Protective factors for children with autism spectrum disorder during COVID-19-related strict lockdowns: a Shanghai autism early developmental cohort study.

BACKGROUND: COVID-19 lockdowns increased the risk of mental health problems, especially for children with autism spectrum disorder (ASD). However, despite its importance, little is known about the protective factors for ASD children during the lockdowns. METHODS: Based on the Shanghai Autism Early Developmental Cohort, 188 ASD children with two visits before and after the strict Omicron lockdown were included; 85 children were lockdown-free, while 52 and 51 children were under the longer and the shorter durations of strict lockdown, respectively. We tested the association of the lockdown group with the clinical improvement and also the modulation effects of parent/family-related factors on this association by linear regression/mixed-effect models. Within the social brain structures, we examined the voxel-wise interaction between the grey matter volume and the identified modulation effects. RESULTS: Compared with the lockdown-free group, the ASD children experienced the longer duration of strict lockdown had less clinical improvement (ß = 0.49, 95% confidence interval (CI) [0.19-0.79], p = 0.001) and this difference was greatest for social cognition (2.62 [0.94-4.30], p = 0.002). We found that this association was modulated by parental agreeableness in a protective way (-0.11 [-0.17 to -0.05], p = 0.002). This protective effect was enhanced in the ASD children with larger grey matter volumes in the brain's mentalizing network, including the temporal pole, the medial superior frontal gyrus, and the superior temporal gyrus. CONCLUSIONS: This longitudinal neuroimaging cohort study identified that the parental agreeableness interacting with the ASD children's social brain development reduced the negative impact on clinical symptoms during the strict lockdown.

Trust-Aware and Fuzzy Logic-Based Reliable Layering Routing Protocol for Underwater Acoustic Networks.

Routing protocols based on trust mechanisms have been widely investigated for wireless sensor networks, and the works have achieved good results, while there are few works on trusted routing for underwater acoustic networks (UANs). However, trust-aware routing is the key to improving the packet delivery rate and the energy efficiency of UANs. Therefore, inspired by the theory of trust evaluation, a trust-aware and fuzzy logic-based reliable layering routing protocol (TAFLRLR) is proposed. In the TAFLRLR protocol, to avoid the problem of the void area and improve the transmission reliability, the candidate nodes of the next-hop forwarding nodes are determined according to the layers of neighbor nodes. Moreover, a fuzzy logic-based trust evaluation mechanism (FLTEM) is provided, which employs the fuzzy comprehensive evaluation decision model to calculate the comprehensive trust value for underwater sensor nodes. Further, the node density of a candidate node and its comprehensive trust value are taken as the input of a fuzzy control system and the forwarding probability (FP) of the node is taken as the output, and the candidate node with the highest FP is selected as the best forwarding node. Simulation results illustrate the superiority and effectiveness of the TAFLRLR protocol in terms of energy efficiency, routing reliability, and transmission reliability.

Management and follow-up of uveal effusion syndrome: a case report.

BACKGROUND: We present the management and follow-up of a case of uveal effusion syndrome (UES). CASE PRESENTATION: We study the relevant recent literature reports and review the aetiology, clinical classification, pathogenesis, diagnostic characteristics, treatment methods, and prognosis of this disease. When we encounter UES patients clinically, we can classify them according to their clinical characteristics and adopt different treatment plans for different types. The retina of this patient reattached 5 months after receiving eight periocular injections of triamcinolone acetonide (TA). CONCLUSIONS: For type III UES patients, local hormone therapy can be applied, and follow-up should be done to optimize the clinical outcome.

Discovery and Validation of Novel Genes in a Large Chinese Autism Spectrum Disorder Cohort.

BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disorder that causes impairments in social communication and stereotypical behaviors, often accompanied by developmental delay or intellectual disability. A growing body of evidence suggests that ASD is highly heritable, and genetic studies have defined numerous risk genes. However, most studies have been conducted with individuals of European and Hispanic ancestry, and there is a lack of genetic analyses of ASD in the East Asian population. METHODS: We performed whole-exome sequencing on 772 Chinese ASD trios and combined the data with a previous study of 369 Chinese ASD trios, identifying de novo variants in 1141 ASD trios. We used single-cell RNA sequencing analysis to identify the cell types in which ASD-related genes were enriched. In addition, we validated the function of a candidate high-functioning autism gene in mouse models using genetic approaches. RESULTS: Our findings showed that ASD without developmental delay or intellectual disability carried fewer disruptive de novo variants than ASD with developmental delay or intellectual disability. Moreover, we identified 9 novel ASD candidate genes that were not present in the current ASD gene database. We further validated one such novel ASD candidate gene, SLC35G1, by showing that mice harboring a heterozygous deletion of Slc35g1 exhibited defects in interactive social behaviors. CONCLUSIONS: Our work nominates novel ASD candidate genes and emphasizes the importance of genome-wide genetic studies with ASD cohorts of different ancestries to reveal the comprehensive genetic architecture of ASD.

Glaucoma in rural China (the Rural Epidemiology for Glaucoma in China (REG-China)): a national cross-sectional study.

OBJECTIVE: This study aimed to investigate the prevalence of glaucoma with associated factors in the rural populations of 10 provinces in China. DESIGN: A population-based cross-sectional study. METHODS: All participants aged 6 years or older from 10 provinces completed visual acuity testing, slit-lamp examination, ophthalmoscopy and non-contact tonometry. Glaucoma suspects underwent fundus photography, Goldmann applanation tonometry, visual field testing and gonioscopy. Glaucoma was determined according to the International Society of Geographical and Epidemiological Ophthalmology classification scheme. Associations of demographics and medical factors with glaucoma were assessed using multiple logistic regression models. RESULTS: From June 2017 to October 2018, 48 398 of 52 041 participants were included in the final analyses. The age-standardised prevalence of glaucoma was 1.7% (95% CI 1.55% to 1.78%) among the participants older than 6 years, which was 2.1% (95% CI 1.93% to 2.23%) in participants aged over 40 years. The constituent ratios of glaucoma were: 44.4% primary angle-closure glaucoma (PACG), 34.7% primary open-angle glaucoma, 2.6% congenital glaucoma and 18.3% other types of glaucoma. Increasing age, smoking, cerebral stroke, type 2 diabetes, higher education (college or more) and higher personal income were significant risk factors for PACG. The unilateral and bilateral blindness rates in the entire study population were 4.692% and 1.068%, respectively. A family history of glaucoma was a significant risk factor for the prevalence of glaucoma and blindness in at least one eye. CONCLUSIONS: Rural populations have a high prevalence of glaucoma, which should be included in chronic disease management programmes in China for long-term care.

SH2B1 Tunes Hippocampal ERK Signaling to Influence Fluid Intelligence in Humans and Mice.

Fluid intelligence is a cognitive domain that encompasses general reasoning, pattern recognition, and problem-solving abilities independent of task-specific experience. Understanding its genetic and neural underpinnings is critical yet challenging for predicting human development, lifelong health, and well-being. One approach to address this challenge is to map the network of correlations between intelligence and other constructs. In the current study, we performed a genome-wide association study using fluid intelligence quotient scores from the UK Biobank to explore the genetic architecture of the associations between obesity risk and fluid intelligence. Our results revealed novel common genetic loci (SH2B1, TUFM, ATP2A1, and FOXO3) underlying the association between fluid intelligence and body metabolism. Surprisingly, we demonstrated that SH2B1 variation influenced fluid intelligence independently of its effects on metabolism but partially mediated its association with bilateral hippocampal volume. Consistently, selective genetic ablation of Sh2b1 in the mouse hippocampus, particularly in inhibitory neurons, but not in excitatory neurons, significantly impaired working memory, short-term novel object recognition memory, and behavioral flexibility, but not spatial learning and memory, mirroring the human intellectual performance. Single-cell genetic profiling of Sh2B1-regulated molecular pathways revealed that Sh2b1 deletion resulted in aberrantly enhanced extracellular signal-regulated kinase (ERK) signaling, whereas pharmacological inhibition of ERK signaling reversed the associated behavioral impairment. Our cross-species study thus provides unprecedented insight into the role of SH2B1 in fluid intelligence and has implications for understanding the genetic and neural underpinnings of lifelong mental health and well-being.

SENP1 in the retrosplenial agranular cortex regulates core autistic-like symptoms in mice.

Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental disorder, causing defects of social interaction and repetitive behaviors. Here, we identify a de novo heterozygous gene-truncating mutation of the Sentrin-specific peptidase1 (SENP1) gene in people with ASD without neurodevelopmental delay. We find that Senp1+/- mice exhibit core autistic-like symptoms such as social deficits and repetitive behaviors but normal learning and memory ability. Moreover, we find that inhibitory and excitatory synaptic functions are severely affected in the retrosplenial agranular (RSA) cortex of Senp1+/- mice. Lack of Senp1 leads to increased SUMOylation and degradation of fragile X mental retardation protein (FMRP), also implicated in syndromic ASD. Importantly, re-introducing SENP1 or FMRP specifically in RSA fully rescues the defects of synaptic function and autistic-like symptoms of Senp1+/- mice. Together, these results demonstrate that disruption of the SENP1-FMRP regulatory axis in the RSA causes autistic symptoms, providing a candidate region for ASD pathophysiology.

A novel mutation in the PRPH2 gene in a Chinese pedigree with retinitis pigmentosa and angle-closure glaucoma.

BACKGROUND: Retinitis pigmentosa (RP) is a rare, progressive, and hereditary disorder that leads to the progressive loss of vision and visual field, and in some cases blindness. The specific relationship between RP and glaucoma has been debated for decades. METHODS: In this study, we examined a Han RP family with concomitant angle-closure glaucoma (ACG), performed an inductive analysis of their clinical features and assistant results, and applied whole-exome sequencing (WES) technology for a molecular diagnosis. RESULTS: A novel transversion mutation (c.626 T > A) was identified in the peripherin-2 (PRPH2) gene in the proband, resulting in the substitution of Valine to aspartic acid in codon 209. A full ophthalmic examination showed that the proband with the c.626 T > A mutation had a typical RP manifestation, with close angles; however, the proband's elder brother, who lacked the novel mutation, had a normal fundus and open angles. CONCLUSION: Our results extend the genetic mutation spectrum of PRPH2 in RP, and provide evidence to support a genetic correlation between RP and ACG.

Gut Microbial Profile Is Associated With the Severity of Social Impairment and IQ Performance in Children With Autism Spectrum Disorder.

Background and Objective: Autism spectrum disorder (ASD) refers to a heterogeneous set of neurodevelopmental disorders with diverse symptom severity and comorbidities. Although alterations in gut microbiota have been reported in individuals with ASD, it remains unclear whether certain microbial pattern is linked to specific symptom or comorbidity in ASD. We aimed to investigate the associations between gut microbiota and the severity of social impairment and cognitive functioning in children with ASD. Methods: A total of 261 age-matched children, including 138 children diagnosed with ASD, 63 with developmental delay or intellectual disability (DD/ID), and 60 typically developing (TD) children, were enrolled from the Shanghai Xinhua Registry. The children with ASD were further classified into two subgroups: 76 children diagnosed with ASD and developmental disorder (ASD+DD) and 62 with ASD only (ASD-only). The gut microbiome of all children was profiled and evaluated by 16S ribosomal RNA sequencing. Results: The gut microbial analyses demonstrated an altered microbial community structure in children with ASD. The alpha diversity indices of the ASD+DD and ASD-only subgroups were significantly lower than the DD/ID or TD groups. At the genus level, we observed a decrease in the relative abundance of Prevotella. Simultaneously, Bacteroides and Faecalibacterium were significantly increased in ASD compared with DD/ID and TD participants. There was a clear correlation between alpha diversity and the Childhood Autism Rating Scale (CARS) total score for all participants, and this correlation was independent of IQ performance. Similar correlations with the CARS total score were observed for genera Bacteroides, Faecalibacterium, and Oscillospira. However, there was no single genus significantly associated with IQ in all participants. Conclusions: Specific alterations in bacterial taxonomic composition and associations with the severity of social impairment and IQ performance were observed in children with ASD or ASD subgroups, when compared with DD/ID or TD groups. These results illustrate that gut microbiota may serve as a promising biomarker for ASD symptoms. Nevertheless, further investigations are warranted.

Improved symptoms following bumetanide treatment in children aged 3-6 years with autism spectrum disorder: a randomized, double-blind, placebo-controlled trial.

With the current limited drug therapy for the core symptoms of autism spectrum disorder (ASD), we herein report a randomized, double-blind, placebo-controlled trial to investigate the efficacy, safety, and potential neural mechanism of bumetanide in children with ASD aged 3-6 years old. A total of 120 children were enrolled into the study and randomly assigned to either 0.5 mg bumetanide or placebo. In the final sample, 119 children received at least one dose of bumetanide (59 children) or placebo (60 children) were included in the final analysis. The primary outcome was a reduction in the Childhood Autism Rating Scale (CARS) score, and the secondary outcomes were the Clinical Global Impressions Scale (CGI) -Global Improvement (CGI-I) score at 3 months and the change from baseline to 3-month in the Autism Diagnostic Observation Schedule (ADOS). Magnetic resonance spectroscopy (MRS) was used to measure γ-aminobutyric acid (GABA) and glutamate neurotransmitter concentrations in the insular cortex (IC) before and after the treatment. As compared with the placebo, bumetanide treatment was significantly better in reducing the severity. No patient withdrew from the trial due to adverse events. The superiority of bumetanide to placebo in reducing insular GABA, measured using MRS, was demonstrated. The clinical improvement was associated with a decrease in insular GABA in the bumetanide group. In conclusion, this trial in a large group of young children with predominantly moderate and severe ASD demonstrated that bumetanide is safe and effective in improving the core symptoms of ASD. However, the clinical significance remains uncertain, and future multi-center clinical trials are required to replicate these findings and confirm the clinical significance using a variety of outcome measures.

Evaluation Preparation of Apatinib-Loaded Polymer Nanoparticles and Its Effect in the Treatment of Advanced Ovarian Cancer.

Ovarian cancer is a common gynecological malignant tumor, second only to cervical cancer and uterine body cancer. In China, ovarian cancer has the highest mortality rate in gynecological tumors. Due to the rapid spread of cancer cells, the prognosis is relatively poor. Because the ovarian epithelial cancer is relatively insidious, there are no obvious clinical manifestations in the early stage. At present, apatinib chemotherapy is widely used, which can reduce the disease of patients by inhibiting the migration and proliferation of vascular endothelial cells. Fluorescence imaging is widely used in biomedical imaging. Organic fluorescent dyes are stable in nature and can be linked to a variety of molecules. They are often used in targeted imaging and therapeutic research. A cyanine dye is an organic molecule formed by two nitrogen-containing aromatic heterocycles connected by a polymethine bridge. Because neither MR contrast agents nor fluorescent dyes are targeted, specific biomolecules and contrast agents are often used in the research to diagnose and treat tumors. In this paper, a polymer nanoparticle loaded with apatinib was prepared and its therapeutic effect in advanced ovarian cancer was explored. The results show that nanoparticles loaded with apatinib are more effective than ordinary therapeutic drugs.

A 29 Mainland Chinese cohort of patients with Phelan-McDermid syndrome: genotype-phenotype correlations and the role of SHANK3 haploinsufficiency in the important phenotypes.

BACKGROUND: Phelan-McDermid syndrome (PMS) or 22q13 deletion syndrome is a rare developmental disorder characterized by hypotonia, developmental delay (DD), intellectual disability (ID), autism spectrum disorder (ASD) and dysmorphic features. Most cases are caused by 22q13 deletions encompassing many genes including SHANK3. Phenotype comparisons between patients with SHANK3 mutations (or deletions only disrupt SHANK3) and 22q13 deletions encompassing more than SHANK3 gene are lacking. METHODS: A total of 29 Mainland China patients were clinically and genetically evaluated. Data were obtained from medical record review and a standardized medical history questionnaire, and dysmorphology evaluation was conducted via photographic evaluation. We analyzed 22q13 deletions and SHANK3 small mutations and performed genotype-phenotype analysis to determine whether neurological features and other important clinical features are responsible for haploinsufficiency of SHANK3. RESULTS: Nineteen patients with 22q13.3 deletions ranging in size from 34 kb to 8.7 Mb, one patient with terminal deletions and duplications, and nine patients with SHANK3 mutations were included. All mutations would cause loss-of function effect and six novel heterozygous variants, c.3838_3839insGG, c.3088delC, c.3526G > T, c.3372dupC, c.3120delC and c.3942delC, were firstly reported. Besides, we demonstrated speech delay (100%), DD/ID (88%), ASD (80%), hypotonia (83%) and hyperactivity (83%) were prominent clinical features. Finally, 100% of cases with monogenic SHANK3 deletion had hypotonia and there was no significant difference between loss of SHANK3 alone and deletions encompassing more than SHANK3 gene in the prevalence of hypotonia, DD/ID, ASD, increased pain tolerance, gait abnormalities, impulsiveness, repetitive behaviors, regression and nonstop crying which were high in loss of SHANK3 alone group. CONCLUSIONS: This is the first work describing a cohort of Mainland China patients broaden the clinical and molecular spectrum of PMS. Our findings support the effect of 22q13 deletions and SHANK3 point mutations on language impairment and several clinical manifestations, such as DD/ID. We also demonstrated SHANK3 haploinsufficiency was a major contributor to the neurological phenotypes of PMS and also responsible for other important phenotypes such as hypotonia, increased pain tolerance, impulsiveness, repetitive behaviors, regression and nonstop crying.

Severe nausea and vomiting in pregnancy: psychiatric and cognitive problems and brain structure in children.

BACKGROUND: Two studies have suggested that severe prolonged nausea and vomiting during pregnancy is associated with emotional and behavioral problems in offspring, with smaller sample size and short-term follow-up. Moreover, little information is available on the role of the brain structure in the associations. METHODS: In a US-based cohort, the association was investigated between severe prolonged nausea and vomiting in pregnancy (extending after the second trimester and termed SNVP), psychiatric and cognitive problems, and brain morphology, from the Adolescent Brain Cognitive Development (ABCD) study, from 10,710 children aged 9-11 years. We validated the emotional including psychiatric findings using the Danish National Cohort Study with 2,092,897 participants. RESULTS: SNVP was significantly associated with emotional and psychiatric problems (t = 8.89, Cohen's d = 0.172, p = 6.9 × 10-19) and reduced global cognitive performance (t = - 4.34, d = - 0.085, p = 1.4 × 10-5) in children. SNVP was associated with low cortical area and volume, especially in the cingulate cortex, precuneus, and superior medial prefrontal cortex. These lower cortical areas and volumes significantly mediated the relation between SNVP and the psychiatric and cognitive problems in children. In the Danish National Cohort, severe nausea and vomiting in pregnancy were significantly associated with increased risks of behavioral and emotional disorders in children (hazard ratio, 1.24; 95% confidence interval, 1.16-1.33). CONCLUSIONS: SNVP is strongly associated with psychiatric and cognitive problems in children, with mediation by brain structure. These associations highlight the clinical importance and potential benefits of the treatment of SNVP, which could reduce the risk of psychiatric disorder in the next generation.

Different strategies, distinguished cooperation efficiency, and brain synchronization for couples: An fNIRS-based hyperscanning study.

INTRODUCTION: Individuals may employ different strategies when cooperating with others. For example, when two participants are asked to press buttons simultaneously, they may press the buttons as quickly as possible (immediate response strategy) or press them in a delayed pattern (delayed response strategy). Despite recognition of interpersonal brain synchronization (IBS) as a fundamental neural mechanism of cooperation, it remains unclear how various strategies influence cooperative behavior and its neural activities. METHODS: To address this issue, 43 married couples were recruited to complete a button-press cooperative task, during which IBS was recorded by functional near-infrared spectroscopy hyperscanning. RESULTS: Behavioral results showed that couples who adopted a delayed response strategy performed better than those who adopted an immediate response strategy and those without any obvious strategy, and a new measure (cooperation coefficient) was used to index the level of cooperation. In addition, stronger IBS in the right frontal cortex was observed in the delayed response condition. The greater couples' perceived parenting stress, the more likely they were to perform well in tasks and the stronger their brain synchronization, since they tended to choose the delayed response strategy. CONCLUSION: The delayed response strategy may better unify dyad partners' response modes, trigger synchronized psychological processes, and enable their brains to become synchronized. The study extends understanding of cooperation by comparing the contributions of different strategies underlying cooperative behavior with corresponding neural evidence.

Symptom improvement in children with autism spectrum disorder following bumetanide administration is associated with decreased GABA/glutamate ratios.

Bumetanide has been reported to alter synaptic excitation-inhibition (E-I) balance by potentiating the action of γ-aminobutyric acid (GABA), thereby attenuating the severity of autism spectrum disorder (ASD) in animal models. However, clinical evidence of its efficacy in young patients with ASD is limited. This was investigated in the present clinical trial of 83 patients, randomised to the bumetanide group (bumetanide treatment, 0.5 mg twice daily) or the control group (no bumetanide treatment). Primary [Children Autism Rating Scale (CARS)], secondary [Clinical Global Impressions (CGI)], and exploratory [inhibitory (γ-aminobutyric acid, GABA) and excitatory (glutamate, Glx) neurotransmitter concentrations measured in the insular cortex (IC) and visual cortex (VC) by magnetic resonance spectroscopy (MRS)] outcome measures were evaluated at baseline and at the 3-month follow-up. Side effects were monitored throughout the treatment course. Compared with the control group, the bumetanide group showed significant reduction in symptom severity, as indicated by both total CARS score and number of items assigned a score ≥ 3. The improvement in clinical symptoms was confirmed by CGI. GABA/Glx ratio in both the IC and VC decreased more rapidly over the 3-month period in the bumetanide group than that in the control group. This decrease in the IC was associated with the symptom improvement in the bumetanide group. Our study confirmed the clinical efficacy of bumetanide on alleviating the core symptoms of ASD in young children and it is the first demonstration that the improvement is associated with reduction in GABA/Glx ratios. This study suggests that the GABA/Glx ratio measured by MRS may provide a neuroimaging biomarker for assessing treatment efficacy for bumetanide.

Correction: Symptom improvement in children with autism spectrum disorder following bumetanide administration is associated with decreased GABA/glutamate ratios.

An important detail was omitted in the Method of the original Article, I.E, The CARS and other evaluations were conducted 'blind' to condition (Bumetanide or no treatment) by experienced clinicians. This has now been updated in the HTML and PDF versions of this Article.

Diode laser transscleral cyclophotocoagulation for uveitis-glaucoma-hyphema syndrome: A case report.

RATIONALE: To report a case of diode laser transscleral cyclophotocoagulation (DLTSC) for uveitis-glaucoma-hyphema syndrome (UGH). PATIENT CONCERNS: The patient developed UGH on the right eye (OD) after vitrectomy and intraocular lens (IOL) implantation. DIAGNOSES: Best corrected visual acuity (BCVA) was HM/50 cm, intraocular pressure (IOP) was 51.3 mm Hg on the OD. He was found to have 3+ anterior chamber cells. A B-scan ultrasound showed vitreous opacity. Ultrasound biomicroscopy (UBM) showed the chafing between the IOL and the posterior surface of the iris. Thus, he was diagnosed as UGH on the OD. INTERVENTIONS: The patient was worried about the complications for removal of the IOL, a DLTSC approach was performed. OUTCOMES: BCVA was 20/40 on the OD, IOP was 12 mm Hg on the OD. There were no anterior chamber inflammation and no vitreous opacity. UBM showed there was no contact between IOL and the posterior surface of the iris, the fundus of the eye was clearly visible. LESSONS: UGH syndrome is a severe complication of cataract extraction. IOL extraction has been the traditional approach to treatment. DLTSC can be an option when the IOL is slightly tilted.

Salidroside mitigates hydrogen peroxide-induced injury by enhancement of microRNA-27a in human trabecular meshwork cells.

Salidroside (Sal) exerted widely pharmacological effects in multitudinous diseases had been certified. The actual study clarified the protective activity of Sal in H2O2-injured human trabecular meshwork (HTM) cells. HTM cells were disposed with H2O2 to construct an oxidative damage model in vitro. Then, Sal was utilized to administrate HTM cells, and cell viability, apoptosis, apoptosis-interrelated proteins and ROS production were appraised using CCK-8, flow cytometry, western blot and DCFH-DA staining. MiR-27a inhibitor and its control were transfected into HTM cells, and the influences of miR-27a inhibition in HTM cells stimulated with H2O2 and Sal were detected. PI3K/AKT and Wnt/ß-catenin pathways were ultimately investigated to uncover the underlying mechanism. We found that H2O2 evoked HTM cells oxidative damage, as evidenced by repressing cell viability, inducing apoptosis, activating cleaved-caspase-3/-9 expression and increasing ROS production. Sal significantly lightened H2O2-evoked oxidative damage in HTM cells. Additionally, miR-27a was up-regulated by Sal, and miR-27a suppression significantly reversed the protective effect of Sal on H2O2-injured HTM cells. Finally, Sal activated PI3K/AKT and Wnt/ß-catenin pathways through enhancement of miR-27a in H2O2-injured HTM cells. In conclusion, these discoveries suggested that Sal could protect HTM cells against H2O2-evoked oxidative damage by activating PI3K/AKT and Wnt/ß-catenin pathways through enhancement of miR-27a. Highlights H2O2 evokes HTM cells oxidative damage; Sal relieves H2O2-induced oxidative damage in HTM cells; Sal enhances miR-27a expression in H2O2-injured HTM cells; Repressed miR-27a reverses the protective impacts of Sal on H2O2-injured HTM cells; Sal activates PI3K/AKT and Wnt/ß-catenin pathways by increasing miR-27a.

Altered social cognition and connectivity of default mode networks in the co-occurrence of autistic spectrum disorder and attention deficit hyperactivity disorder.

OBJECTIVE: As two common neurodevelopmental disorders, autistic spectrum disorder and attention deficit hyperactivity disorder frequently occur together. Until now, only a few studies have investigated the co-occurrence of attention deficit hyperactivity disorder and autistic spectrum disorder, this is due to restrictions associated with previous Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Most previous research has focused on the developmental trajectories for autistic spectrum disorder and attention deficit hyperactivity disorder separately, while the neural mechanisms underpinning the co-occurrence of autistic spectrum disorder and attention deficit hyperactivity disorder remain largely unknown. METHODS: We studied 162 autistic spectrum disorder individuals (including 79 co-attention deficit hyperactivity disorder and 83 non-attention deficit hyperactivity disorder patients) and 177 typical developing individuals using resting-state functional magnetic resonance imaging data from the Autism Brain Imaging Data Exchange II, an aggregated magnetic resonance imaging dataset from 19 centers. Independent component analysis was used to extract sub-networks from the classic resting-state networks. Functional connectivity values within (intra-iFC) and between (inter-iFC) these networks were then determined. Subsequently, we compared the ASD_coADHD group with the ASD_nonADHD group in relation to the abnormal intra-iFC and inter-iFC of autistic spectrum disorder group relative to the typical developing group. RESULTS: The ASD_coADHD group showed more severe social impairment and decreased intra-iFC in the bilateral posterior cingulate cortex of the default mode network (independent component 17) and increased inter-iFC between the default mode network (independent component 8) and the somatomotor networks (independent component 2) compared to the ASD_nonADHD group. In addition, the strength of the intra-iFC in the default mode network was associated with the severity of autistic traits across the entire autistic spectrum disorder group and particularly the ASD_coADHD group. CONCLUSION: Our results showed that dysfunction of the default mode network is a central feature in the co-occurrence of autistic spectrum disorder and attention deficit hyperactivity disorder, including connectivity within the default mode network as well as between the default mode network and the somatomotor networks, thus supporting the existence of a clinically combined phenotype (autistic spectrum disorder + attention deficit hyperactivity disorder).

One-pot synthesis of dual carbon dots using only an N and S co-existed dopant for fluorescence detection of Ag.

Luminescent carbon-based nanoparticles, named often as carbon dots (CDs), were synthesized from citric acid (CA) and guanidine thiocyanate (GITC) via an N and S co-doped hydrothermal procedure. In the present structure characterization, N and S elements could be sufficiently doped by means of the heteroatom or the functional groups bonded on the surface of CDs. The as-prepared CDs solution showed blue color fluorescence under ultraviolet excitation, yet the PL spectra exhibited a repetitive emission process from excitation-independent to excitation-dependent. In view of the triexponential feature of fluorescence lifetimes of CDs, one possibility was proposed to be co-existence of two types of CDs with different surface states. Additionally, the as-prepared CDs were used as a sensing probe for the detection of Ag+ taking into consideration of the possible interactions between Ag+ and various fluorophores attached to the CD surface. As expected, the changes of fluorescence intensities were linearly proportional to the different concentration ranges of Ag+, which suggests the complex nature of the quenching mechanism. And for the first time, the SCN group was found to accelerate the quenching of CDs towards Ag+, promising a new approach for efficient detection of Ag+ for the application in industrial pollutants.