatment of BM. However, it cannot be ignored that WBRT might induce a series of neuropsychiatric side effects, including cognitive dysfunction (CD). Accumulating evidence shows that the gut microbiota and the gut-microbiota–brain axis may play a vital role in the pathogenesis of CD.Objective and methodsWe adopted WBRT to mimic CD after a hierarchical cluster analysis of the Morris water maze test (MWMT) results. In addition, we observed the effects of antibiotics and prebiotics on WBRT-induced CD. Variations were revealed via the 16S rRNA sequencing analysis at different levels.ResultsThe 16S rRNA sequencing analysis revealed an altered composition of gut microbiota between CD and non-CD phenotypes. Furthermore, we observed a decrease in the levels of Phylum-Bacteroidete, Class-Bacteroidia, and Order-Bacteroidales in the CD group and an increase in the Genus-Allobaculum level after WBRT. Pretreatment with antibiotics caused a significant decrease in the level of Phylum-TM7 01, whereas an increase in the levels of Class-Gammaproteobacteria, Order-Enterobacteriales, and Species-Escherichia coli. After pretreatment with probiotics, the levels of Phylum-Cyanobacteria, Class-4C0d-2, and Order-YS2 were decreased, while the levels of Family-Bacteroidaceae, Genus-Bacteroides, and Species-Parabacteroides distasonis were increased.ConclusionsWBRT-induced CD might be highly related to abnormal composition of gut microbiota. Strategies improving the composition of the gut microbiota may provide beneficial effects on CD in individuals exposed to WBRT.

The journal retracts the article titled \"Kinetics of Martensite/Austenite Decomposition during Tempering of Ultrafine Nano-Bainitic Steels\" [...].The journal retracts the article titled \"Kinetics of Martensite/Austenite Decomposition during Tempering of Ultrafine Nano-Bainitic Steels\" [...].

Cardiovascular disease remains the leading cause of morbidity and mortality, imposing a major disease burden worldwide. Therefore, there is an urgent need to identify new therapeutic targets. Recently, the concept that the heart acts as a secretory organ has attracted increasing attention. Proteins secreted by the heart are called cardiokines, and they play a critical physiological role in maintaining heart homeostasis or responding to myocardial damage and thereby influence the development of heart diseases. Given the critical role of cardiokines in heart disease, they might represent a promising therapeutic target. This review will focus on several cardiokines and discuss their roles in the pathogenesis of heart diseases and as potential therapeutics.

Due to the exotic electronic and optical properties, two-dimensional (2D) materials, such as graphene, topological insulators, transition metal dichalcogenides, black phosphorus, MXenes, graphitic carbon nitride, metal-organic frameworks, and so on, have attracted enormous interest in the scientific communities dealing with electronics and photonics. Combing the 2D materials with the microfiber, the 2D material-decorated microfiber photonic devices could be assembled. They offer the advantages of a high nonlinear effect, all fiber structure, high damage threshold, and so on, which play important roles in fields of pulse shaping and all-optical signal processing. In this review, first, we introduce the fabrication methods of 2D material-decorated microfiber photonic devices. Then the pulse generation and the nonlinear soliton dynamics based on pulse shaping method in fiber lasers and all-optical signal processing based on 2D material-decorated microfiber photonic devices, such as optical modulator and wavelength converter, are summarized, respectively. Finally, the challenges and opportunities in the future development of 2D material-decorated microfiber photonic devices are given. It is believed that 2D material-decorated microfiber photonic devices will develop rapidly and open new opportunities in the related fields.

In this study, the decomposition of a martensite/austenite (M/A) microconstituent in bainitic steels was analyzed using differential scanning calorimetry (DSC) data in conjunction with Kissinger’s and Johnson–Mehl–Avrami–Kolmogorov (JMAK)’s formulas. In bainitic steel subjected to austempering heat treatment, the presence of an M/A microstructure adversely affects the mechanical properties. According to the kinetic equations derived, it is observed that after tempering the sample at 600 °C for 4000 s, the generation of each phase reaches its maximum. The SEM images taken before and after tempering reveal extensive decomposition of the M/A constituent in the microstructure. The proportion of the M/A microstructure decreased significantly from about 10% before tempering to less than 1% after. Additionally, the content of residual austenite also reduced nearly to zero. These observations are consistent with the predictions of the kinetic equations.

BackgroundThe genetic causes of the majority of male and female infertility caused by human non-obstructive azoospermia (NOA) and premature ovarian insufficiency (POI) with meiotic arrest are unknown.ObjectiveTo identify the genetic cause of NOA and POI in two affected members from a consanguineous Chinese family.MethodsWe performed whole-exome sequencing of DNA from both affected patients. The identified candidate causative gene was further verified by Sanger sequencing for pedigree analysis in this family. In silico analysis was performed to functionally characterise the mutation, and histological analysis was performed using the biopsied testicle sample from the male patient with NOA.ResultsWe identified a novel homozygous missense mutation (NM_007068.3: c.106G>A, p.Asp36Asn) in DMC1, which cosegregated with NOA and POI phenotypes in this family. The identified missense mutation resulted in the substitution of a conserved aspartic residue with asparaginate in the modified H3TH motif of DMC1. This substitution results in protein misfolding. Histological analysis demonstrated a lack of spermatozoa in the male patient’s seminiferous tubules. Immunohistochemistry using a testis biopsy sample from the male patient showed that spermatogenesis was blocked at the zygotene stage during meiotic prophase I.ConclusionsTo the best of our knowledge, this is the first report identifying DMC1 as the causative gene for human NOA and POI. Furthermore, our pedigree analysis shows an autosomal recessive mode of inheritance for NOA and POI caused by DMC1 in this family.

Accumulating evidence has shown that neuropsychiatric diseases are frequently associated with gut microbiota disorders. 2 It has been widely recognised that toxins within the human body mainly stem from the gut. 3 The opening of intercellular tight junctions in the gut allow many toxins into the bloodstream that then have a deleterious effect on the brain, finally resulting in a series of neuropsychiatric symptoms. 3 In their study, Stevens and colleagues suggested that overexpression of the tight junction protein zonulin, LPS and its synthesis proteins are associated with the onset of depression and anxiety. 1 We suggest, however, that while solely reducing intestinal epithelium permeability by strengthening tight junctions may have a facilitating effect on decreasing peripheral levels of LPS and inflammatory cytokines, it would fail to elicit beneficial effects on neuropsychiatric diseases. [...]our results directly support the idea that ECs are of importance in enabling ketamine to exert pharmacologically beneficial effects on depression. [...]ECs play an important role in the pathogenesis and therapeutic mechanisms of neuropsychiatric diseases.

Porcine epidemic diarrhea virus (PEDV) is the major pathogen that causes diarrhea and high mortality in newborn piglets, with devastating impact on the pig industry. To further understand the molecular epidemiology and genetic diversity of PEDV field strains, in this study the complete genomes of four PEDV variants (HN2021, CH-HNYY-2018, CH-SXWS-2018, and CH-HNKF-2016) obtained from immunized pig farms in central China between 2016 to 2021 were characterized and analyzed. Phylogenetic analysis of the genome and S gene showed that the four strains identified in the present study had evolved into the subgroup G2a, but were distant from the vaccine strain CV777. Additionally, it was noteworthy that a new PEDV strain (named HN2021) belonging to the G2a PEDV subgroup was successfully isolated in vitro and it was further confirmed by RT-PCR that this isolate had a large natural deletion at 207–373 nt of the ORF3 gene, which has never been reported before. Particularly, in terms of pathogenicity evaluation, colostrum deprivation piglets challenged with PEDV HN2021 showed severe diarrhea and high mortality, confirming that PEDV HN2021 was a virulent strain. Hence, PEDV strain HN2021 of subgroup G2a presents a promising vaccine candidate for the control of recurring porcine epidemic diarrhea (PED) in China. This study lays the foundation for better understanding of the genetic evolution and molecular pathogenesis of PEDV.