Enhanced Adsorptive Removal of Tetracycline by Phosphomolybdic Acid-Modified Low-Temperature Sludge Biochar.

Increasing the adsorption capacity and reducing the energy consumption of sludge biochar during preparation is important. In this study, a new modification method was developed to prepare phosphomolybdic acid-modified sludge biochar through the low-temperature pyrolysis of sewage sludge using phosphomolybdic acid as a modifier. Tetracycline was used to assess the adsorption performance of sludge biochar, and phosphomolybdic acid-modified sludge biochar was prepared at different temperatures. The results showed that the adsorption capacity of sludge biochar improved from 84.49 to 120.86 mg/g through modification with phosphomolybdic acid at 200 °C. The maximum adsorption capacities of phosphomolybdic acid-modified sludge biochar (200 °C pyrolysis temperature) at 298, 308, and 318 K were 283.87, 421.39, and 545.48 mg/g, respectively. Both liquid film and intraparticle diffusion were the main rate-limiting steps of tetracycline adsorption by phosphomolybdic acid-modified sludge biochar. Furthermore, the adsorption of tetracycline by phosphomolybdic acid-modified sludge biochar was mainly attributed to π-π interactions, electrostatic interactions, hydrogen bonding, and pore filling.

Efferocytosis induces a novel SLC program to promote glucose uptake and lactate release.

Development and routine tissue homeostasis require a high turnover of apoptotic cells. These cells are removed by professional and non-professional phagocytes via efferocytosis1. How a phagocyte maintains its homeostasis while coordinating corpse uptake, processing ingested materials and secreting anti-inflammatory mediators is incompletely understood1,2. Here, using RNA sequencing to characterize the transcriptional program of phagocytes actively engulfing apoptotic cells, we identify a genetic signature involving 33 members of the solute carrier (SLC) family of membrane transport proteins, in which expression is specifically modulated during efferocytosis, but not during antibody-mediated phagocytosis. We assessed the functional relevance of these SLCs in efferocytic phagocytes and observed a robust induction of an aerobic glycolysis program, initiated by SLC2A1-mediated glucose uptake, with concurrent suppression of the oxidative phosphorylation program. The different steps of phagocytosis2-that is, 'smell' ('find-me' signals or sensing factors released by apoptotic cells), 'taste' (phagocyte-apoptotic cell contact) and 'ingestion' (corpse internalization)-activated distinct and overlapping sets of genes, including several SLC genes, to promote glycolysis. SLC16A1 was upregulated after corpse uptake, increasing the release of lactate, a natural by-product of aerobic glycolysis3. Whereas glycolysis within phagocytes contributed to actin polymerization and the continued uptake of corpses, lactate released via SLC16A1 promoted the establishment of an anti-inflammatory tissue environment. Collectively, these data reveal a SLC program that is activated during efferocytosis, identify a previously unknown reliance on aerobic glycolysis during apoptotic cell uptake and show that glycolytic by-products of efferocytosis can influence surrounding cells.

Facial emotion recognition function and white matter microstructural alterations in drug-naive, comorbidity-free autism.

Individuals with autism spectrum disorder have deficits in facial emotion recognition and white matter microstructural alterations. Nonetheless, most previous studies were confounded by different variables, such as psychiatric comorbidities and psychotropic medications used by ASD participants. Also, it remains unclear how exactly FER deficits are related to white matter microstructural alterations in ASD. Accordingly, we aimed to investigate the FER functions, white matter microstructure, and their relationship in drug-naive and comorbidity-free ASD individuals. 59 ASD individuals and 59 typically developed individuals were included, where 46 ASD and 50 TD individuals completed FER tasks. Covariance analysis showed scores were lower in both basic and complex FER tasks in the ASD group. Tract-Based Spatial Statistics showed FA values in widespread white matter fibers were lower in the ASD group than in the TD group, including forceps major and forceps minor of the corpus callosum, anterior thalamic radiation, corticospinal tract, cingulum, inferior frontal-occipital fasciculus, inferior longitudinal fasciculus, superior longitudinal fasciculus. Moreover, in the TD group but not the ASD group, the performance in the complex FER task was negatively correlated with the FA value in some white matter fibers, including forceps major of the corpus callosum, ATR, CT, cingulum, IFOF, ILF, SLF. Our study suggests children with ASD may experience deficits in facial emotion recognition and exhibit alterations in white matter microstructure. More importantly, our study indicates that white matter microstructural alterations may be involved in FER deficits in children with ASD.

Relationship between autism and brain cortex surface area: genetic correlation and a two-sample Mendelian randomization study.

BACKGROUND: Alterations in surface area (SA) in specific regions of the cortex have been reported in many individuals with autism spectrum disorder (ASD), however, the genetic background between ASD and SA is still unclear. This study estimated the genetic correlation and causal effect of ASD and cortical SA. METHODS: Summarized data of genome-wide association studies (GWAS) were separately downloaded from the Psychiatric Genomics Consortium (18,381 cases of ASD, and 27,969 controls) and the Enhancing Neuroimaging Genetics through Meta-Analysis Consortium (33,992 participants of Europeans). We used Linkage disequilibrium score regression (LDSC) and Heritability Estimation from Summary Statistics (HESS) to calculate the heritability of each trait. As for the genetic correlation between ASD and SA, LDSC was used for global correlation and HESS was used to examine the local genetic covariance further. We used three Mendelian randomization (MR) methods, Inverse-variance weighted, MR-Egger, and weighted median to estimate the causal relationship. RESULTS: LDSC observed a nominal significant genetic correlation (rg = 0.1229, P-value = 0.0346) between ASD and SA of the rostral anterior cingulate gyrus whereas analysis through HESS did not reveal any significant loci having genetic covariance. Based on MR results, statistically meaningful estimations were found in the following areas, postcentral cortex (ß (SE) = 21.82 (7.84) mm, 95% CI: 6.46 to 37.19 mm, PIVW = 5.38 × 10- 3, PFDR = 3.09 × 10- 2), posterior cingulate gyrus (ß (SE) = 6.23 (2.69) mm, 95% CI: 0.96 to 11.49 mm, PIVW = 2.05 × 10- 2, PFDR = 4.26 × 10- 2), supramarginal gyrus (ß (SE) = 19.25 (8.43) mm, 95% CI: 29.29 to 35.77 mm, PIVW = 2.24 × 10- 2, PFDR = 4.31 × 10- 2). CONCLUSION: Our results provided genetic evidence to support the opinion that individuals with ASD tend to develop differences in cortical SA of special areas. The findings contributed to understanding the genetic relationship between ASD and cortical SA.

Digital transformation of the agricultural industry: Behavioral decision-making, influencing factors, and simulation practices in the Yunnan highlands.

Motivating the agricultural industry to engage in digital transformation is a challenge academically and socially. It is of great significance to study the choice of digital transformation mode of agricultural industrial organization and analyze its driving factors for promoting the sustainable development of agricultural industrial organization. This study adopts a bilateral evolutionary game to construct a decision-making model for behavioral decision-making during the digital transformation of the agricultural industry. The contingent-actual logical framework and multiple case studies of Yunnan highland agriculture are used to explore the impact of various factors on behavioral decision-making during the digital transformation of the agricultural industry. Additionally, a simulation analysis is used to verify the validity of the bilateral evolutionary game model. The results demonstrate that: (1) When the agricultural industry chooses "active transformation," behavioral decision-making during the digital transformation of the agricultural industry reaches a Nash equilibrium; (2) transformation costs, industry revenue, and reward and penalty mechanisms are the main driving factors for whether or not the agricultural industry chooses to actively engage in digital transformation; and (3) the probability of active digital transformation increases when agricultural industry organizations obtain higher returns at lower costs. Simultaneously, the higher the government's incentives, the greater the enthusiasm. However, when the penalty is excessive, the digital transformation takes the shape of either passive transformation or forced active transformation. Subsequently, it is necessary to improve the digital transformation planning of the agricultural industry, strengthen this field's cooperation mechanism, and formulate a reasonable reward and penalty system for digital transformation.

Reply to Chan et al.

We agree that smoking might be a risk factor for the severity of COVID-19, but in our previous study, smoking was not so robust compared with our conclusion. Also, we strongly agreed that COVID-19 patients with diabetes or other chronic diseases might worsen the situation of the disease. But these factors were out of the scope of our study and we had published other research on this topic related to diabetes. Because of the limited sample size and original medical records, our study could not cover many factors. But we wish our study will be a useful and meaningful pilot study for future studies.

The clinical and bioinformatics analysis for the role of antihypertension drugs on mortality among patients with hypertension hospitalized with COVID-19.

Comorbidities such as hypertension could exacerbate symptoms of coronaviral disease 2019 (COVID)-19 infection. Patients with hypertension may receive both anti-COVID-19 and antihypertension therapies when infected with COVID-19. However, it is not clear how different classes of anti-hypertension drugs impact the outcome of COVID-19 treatment. Herein, we explore the association between the inpatient use of different classes of anti-hypertension drugs and mortality among patients with hypertension hospitalized with COVID-19. We totally collected data from 278 patients with hypertension diagnosed with COVID-19 admitted to hospitals in Wuhan from February 1 to April 1, 2020. A retrospective study was conducted and single-cell RNA-sequencing (RNA-Seq) analysis of treatment-related genes was performed. The results showed that Angiotensin II receptor blocker (ARB) and calcium channel blocker (CCB) drugs significantly increased the survival rate but the use of angiotensin-converting enzyme inhibitor/ß-block/diuretic drugs did not affect the mortality caused by COVID-19. Based on the analysis of four public data sets of single-cell RNA-Seq on COVID-19 patients, we concluded that JUN, LST1 genes may play a role in the effect of ARB on COVID-19-related mortality, whereas CALM1 gene may contribute to the effect of CCB on COVID-19-related mortality. Our results provide guidance on the selection of antihypertension drugs for hypertensive patients infected with COVID-19.

Myeloid Slc2a1-Deficient Murine Model Revealed Macrophage Activation and Metabolic Phenotype Are Fueled by GLUT1.

Macrophages (MΦs) are heterogeneous and metabolically flexible, with metabolism strongly affecting immune activation. A classic response to proinflammatory activation is increased flux through glycolysis with a downregulation of oxidative metabolism, whereas alternative activation is primarily oxidative, which begs the question of whether targeting glucose metabolism is a viable approach to control MΦ activation. We created a murine model of myeloid-specific glucose transporter GLUT1 (Slc2a1) deletion. Bone marrow-derived MΦs (BMDM) from Slc2a1M-/- mice failed to uptake glucose and demonstrated reduced glycolysis and pentose phosphate pathway activity. Activated BMDMs displayed elevated metabolism of oleate and glutamine, yet maximal respiratory capacity was blunted in MΦ lacking GLUT1, demonstrating an incomplete metabolic reprogramming. Slc2a1M-/- BMDMs displayed a mixed inflammatory phenotype with reductions of the classically activated pro- and anti-inflammatory markers, yet less oxidative stress. Slc2a1M-/- BMDMs had reduced proinflammatory metabolites, whereas metabolites indicative of alternative activation-such as ornithine and polyamines-were greatly elevated in the absence of GLUT1. Adipose tissue MΦs of lean Slc2a1M-/- mice had increased alternative M2-like activation marker mannose receptor CD206, yet lack of GLUT1 was not a critical mediator in the development of obesity-associated metabolic dysregulation. However, Ldlr-/- mice lacking myeloid GLUT1 developed unstable atherosclerotic lesions. Defective phagocytic capacity in Slc2a1M-/- BMDMs may have contributed to unstable atheroma formation. Together, our findings suggest that although lack of GLUT1 blunted glycolysis and the pentose phosphate pathway, MΦ were metabolically flexible enough that inflammatory cytokine release was not dramatically regulated, yet phagocytic defects hindered MΦ function in chronic diseases.

Defective fatty acid oxidation in mice with muscle-specific acyl-CoA synthetase 1 deficiency increases amino acid use and impairs muscle function.

Loss of long-chain acyl-CoA synthetase isoform-1 (ACSL1) in mouse skeletal muscle (Acsl1M-/-) severely reduces acyl-CoA synthetase activity and fatty acid oxidation. However, the effects of decreased fatty acid oxidation on skeletal muscle function, histology, use of alternative fuels, and mitochondrial function and morphology are unclear. We observed that Acsl1M-/- mice have impaired voluntary running capacity and muscle grip strength and that their gastrocnemius muscle contains myocytes with central nuclei, indicating muscle regeneration. We also found that plasma creatine kinase and aspartate aminotransferase levels in Acsl1M-/- mice are 3.4- and 1.5-fold greater, respectively, than in control mice (Acsl1flox/flox ), indicating muscle damage, even without exercise, in the Acsl1M-/- mice. Moreover, caspase-3 protein expression exclusively in Acsl1M-/- skeletal muscle and the presence of cleaved caspase-3 suggested myocyte apoptosis. Mitochondria in Acsl1M-/- skeletal muscle were swollen with abnormal cristae, and mitochondrial biogenesis was increased. Glucose uptake did not increase in Acsl1M-/- skeletal muscle, and pyruvate oxidation was similar in gastrocnemius homogenates from Acsl1M-/- and control mice. The rate of protein synthesis in Acsl1M-/- glycolytic muscle was 2.1-fold greater 30 min after exercise than in the controls, suggesting resynthesis of proteins catabolized for fuel during the exercise. At this time, mTOR complex 1 was activated, and autophagy was blocked. These results suggest that fatty acid oxidation is critical for normal skeletal muscle homeostasis during both rest and exercise. We conclude that ACSL1 deficiency produces an overall defect in muscle fuel metabolism that increases protein catabolism, resulting in exercise intolerance, muscle weakness, and myocyte apoptosis.

Long-chain acyl-CoA synthetase 1 interacts with key proteins that activate and direct fatty acids into niche hepatic pathways.

Fatty acid channeling into oxidation or storage modes depends on physiological conditions and hormonal signaling. However, the directionality of this channeling may also depend on the association of each of the five acyl-CoA synthetase isoforms with specific protein partners. Long-chain acyl-CoA synthetases (ACSLs) catalyze the conversion of long-chain fatty acids to fatty acyl-CoAs, which are then either oxidized or used in esterification reactions. In highly oxidative tissues, ACSL1 is located on the outer mitochondrial membrane (OMM) and directs fatty acids into mitochondria for ß-oxidation. In the liver, however, about 50% of ACSL1 is located on the endoplasmic reticulum (ER) where its metabolic function is unclear. Because hepatic fatty acid partitioning is likely to require the interaction of ACSL1 with other specific proteins, we used an unbiased protein interaction technique, BioID, to discover ACSL1-binding partners in hepatocytes. We targeted ACSL1 either to the ER or to the OMM of Hepa 1-6 cells as a fusion protein with the Escherichia coli biotin ligase, BirA*. Proteomic analysis identified 98 proteins that specifically interacted with ACSL1 at the ER, 55 at the OMM, and 43 common to both subcellular locations. We found subsets of peroxisomal and lipid droplet proteins, tethering proteins, and vesicle proteins, uncovering a dynamic role for ACSL1 in organelle and lipid droplet interactions. Proteins involved in lipid metabolism were also identified, including acyl-CoA-binding proteins and ceramide synthase isoforms 2 and 5. Our results provide fundamental and detailed insights into protein interaction networks that control fatty acid metabolism.

Phenanthrene, but not its isomer anthracene, effectively activates both human and mouse nuclear receptor constitutive androstane receptor (CAR) and induces hepatotoxicity in mice.

Polycyclic aromatic hydrocarbons (PAHs) are a class of pervasive global environmental pollutants and adversely affect human health. Among PAHs, phenanthrene and anthracene are isomers consisting of three benzene rings. In the present study, we have made comparisons of constitutive androstane receptor (CAR) activation and toxic effects on the liver between these two isomers. Phenanthrene, but not anthracene, significantly induced promoter activity and gene expression of human drug metabolizing enzyme CYP2B6 in HepG2 cells and human primary hepatocytes, respectively. Phenanthrene, but not anthracene, significantly increased CYP2B10 expression levels and caused hepatotoxicity in mice. Phenanthrene induced the nuclear accumulation of CAR in the liver of wild-type mice, but not CAR-/- mice. Hepatocellular necrosis, elevated expression levels of some CAR-related genes such as CYP2B10, CYP3A11, UGT1A1, SULT2A1 and GSTM3, and lower hepatic glutathione levels were found in phenanthrene-exposed wild-type mice but not CAR-/- mice. Additionally, phenanthrene and anthracene were detected in both raw and grilled lamb samples. The average concentrations of phenanthrene were much higher than those of anthracene in these samples. This study is the first to demonstrate that phenanthrene, but not its isomer anthracene, effectively activates both human and mouse nuclear receptor CAR, and CAR plays a crucial role in phenanthrene-induced mouse hepatotoxicity. Compared with anthracene, K region may be an important electronic structure of phenanthrene for activation of CAR. Dietary consumption of PAHs-contaminated food is an important exposure route for humans. Exposure to phenanthrene may affect human health especially associated with liver.

Pumping a Ring-Sliding Molecular Motion by a Light-Powered Molecular Motor.

Designing artificial molecular machines to execute complex mechanical tasks, like coupling rotation and translation to accomplish transmission of motion, continues to provide important challenges. Herein, we demonstrated a novel molecular machine comprising a second-generation light-driven molecular motor and a bistable [1]rotaxane unit. The molecular motor can rotate successfully even in an interlocked [1]rotaxane system through a photoinduced cis-to -trans isomerization and a thermal helix inversion, resulting in concomitant transitional motion of the [1]rotaxane. The transmission process was elucidated via 1H NMR, 1H-1H COSY, HMQC, HMBC, and 2D ROESY NMR spectroscopies, UV-visible absorption spectrum, and density functional theory calculations. This is the first demonstration of a molecular motor to rotate against the appreciably noncovalent interactions between dibenzo-24-crown-8 and N-methyltriazolium moieties comprising the rotaxane unit, showing operational capabilities of molecular motors to perform more complex tasks.

Identification of hepatotoxicity and renal dysfunction of pyrene in adult male rats.

Polycyclic aromatic hydrocarbons (PAHs) are a group of persistent organic pollutants primarily formed from the incomplete combustion of carbonaceous materials, and have adverse effects on human health. In this study, we investigated whether pyrene, a PAH consisting of 4 fused benzene rings, has adverse effects on rat. Adult male Sprague-Dawly rats were treated daily by oral gavage with vehicle (corn oil) or pyrene at doses of 375, 750, 1500, or 2200 mg/kg/day for 4 days. The results showed that pyrene caused hepatotoxicity in rats. When compared with the control group, relative liver weights, plasma alanine aminotransferase, and direct bilirubin levels significantly increased after pyrene exposure. Hepatocyte swelling and degeneration and decreased hepatic total glutathione (GSH) levels were also found in pyrene-exposed rats. We further observed that mRNA levels of several hepatic metabolizing enzymes regulated by constitutive androstane receptor (CAR) such as CYP2B1 and CYP2B2 significantly increased in pyrene-exposed rats. These results suggest that decreased GSH levels, elevated hepatic metabolizing enzyme gene expression, and CAR activation are important contributors for pyrene-induced hepatotoxicity in rats. Additionally, we found pyrene significantly induced plasma inflammatory indices including white blood cell and lymphocyte counts. We also observed that pyrene exposure increased relative weight of kidneys and disrupted kidney function with elevated urea and creatinine levels in rats.

A phosphorylation-sensitive tyrosine-tailored magnetic particle for electrochemically probing free organophosphates in blood.

A simple, rapid, sensitive, selective, and field-deployable detection protocol has been initially proposed for the early warning and diagnosis of exposure to organophosphates (OPs) by electrochemically monitoring the direct biomarkers of free OPs in blood. Phosphorylation-sensitive tyrosine (Tyr), which was tested with unique electroactivity, was bound onto Fe3O4 particles mediated by the mussel-inspired dopamine to form Fe3O4@Tyr particles with well-defined shape and well-retained Tyr electroactivities, as characterized separately by electron microscopy and electrochemical measurements. A "lab-on-a-particle"-based detection procedure combined with a magnetic electrode was thus developed by employing Fe3O4@Tyr particles as capturing probes for detecting free OPs in blood, dimethyl-dichloro-vinyl phosphate (DDVP) as an example. A significant difference in electrochemical responses could be obtained for Fe3O4@Tyr particles before and after DDVP exposure, based on the phosphorylation-induced inhibition of electroactivities of loaded Tyr. Investigation results indicate that highly specific and sensitive phosphorylation for the inhibition of Tyr electroactivities by sensitive electrochemical outputs could endow the OP detection with high selectivity and sensitivity (i.e., down to about 0.16 nM DDVP in blood). Moreover, strong and stable Tyr-OP bindings especially irreversible electrochemical oxidization of the Tyr probe could facilitate the OP evaluation with high reproducibility and stability over time. In particular, the simple "lab-on-a-particle"-based detection procedure equipped with a portable electrochemical transducer can be tailored for the field-deployable or on-site monitoring of the exposure to various nerve agents and pesticides.

Adsorption Performance and Mechanisms of Tetracycline on Clay Minerals in Estuaries and Nearby Coastal Areas.

Clay minerals in sediments have strong adsorption capacities for pollutants, but their role in the distribution of antibiotics in estuaries and nearby coastal areas is unclear. We evaluated the clay mineral montmorillonite (SWy-2) adsorption capacity for tetracycline (TC). We assessed the adsorption capacity of SWy-2 for TC by measuring the removal percentage of 30 mg/L TC over time. The effects of pH and ionic strength on the TC adsorption onto SWy-2 were investigated. We analyzed the kinetics of TC adsorption using a pseudo-second-order model and determined the adsorption isotherm using the Langmuir equation. SWy-2 particles were characterized using zeta potential, Fourier transform infrared (FTIR), and X-ray diffraction (XRD) analyses before and after TC adsorption. The removal percentage of 30 mg/L TC by SWy-2 reached 70.76% within 0.25 h and gradually increased to 78.64% at 6 h. TC adsorption was influenced by pH and ionic strength, where low pH enhanced and high ionic strength reduced the adsorption. The kinetics of TC adsorption followed a pseudo-second-order model, and the adsorption isotherm adhered to the Langmuir equation. The saturated adsorption capacity (qmax) of SWy-2 for TC was 227.27 mg/g. Zeta potential, FTIR, and XRD analyses confirmed that electrostatic interactions and chemical bonds played a significant role in the TC adsorption by SWy-2. SWy-2 clay mineral exhibits a substantial adsorption capacity for TC, indicating its potential as an effective sorbent to mitigate antibiotic contamination in estuaries and nearby coastal areas. The observed effects of pH and ionic strength on TC adsorption have implications for the environmental fate and transport of antibiotics. The pseudo-second-order kinetic model and Langmuir isotherm equation provide valuable insights into the adsorption behavior and capacity of TC on SWy-2. Characterization analyses support the involvement of electrostatic interactions and chemical bonds in the SWy-2-TC adsorption mechanism.

Self-endowed magnetic photocatalysts derived from iron-rich sludge and its recycling in photocatalytic process for tetracycline degradation.

The disposal of iron-rich sludge by landfill or incineration poses environmental risks and wastes resources. The utilization of iron-rich sludge for magnetic material preparation offers a sustainable and resource-efficient solution for its disposal. Herein, self-endowed magnetic photocatalysts were initially prepared by pyrolysis using iron-rich sludge without any additives. The photocatalysts performance were evaluated for tetracycline degradation, with the highest degradation rate of 95.3 % at a concentration of 10 mg·L-1 (pH = 7) within 5 h being achieved for the photocatalyst prepared at 800 °C. The reactive radical species in the photocatalysis process were confirmed to be •OH and O2•- activated by ferrous oxygen species under light irradiation. Furthermore, quinone-like structures induced bound persistent free radicals, which emerged as the predominant factors influencing 1O2 formation. The employed photocatalyst can be efficiently separated and recovered owing to its magnetism. This work presents an economic solution for antibiotic removal using waste iron-rich sludge.

Spatiotemporal evolution of healthcare service capacity at township health centers in China.

Introduction: This study analyzes the efficiency, spatiotemporal evolution, and influencing factors of provincial township health centers' healthcare service capacity in China. Method: It utilizes an unexpected output super-efficiency slacks-based measure (SBM) model, exploratory spatiotemporal data analysis methods, and a quantile regression model. Results: The results show that the healthcare service capacity of township health centers is better in provinces with a larger proportion of hierarchical diagnoses and treatments pilot projects in cities, and the regional efficiency trend is ordered central > eastern > western > northeastern. The healthcare service capacity of provincial township health centers mainly shows significant spatial correlation and a spatiotemporal distribution pattern of "high agglomeration, low differentiation." Discussion: Rural population density and per capita GDP significantly improve the healthcare service capacity of township health centers, while local governments' healthcare and health expenditure increases the healthcare service capacity of township health centers in certain quantiles. The urbanization rate and per capita disposable income inhibit the improvement of the healthcare service capacity of township health centers in certain quantiles. The provinces should accelerate the promotion of hierarchical diagnoses and treatment pilot projects in cities and establish national cooperative development models to promote public health.

Autism spectrum disorder research: knowledge mapping of progress and focus between 2011 and 2022.

Background: In recent years, a large number of studies have focused on autism spectrum disorder (ASD). The present study used bibliometric analysis to describe the state of ASD research over the past decade and identify its trends and research fronts. Methods: Studies on ASD published from 2011 to 2022 were obtained from the Web of Science Core Collection (WoSCC). Bibliometrix, CiteSpace, and VOSviewer were used for bibliometric analysis. Results: A total of 57,108 studies were included in the systematic search, and articles were published in more than 6,000 journals. The number of publications increased by 181.7% (2,623 in 2011 and 7,390 in 2021). The articles in the field of genetics are widely cited in immunology, clinical research, and psychological research. Keywords co-occurrence analysis revealed that "causative mechanisms," "clinical features," and "intervention features" were the three main clusters of ASD research. Over the past decade, genetic variants associated with ASD have gained increasing attention, and immune dysbiosis and gut microbiota are the new development frontiers after 2015. Conclusion: This study uses a bibliometric approach to visualize and quantitatively describe autism research over the last decade. Neuroscience, genetics, brain imaging studies, and gut microbiome studies improve our understanding of autism. In addition, the microbe-gut-brain axis may be an exciting research direction for ASD in the future. Therefore, through visual analysis of autism literature, this paper shows the development process, research hotspots, and cutting-edge trends in this field to provide theoretical reference for the development of autism in the future.

Calcium Homeostasis and Psychiatric Disorders: A Mendelian Randomization Study.

Observational studies have investigated the impact of calcium homeostasis on psychiatric disorders; however, the causality of associations is yet to be established. Bidirectional Mendelian randomization (MR) analysis of calcium homeostasis hormones was conducted on nine psychiatric disorders. Calcium, serum 25-hydroxyvitamin D levels (25OHD), parathyroid hormone, and fibroblast growth factor 23 are the major calcium homeostasis hormones. The causality was evaluated by the inverse variance weighted method (IVW) and the MR Steiger test, while Cochran's Q test, the MR-Egger intercept test, funnel plot, and the leave-one-out method were used for sensitivity analyses. Bonferroni correction was used to determine the causative association features (p < 6.94 × 10-4). Schizophrenia (SCZ) was significantly associated with decreased 25OHD concentrations with an estimated effect of -0.0164 (Prandom-effect IVW = 2.39 × 10-7). In the Multivariable MR (MVMR) analysis adjusting for potentially confounding traits including body mass index, obesity, mineral supplements (calcium, fish oil, and vitamin D) and outdoor time (winter and summer), the relationship between SCZ and 25OHD remained. The genetically predicted autism spectrum disorder and bipolar disorder were also nominally associated with decreased 25OHD. This study provided evidence for a causal effect of psychiatric disorders on calcium homeostasis. The clinical monitoring of 25OHD levels in patients with psychiatric disorders is beneficial.

Cervical cancer immune infiltration microenvironment identification, construction of immune scores, assisting patient prognosis and immunotherapy.

Background: The immune microenvironment is of great significance in cervical cancer. However, there is still a lack of systematic research on the immune infiltration environment of cervical cancer. Methods: We obtained cervical cancer transcriptome data and clinical information from the Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases, evaluated the immune microenvironment of cervical cancer, determined immune subsets, constructed an immune cell infiltration scoring system, screened key immune-related genes, and performed single-cell data analysis and cell function analysis of key genes. Results: We combined the TCGA and GEO data sets and obtained three different immune cell populations. We obtained two gene clusters, extracted 119 differential genes, and established an immune cell infiltration (ICI) scoring system. Finally, three key genes, IL1B, CST7, and ITGA5, were identified, and single-cell sequencing data were mined to distribute these key genes in different cell types. By up-regulating CST7 and down-regulating IL1B and ITGA5, cervical cancer cells' proliferation ability and invasion ability were successfully reduced. Conclusion: We conducted a comprehensive assessment of the state of the tumor immune microenvironment in cervical cancer, constructed the ICI scoring system, and identified the ICI scoring system as a potential indicator of susceptibility to immunotherapy for cervical cancer, identifying key genes suggesting that IL1B, CST7, and ITGA5 play an essential role in cervical cancer.