A Comprehensive Review of Vision-Based 3D Reconstruction Methods.

With the rapid development of 3D reconstruction, especially the emergence of algorithms such as NeRF and 3DGS, 3D reconstruction has become a popular research topic in recent years. 3D reconstruction technology provides crucial support for training extensive computer vision models and advancing the development of general artificial intelligence. With the development of deep learning and GPU technology, the demand for high-precision and high-efficiency 3D reconstruction information is increasing, especially in the fields of unmanned systems, human-computer interaction, virtual reality, and medicine. The rapid development of 3D reconstruction is becoming inevitable. This survey categorizes the various methods and technologies used in 3D reconstruction. It explores and classifies them based on three aspects: traditional static, dynamic, and machine learning. Furthermore, it compares and discusses these methods. At the end of the survey, which includes a detailed analysis of the trends and challenges in 3D reconstruction development, we aim to provide a comprehensive introduction for individuals who are currently engaged in or planning to conduct research on 3D reconstruction. Our goal is to help them gain a comprehensive understanding of the relevant knowledge related to 3D reconstruction.

A Novel Grading System for Diffuse Chorioretinal Atrophy in Pathologic Myopia.

INTRODUCTION: This study aims to quantitatively assess diffuse chorioretinal atrophy (DCA) in pathologic myopia and establish a standardized classification system utilizing artificial intelligence. METHODS: A total of 202 patients underwent comprehensive examinations, and 338 eyes were included in the study. The methodology involved image preprocessing, sample labeling, employing deep learning segmentation models, measuring and calculating the area and density of DCA lesions. Lesion severity of DCA was graded using statistical methods, and grades were assigned to describe the morphology of corresponding fundus photographs. Hierarchical clustering was employed to categorize diffuse atrophy fundus into three groups based on the area and density of diffuse atrophy (G1, G2, G3), while high myopic fundus without diffuse atrophy was designated as G0. One-way analysis of variance (ANOVA) and nonparametric tests were conducted to assess the statistical association with different grades of DCA. RESULTS: On the basis of the area and density of DCA, the condition was classified into four grades: G0, G1 (0 < density ≤ 0.093), G2 (0.093 < density ≤ 0.245), and G3 (0.245 < density ≤ 0.712). Fundus photographs depicted a progressive enlargement of atrophic lesions, evolving from punctate-shaped to patchy with indistinct boundaries. DCA atrophy lesions exhibited a gradual shift in color from brown-yellow to yellow-white, originating from the temporal side of the optic disc and extending towards the macula, with severe cases exhibiting widespread distribution throughout the posterior pole. Patients with DCA were significantly older [34.00 (27.00, 48.00) vs 29.00 (26.00, 34.00) years], possessed a longer axial length (28.85 ± 1.57 vs 27.11 ± 1.01 mm), and exhibited a more myopic spherical equivalent [- 13.00 (- 16.00, - 10.50) vs - 9.09 ± 2.41 D] compared to those without DCA (G0) (all P < 0.001). In eyes with DCA, a trend emerged as grades increased from G1 to G3, showing associations with older age, longer axial length, deeper myopic spherical equivalent, larger area of parapapillary atrophy, and increased fundus tessellated density (all P < 0.001). CONCLUSIONS: The novel grading system for DCA, based on assessments of area and density, serves as a reliable measure for evaluating the severity of this condition, making it suitable for widespread application in the screening of pathologic myopia.

Analysis of four hereditary protein C deficiencies associated with vascular thromboembolism.

OBJECTIVE: To analyze the clinical features and gene mutations in four families with hereditary protein C (PC) deficiency and explore their association with vascular thromboembolism. METHODS: The clinical data of four patients with PC deficiency were retrospectively analyzed. Venous blood samples were collected from the four affected patients and their family members, and relevant coagulation indexes and thrombin production and inhibition tests were performed. PCR was used to amplify and directly sequence the PROC gene of the probands. Software analysis was conducted to assess the conservativeness and pathogenicity of the mutated loci. Protein models were constructed to analyze the spatial structure before and after the mutation. RESULTS: Thrombin generation and inhibition assays demonstrated impaired anticoagulation in all four probands. Proband 1 and 4 presented clinically with pulmonary embolism and lower extremity deep vein thrombosis (DVT), Proband 2 with cerebral infarction, and Proband 3 with DVT. Genetic analysis revealed the presence of the following mutations: c.541T > G heterozygous missense mutation, c.577-579delAAG heterozygous deletion mutation, c.247-248insCT heterozygous insertion mutation, c.659G > A heterozygous missense mutation, and a new variant locus c.1146_1146delT heterozygous deletion mutation in the four probands, respectively. In particular, c.1146_1146delT heterozygous deletion mutations not reported previously. Conservativeness and pathogenicity analyses confirmed that most of these amino acid residues were conserved, and all the mutations were found to be pathogenic. Analysis of protein modeling revealed that these mutations induced structural alterations in the protein or led to the formation of truncated proteins. According to the American College of Medical Genetics and Genomics (ACMG) classification criteria and guidelines for genetic variants, c.1146_1146delT was rated as pathogenic (PVS1 + M2 + PM4 + PP1 + PP3 + PP4). CONCLUSION: The identified mutations are likely associated with decreased PC levels in each of the four families. The clinical manifestations of hereditary PC deficiency exhibit considerable diversity.

An analysis of POMC gene methylation and expression in patients with schizophrenia.

Schizophrenia is a chronic mental disorder that affects millions of people and is believed to be caused by both environmental and genetic factors. Despite extensive research, the exact mechanisms underlying schizophrenia are still unclear. Studies have shown that numerous psychiatric disorders are associated with methylation of the POMC gene, which encodes adrenocorticotropic hormone, a critical player in the hypothalamic-pituitary-adrenal axis. However, the association between DNA methylation in POMC patients and schizophrenia remains unclear. In this study, we evaluated three fragments of the POMC promoter region, including 51 CpG sites, in the peripheral blood of schizophrenia patients and healthy controls. The POMC protein level was measured via enzyme-linked immunosorbent assay (ELISA). The schizophrenia group exhibited significantly greater levels of methylation of the POMC gene than those in the control group. The methylation level of the POMC-2 fragment was significantly greater in the patient group than in the control group. There were 17 significantly hypermethylated CpG sites in the patient group. After stratification by sex, POMC methylation levels were found to be significantly greater in male schizophrenia patients than in healthy controls; the methylation levels of POMC-2 fragments were greater in the male patient group; nine CpG sites were significantly hypermethylated in the male patient group; and only one CpG site was significantly hypermethylated in the female patient group. The POMC protein level in patients was significantly lower than that in healthy controls. These findings demonstrate that the DNA methylation of POMC might be associated with the pathophysiology of schizophrenia. Overall, studying the correlation between POMC methylation and schizophrenia may contribute to the diagnosis and evaluation of neuropsychiatric disorders.

Time series prediction of insect pests in tea gardens.

BACKGROUND: Tea-garden pest control is crucial to ensure tea quality. In this context, the time-series prediction of insect pests in tea gardens is very important. Deep-learning-based time-series prediction techniques are advancing rapidly but research into their use in tea-garden pest prediction is limited. The current study investigates the time-series prediction of whitefly populations in the Tea Expo Garden, Jurong City, Jiangsu Province, China, employing three deep-learning algorithms, namely Informer, the Long Short-Term Memory (LSTM) network, and LSTM-Attention. RESULTS: The comparative analysis of the three deep-learning algorithms revealed optimal results for LSTM-Attention, with an average root mean square error (RMSE) of 2.84 and average mean absolute error (MAE) of 2.52 for 7 days' prediction length, respectively. For a prediction length of 3 days, LSTM achieved the best performance, with an average RMSE of 2.60 and an average MAE of 2.24. CONCLUSION: These findings suggest that different prediction lengths influence model performance in tea garden pest time series prediction. Deep learning could be applied satisfactorily to predict time series of insect pests in tea gardens based on LSTM-Attention. Thus, this study provides a theoretical basis for the research on the time series of pest and disease infestations in tea plants. © 2024 Society of Chemical Industry.

Cross-talk between immunity and behavior: insights from entomopathogenic fungi and their insect hosts.

Insects are one of the most successful animals in nature, and entomopathogenic fungi play a significant role in the natural epizootic control of insect populations in many ecosystems. The interaction between insects and entomopathogenic fungi has continuously coevolved over hundreds of millions of years. Many components of the insect innate immune responses against fungal infection are conserved across phyla. Additionally, behavioral responses, which include avoidance, grooming, and/or modulation of body temperature, have been recognized as important mechanisms for opposing fungal pathogens. In an effort to investigate possible cross-talk and mediating mechanisms between these fundamental biological processes, recent studies have integrated and/or explored immune and behavioral responses. Current information indicates that during discrete stages of fungal infection, several insect behavioral and immune responses are altered simultaneously, suggesting important connections between the two systems. This review synthesizes recent advances in our understanding of the physiological and molecular aspects influencing cross-talk between behavioral and innate immune antifungal reactions, including chemical perception and olfactory pathways.

Advanced nanozymes possess peroxidase-like catalytic activities in biomedical and antibacterial fields: review and progress.

Infectious diseases caused by bacterial invasions have imposed a significant global health and economic burden. More worryingly, multidrug-resistant (MDR) pathogenic bacteria born under the abuse of antibiotics have further escalated the status quo. Nowadays, at the crossroads of multiple disciplines such as chemistry, nanoscience and biomedicine, nanozymes, as enzyme-mimicking nanomaterials, not only possess excellent bactericidal ability but also reduce the possibility of inducing resistance. Thus, nanozymes are promising to serve as an alternative to traditional antibiotics. Nanozymes that mimic peroxidase (POD) activity are also known as POD nanozymes. In recent years, POD nanozymes have become one of the most frequently reported and effective nanozymes due to their broad-spectrum bactericidal properties and unique sterilization mechanism. In this review, we introduce the mechanism as well as the classification of POD nanozymes. More importantly, to further improve the antibacterial efficacy of POD nanozymes, we elaborate on three aspects: (1) improving the physicochemical properties; (2) regulating the catalytic microenvironment; and (3) designing multimodel POD nanozymes. In addition, we review the nanosafety of POD nanozymes for discussing their potential toxicity. Finally, the remaining challenges of POD nanozymes and possible future directions are discussed. This work provides a systematic summary of POD nanozymes and hopefully contributes to the early clinical translation.

Cognitive impairment associated with cerebellar volume loss in spinocerebellar ataxia type 3.

BACKGROUND: Many neuroscience and neurology studies have forced a reconsideration of the traditional motor-related scope of cerebellar function, which has now expanded to include various cognitive functions. Spinocerebellar ataxia type 3 (SCA3; the most common hereditary ataxia) is neuropathologically characterized by cerebellar atrophy and frequently presents with cognitive impairment. OBJECTIVE: To characterize cognitive impairment in SCA3 and investigate the cerebellum-cognition associations. METHODS: This prospective, cross-sectional cohort study recruited 126 SCA3 patients and 41 healthy control individuals (HCs). Participants underwent a brain 3D T1-weighted images as well as neuropsychological tests. Voxel-based morphometry (VBM) and region of interest (ROI) approaches were performed on the 3D T1-weighted images. CERES was used to automatically segment cerebellums. Patients were grouped into cognitively impaired (CI) and cognitively preserved (CP), and clinical and MRI parameters were compared. Multivariable regression models were fitted to examine associations between cerebellar microstructural alterations and cognitive domain impairments. RESULTS: Compared to HCs, SCA3 patients showed cognitive domain impairments in information processing speed, verbal memory, executive function, and visuospatial perception. Between CI and CP subgroups, the CI subgroup was older and had lower education, as well as higher severity scores. VBM and ROI analyses revealed volume loss in cerebellar bilateral lobule VI, right lobule Crus I, and right lobule IV of the CI subgroup, and all these cerebellar lobules were associated with the above cognitive domain impairments. CONCLUSIONS: Our findings demonstrate the multiple cognitive domain impairments in SCA3 patients and indicate the responsible cerebellar lobules for the impaired cognitive domain(s).

Fundus Tessellated Density of Pathologic Myopia.

PURPOSE: The study aimed to quantitatively evaluate the fundus tessellated density (FTD) in different categories of pathologic myopia (PM) using fundus photographs with the application of artificial intelligence. METHODS: A retrospective review of 407 PM (META-PM, Category 2-Category 4) eyes was conducted, employing a biomimetic mechanism of human vision and integrated image processing technologies for FTD extraction and calculation. Different regions of interest were analyzed, including circle O4.5 (optic disc centered, diameter of 4.5 mm) and circle M1.0, M3.0, M6.0 (macular centered, diameter of 1.0, 3.0, and 6.0 mm), using 2 partitioning methods ("X" and "+"). The density of patchy (Category 3) or macular atrophy (Category 4) areas was quantified. Univariate and multivariate linear regression analyses were performed to assess the association with FTD. RESULTS: The mean FTD of total PM eyes was 0.283, ranging from 0.002 to 0.500, and demonstrating a negative correlation with the PM category. In multivariate analysis, age was found to be significantly associated with FTD ( P <0.05), while axial length did not show a significant association. Fundus tessellation of circle O4.5 and circle M6.0 displayed associations with the FTD across different PM categories. The "X" partitioning method better fit the circle M6.0 region, while both methods were suitable for the circle O4.5 region. After excluding the patchy and macular atrophic areas, the mean FTD values were 0.346 in Category 2, 0.261 in Category 3, and 0.186 in Category 4. CONCLUSIONS: The study revealed a decreasing trend in FTD values across different categories of PM, regardless of the presence or absence of patchy or macular atrophic areas. Quantifying FTD in PM could be a valuable tool for improving the existing PM classification system and gaining insights into the origin of posterior staphyloma and visual field defects in high myopia.

Transcriptomic Analysis of the Response of Susceptible and Resistant Bitter Melon (Momordica charantia L.) to Powdery Mildew Infection Revealing Complex Resistance via Multiple Signaling Pathways.

The challenge of mitigating the decline in both yield and fruit quality due to the intrusion of powdery mildew (PM) fungus looms as a pivotal concern in the domain of bitter melon cultivation. Yet, the intricate mechanisms that underlie resistance against this pathogen remain inscrutable for the vast majority of bitter melon variants. In this inquiry, we delve deeply into the intricate spectrum of physiological variations and transcriptomic fluctuations intrinsic to the PM-resistant strain identified as '04-17-4' (R), drawing a sharp contrast with the PM-susceptible counterpart, designated as '25-15' (S), throughout the encounter with the pathogenic agent Podosphaera xanthii. In the face of the challenge presented by P. xanthii, the robust cultivar displays an extraordinary capacity to prolong the initiation of the pathogen's primary growth stage. The comprehensive exploration culminates in the discernment of 6635 and 6954 differentially expressed genes (DEGs) in R and S strains, respectively. Clarification through the lens of enrichment analyses reveals a prevalence of enriched DEGs in pathways interconnected with phenylpropanoid biosynthesis, the interaction of plants with pathogens, and the signaling of plant hormones. Significantly, in the scope of the R variant, DEGs implicated in the pathways of plant-pathogen interaction phenylpropanoid biosynthesis, encompassing components such as calcium-binding proteins, calmodulin, and phenylalanine ammonia-lyase, conspicuously exhibit an escalated tendency upon the encounter with P. xanthii infection. Simultaneously, the genes governing the synthesis and transduction of SA undergo a marked surge in activation, while their counterparts in the JA signaling pathway experience inhibition following infection. These observations underscore the pivotal role played by SA/JA signaling cascades in choreographing the mechanism of resistance against P. xanthii in the R variant. Moreover, the recognition of 40 P. xanthii-inducible genes, encompassing elements such as pathogenesis-related proteins, calmodulin, WRKY transcription factors, and Downy mildew resistant 6, assumes pronounced significance as they emerge as pivotal contenders in the domain of disease control. The zenith of this study harmonizes multiple analytical paradigms, thus capturing latent molecular participants and yielding seminal resources crucial for the advancement of PM-resistant bitter melon cultivars.

N/O Co-doped hierarchical nanoporous biochar derived from waste polypropylene nonwoven for high-performance supercapacitors.

How to efficiently treat municipal solid waste (MSW) has become one of the critical solutions in response to the call for "carbon neutrality". Here, the waste polypropylene nonwoven fabric of waste diapers was converted into hierarchical nanoporous biochar (HPBC) through pre-carbonization and activation processes as an ideal precursor for supercapacitors (SCs) with excellent performance. The prepared HPBC-750-4 with an ultrahigh specific surface area (3838.04 m2 g-1) and abundant heteroatomic oxygen (13.25%) and nitrogen (1.16%) codoped porous biochar structure. Given its structural advantages, HPBC-750-4 achieved a specific capacitance of 340.9 F g-1 at a current density of 1 A g-1 in a three-electrode system. Its capacitance retention rate was above 99.2% after 10 000 cycles at a current density of 10 A g-1, which indicated an excellent rate capability and long-term cycling stability. Furthermore, the HPBC-750-4//HPBC-750-4 symmetric SC exhibited a superb energy density of 10.02 W h kg-1 with a power density of 96.15 W kg-1 in a 6 M KOH electrolyte. This work not only demonstrates the enormous potential of waste polypropylene nonwoven fabric in the SC industry but also provides an economically feasible means of managing MSW.

In Situ N, O-Dually Doped Nanoporous Biochar Derived from Waste Eutrophic Spirulina for High-Performance Supercapacitors.

Sustainable and high-performance energy storage materials are crucial to address global energy and environmental challenges. In this study, Spirulina platensis was used as the carbon and nitrogen source, and Spirulina-based nanoporous biochar (SNPB) was synthesized through chemical activation using KOH as the activating agent in N2 atmosphere. SNPB-800-4 was characterized by N2 adsorption-desorption and XPS, showing a high specific surface area (2923.7 m2 g-1) and abundant heteroatomic oxygen (13.78%) and nitrogen (2.55%). SNPB-800-4 demonstrated an exceptional capacitance of 348 F g-1 at a current density of 1 A g-1 and a remarkable capacitance retention of 94.14% after 10,000 cycles at a current density of 10 A g-1 in 6 M KOH. Notably, symmetric supercapacitors SNPB-800-4//SNPB-800-4 achieved the maximum energy and power densities of 17.99 Wh kg-1 and 162.48 W kg-1, respectively, at a current density of 0.5 A g-1, and still maintained 2.66 Wh kg-1 when the power density was increased to 9685.08 W kg-1 at a current density of 30 A g-1. This work provides an easily scalable and straightforward way to convert waste algae biomass into in situ N, O-dually doped biochar for ultra-high-power supercapacitors.

Heterogeneous treatment effects of coronary artery bypass grafting in ischemic cardiomyopathy: A machine learning causal forest analysis.

OBJECTIVES: We aim to evaluate the heterogeneous treatment effects of coronary artery bypass grafting in patients with ischemic cardiomyopathy and to identify a group of patients to have greater benefits from coronary artery bypass grafting compared with medical therapy alone. METHODS: Machine learning causal forest modeling was performed to identify the heterogeneous treatment effects of coronary artery bypass grafting in patients with ischemic cardiomyopathy from the Surgical Treatment for Ischemic Heart Failure trial. The risks of death from any cause and death from cardiovascular causes between coronary artery bypass grafting and medical therapy alone were assessed in the identified subgroups. RESULTS: Among 1212 patients enrolled in the Surgical Treatment for Ischemic Heart Failure trial, left ventricular end-systolic volume index, serum creatinine, and age were identified by the machine learning algorithm to distinguish patients with heterogeneous treatment effects. Among patients with left ventricular end-systolic volume index greater than 84 mL/m2 and age 60.27 years or less, coronary artery bypass grafting was associated with a significantly lower risk of death from any cause (adjusted hazard ratio, 0.61; 95% CI, 0.45-0.84) and death from cardiovascular causes (adjusted hazard ratio, 0.63; 95% CI, 0.45-0.89). By contrast, the survival benefits of coronary artery bypass grafting no longer exist in patients with left ventricular end-systolic volume index 84 mL/m2 or less and serum creatinine 1.04 mg/dL or less, or patients with left ventricular end-systolic volume index greater than 84 mL/m2 and age more than 60.27 years. CONCLUSIONS: The current post hoc analysis of the Surgical Treatment for Ischemic Heart Failure trial identified heterogeneous treatment effects of coronary artery bypass grafting in patients with ischemic cardiomyopathy. Younger patients with severe left ventricular enlargement were more likely to derive greater survival benefits from coronary artery bypass grafting.

MicroRNA-375 Is Induced during Astrocyte-to-Neuron Reprogramming and Promotes Survival of Reprogrammed Neurons when Overexpressed.

While astrocyte-to-neuron (AtN) reprogramming holds great promise in regenerative medicine, the molecular mechanisms that govern this unique biological process remain elusive. To understand the function of miRNAs during the AtN reprogramming process, we performed RNA-seq of both mRNAs and miRNAs on human astrocyte (HA) cultures upon NeuroD1 overexpression. Bioinformatics analyses showed that NeuroD1 not only activated essential neuronal genes to initiate the reprogramming process but also induced miRNA changes in HA. Among the upregulated miRNAs, we identified miR-375 and its targets, neuronal ELAVL genes (nELAVLs), which encode a family of RNA-binding proteins and were also upregulated by NeuroD1. We further showed that manipulating the miR-375 level regulated nELAVLs' expression during NeuroD1-mediated reprogramming. Interestingly, miR-375/nELAVLs were also induced by the reprogramming factors Neurog2 and ASCL1 in HA, suggesting a conserved function to neuronal reprogramming, and by NeuroD1 in the mouse astrocyte culture and spinal cord. Functionally, we showed that miR-375 overexpression improved NeuroD1-mediated reprogramming efficiency by promoting cell survival at early stages in HA and did not appear to compromise the maturation of the reprogrammed neurons. Lastly, overexpression of miR-375-refractory ELAVL4 induced apoptosis and reversed the cell survival-promoting effect of miR-375 during AtN reprogramming. Together, we demonstrated a neuroprotective role of miR-375 during NeuroD1-mediated AtN reprogramming.

Clinical Features of Fundus Tessellation and Its Relationship with Myopia: A Systematic Review and Meta-analysis.

INTRODUCTION: This study aims to assess the existing literature on fundus tessellation (FT), focusing on its prevalence, associated factors, distribution, and progression. METHODS: Systemic methods were employed to search and gather published literature on FT from databases such as the National Library of Medicine (PubMed), Web of Science (WOS), and Elsevier on July 1, 2023. The quality of the studies was evaluated using the Newcastle-Ottawa Scale (NOS) and the Healthcare Research and Quality (AHRQ) criteria. A meta-analysis was conducted to compare tessellated and normal fundus with respect to age, gender, axial length, and spherical equivalent. RESULTS: The systematic review included 23 articles, encompassing a total of 3053 eyes in the meta-analysis. The prevalence of FT varied from 43.00 to 94.35%. The severity of FT was significantly associated with older age, male sex, lower body weight index, longer axial length, larger peripapillary atrophy, thinner choroid, thinner sclera, and larger corneal radius of curvature, suggesting a potential progression pattern. Notably, FT was observed predominantly in the macular and peripapillary regions. The meta-analysis revealed that tessellated fundus tended to be associated with older age (mean difference [MD] 4.76, 95% confidence interval [CI] 1.71-7.80, P < 0.01), longer axial length (MD 0.86, 95% CI 0.70-1.02, P < 0.01), and a lower spherical equivalent (MD - 1.16, 95% CI - 1.68 to 0.65, P < 0.01) compared to normal fundus. However, there was no significant difference in the proportion of males between individuals with tessellated and normal fundus (odds ratio [OR] 1.12, 95% CI 0.89-1.42, P = 0.32). CONCLUSIONS: Overall, this systematic review and meta-analysis shed light on the prevalence, characteristics, and factors associated with FT, offering valuable insights for clinicians and researchers in the field of ophthalmology. STUDY REGISTRATION: The study protocol was registered on the International Prospective Register of Systematic Reviews (PROSPERO) (CRD42023442486).

In situ N, O co-doped porous carbon derived from antibiotic fermentation residues as electrode material for high-performance supercapacitors.

With the widespread use of antibiotics, the safe utilization of waste antibiotic fermentation residues has become an urgent issue to be resolved. In this study, in situ N, O co-doped porous carbon was prepared using fresh oxytetracycline fermentation residue under the mild activation of the green activator K2CO3. The optimal sample exhibited a 3D grid carbon skeleton structure, excellent specific surface area (SBET = 948 m2 g-1), and high nitrogen and oxygen content (N = 3.42 wt%, O = 14.86 wt%). Benefiting from its developed morphology, this sample demonstrated excellent electrochemical performance with a high specific capacitance of 310 F g-1 at a current density of 0.5 A g-1 in the three-electrode system. Moreover, it exhibited superior cycling stability with only a 5.32% loss of capacity after 10 000 cycles in 6 M KOH aqueous electrolyte. Furthermore, the symmetric supercapacitor prepared from it exhibited a maximum energy density of 7.2 W h kg-1 at a power density of 124.9 W kg-1, demonstrating its promising application prospects. This study provided a green and facile process for the sustainable and harmless treatment of antibiotic fermentation residues.

MicroRNA-375 is induced during astrocyte-to-neuron reprogramming and promotes survival of reprogrammed neurons when overexpressed.

While astrocyte-to-neuron (AtN) reprogramming holds great promise in regenerative medicine, the molecular mechanisms that govern this unique biological process remain elusive. MicroRNAs (miRNAs), as post-transcriptional regulators of gene expression, play crucial roles during development and under various pathological conditions. To understand the function of miRNAs during AtN reprogramming process, we performed RNA-seq of both mRNAs and miRNAs on human astrocyte (HA) cultures upon NeuroD1 overexpression. Bioinformatics analyses showed that NeuroD1 not only activates essential neuronal genes to initiate reprogramming process but also induces miRNA changes in HA. Among the upregulated miRNAs, we identified miR-375 and its targets, neuronal ELAVL genes ( nELAVLs ), which encode a family of RNA-binding proteins and are also upregulated by NeuroD1. We further showed that manipulating miR-375 level regulates nELAVLs expression during NeuroD1-mediated reprogramming. Interestingly, miR-375/ nELAVLs are also induced by reprogramming factors Neurog2 and ASCL1 in HA suggesting a conserved function to neuronal reprogramming, and by NeuroD1 in the mouse astrocyte culture and spinal cord. Functionally, we showed that miR-375 overexpression improves NeuroD1-mediated reprogramming efficiency by promoting cell survival at early stages in HA even in cultures treated with the chemotherapy drug Cisplatin. Moreover, miR-375 overexpression doesn't appear to compromise maturation of the reprogrammed neurons in long term HA cultures. Lastly, overexpression of miR-375-refractory ELAVL4 induces apoptosis and reverses the cell survival-promoting effect of miR-375 during AtN reprogramming. Together, we demonstrate a neuro-protective role of miR-375 during NeuroD1-mediated AtN reprogramming and suggest a strategy of combinatory overexpression of NeuroD1 and miR-375 for improving neuronal reprogramming efficiency.

Plasma Electrolytic Oxidation Coatings of a 6061 Al Alloy in an Electrolyte with the Addition of K2ZrF6.

In this study, white thermal control coatings were produced on a 6061 Al alloy using plasma electrolytic oxidation (PEO). The coatings were mainly formed by incorporating K2ZrF6. The phase composition, microstructure, thickness, and roughness of the coatings were characterized using X-ray diffraction (XRD), scanning electron microscopy (SEM), a surface roughness tester, and an eddy current thickness meter, respectively. The solar absorbance and infrared emissivity of the PEO coatings were measured using a UV-Vis-NIR spectrophotometer and FTIR spectrometer, respectively. The addition of K2ZrF6 to the trisodium phosphate electrolyte was found to significantly enhance the thickness of the white PEO coating on the Al alloy, with the coating thickness increasing in proportion to the concentration of K2ZrF6. Meanwhile, the surface roughness was observed to stabilize at a certain level as the K2ZrF6 concentration increased. At the same time, the addition of K2ZrF6 altered the growth mechanism of the coating. In the absence of K2ZrF6 in the electrolyte, the PEO coating on the Al alloy surface predominantly developed outwards. However, with the introduction of K2ZrF6, the coating's growth mode transitioned to a combination of outward and inward growth, with the proportion of inward growth progressively increasing in proportion to the concentration of K2ZrF6. The addition of K2ZrF6 substantially enhanced the adhesion of the coating to the substrate and endowed it with exceptional thermal shock resistance, as the inward growth of the coating was facilitated by the presence of K2ZrF6. In addition, the phase composition of the aluminum alloy PEO coating in the electrolyte containing K2ZrF6 was dominated by tetragonal zirconia (t-ZrO2) and monoclinic zirconia (m-ZrO2). With the increase in K2ZrF6 concentration, the L* value of the coating increased from 71.69 to 90.53. Moreover, the coating absorbance α decreased, while the emissivity ε increased. Notably, at a K2ZrF6 concentration of 15 g/L, the coating exhibited the lowest absorbance (0.16) and the highest emissivity (0.72), which are attributed to the enhanced roughness resulting from the substantial increase in coating thickness caused by the addition of K2ZrF6, as well as the presence of ZrO2 with higher emissivity within the coating.

The Temporal and Spatial Changes of Autophagy and PI3K Isoforms in Different Neural Cells After Hypoxia/Reoxygenation Injury.

There are limited therapeutic options for patient with traumatic spinal cord injury (SCI). Phosphoinositide 3-kinase family (PI3Ks) are the key molecules for regulating cell autophagy, which is a possible way of treating SCI. As we know, PI3K family are composed of eight isoforms, which are distributed into three classes. While the role of PI3Ks in regulating autophagy is controversial and the effects may be in a cell-specific manner. Different isoforms do not distribute in neural cells consistently and it is not clear how the PI3K isoforms regulate and interact with autophagy. Therefore, we explored the distributions and expression of different PI3K isoforms in two key neural cells (PC12 cells and astrocytes). The results showed that the expression of LC3II/I and p62, which are the markers of autophagy, changed in different patterns in PC12 cells and astrocytes after hypoxia/reoxygenation injury (H/R). Furthermore, the mRNA level of eight PI3K isoforms did not change in the same way, and even for the same isoform the mRNA activities are different between PC12 cells and astrocytes. What is more, the results of western blot of PI3K isoforms after H/R were inconsistent with the relevant mRNA. Based on this study, the therapeutic effects of regulating autophagy on SCI are not confirmed definitely, and its molecular mechanisms may be related with different temporal and spatial patterns of activation and distributions of PI3K isoforms.