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Background The hospital-based cross-sectional study aimed to explore the high risk for Attention-Deficit Hyperactive Disorder (ADHD) in Pediatric inpatients with Strabismus. Methods Using data from the Tianjin Eye Hospital, we performed a study comparing the incidence, risk factors, and severity of ADHD in children with and without strabismus by the SNAP-IV tool. Results A total of 401 patients with strabismus (exotropia:313; esotropia:42; vertical deviation:46) that ranged from 4 to 24 yrs and 200 healthy controls. SNAP screening detected that incidence of ADHD with strabismus was higher than controls (P=0.005).'' Inattentiveness '', as one subitem of SNAP, showed higher score in strabismic patients than control groups (P=0.027) and significantly associated with age (r=-0.126, P=0.011) and gender (r=-0.129, P=0.010). ADHD with exotropia was higher than other strabismus types(P=0.019), especially in intermittent exotropia patients (P=0.025). Additionally, the incidence of ADHD was significantly greater in male (HR = 0.539; 95% CI 0.331 - 0.331; P = 0.013) and left eye corrected visual acuity (the most dominant eyes) (HR = 0.097; 95% CI 0.012 - 0.775; P = 0.028) for strabismus patients. Subitems analysis of SNAP, except for inattentiveness, were only influenced by gender in strabismus group. Concomitant strabismic patients were more likely presented with oppositional defiant (P=0.009). Conclusions Patients with strabismus, especially in those with exotropia, had a high possibility of ADHD, which were closely linked to gender and the dominant eye‘s visual acuity, and might have an increased risk for ADHD .

BackgroundMost children with cerebral palsy and mental retardation cannot express independently, parents or guardians usually ignored the visual impairment. To investigate the ocular development and characteristics of visual function of children with cerebral palsy and mental retardation in special schools in Beijing's Chaoyang District.MethodsA total of 160 children (320 eyes) with cerebral palsy and mental retardation, including 86 boys and 74 girls, aged between 6 and 18 years old were included in this study. Subjective far vision, objective far vision (electrophysiological sweep VEP), near stereopsis, diopter, anterior segment, and fundus were examined. Statistical analysis was performed on the data obtained from children of different age groups, genders, degrees of intellectual impairment, and different etiology.Results156 eyes (54.93%) were greater than or equal to 20/40 for subjective far vision, 259 eyes (84.09%) were greater than or equal to 20/40 for objective far vision, 214 eyes with ametropia (70.39%), 94 eyes with astigmatism (30.92%), 8 eyes with hyperopia (2.63%), 112 eyes with myopia (36.84%), and 8 children with glasses, which was a correction rate of 7.69%, 192 eyes needed glasses to correct, which is an uncorrected rate of 92.31%. 64 children had strabismus (40%), 8 children had a color weakness (5%), and 24 children had nystagmus (15%). 72 children (64.29%) had 100″and less, while 40 children (35.71%) had between 200″ and 900″in the near stereopsis test. There were no significant differences in subjective far vision, objective far vision, corrected vision, diopter, and near stereopsis acuity among various degrees of mental retardation,various pathogenys and two age groups.ConclusionThe prevalence of abnormal visual function in children with cerebral palsy and intellectual disability was significantly higher than in typically developing children. Some of children with cerebral palsy and intellectual disability may have visual pathway damage, in a condition known as central visual impairment. Severe intellectual disability caused by craniocerebral diseases had the worst visual function, which undoubtedly demands significant attention of caregivers and the entire society.Fund Program: National Natural Science Foundation of China (81800861)Key Programme: Tianjin Key Research and Development Plan Science and Technology Support (19YFZCSY00990)

This study explored the advantageous effects of purple sweet potato anthocyanin extract (PSPAE) on redox state in obese mice. The normal chow diet (NCD) group, high-fat/cholesterol diet (HCD) group, and three groups based on HCD and added with low, middle, and high dose of PSPAE (PAL, PAM, and PAH) were raised for 12 weeks. High dose of PSPAE treatment decreased the elevations of the body weight by 24.7%, serum total cholesterol by 48.3%, serum triglyceride by 42.4%, and elevated serum activities of glutathione peroxidase by 53.3%, superoxide dismutase by 57.8%, catalase by 75.4%, decreased serum contents of malondialdehyde by 27.1% and lipopolysaccharides by 40.5%, as well as increased caecal total short-chain fatty acid by 2.05-fold. Additionally, PSPAE depressed toll-like receptor 4 (TLR-4), nuclear factor kappa-B (NF-κB), interleukin 6, tumor necrosis factor α, and preserved nuclear factor erythroid-2-related factor 2 (Nrf2) gene expression. Similarly, the protein expression of Nrf2 was enhanced, while TLR-4 and p-NF-κB/NF-κB were depressed by PSPAE treatment. Moreover, PSPAE administration promoted the protection of intestinal barrier function and rebuilt gut microbiota homeostasis by blooming g_Akkermansia, g_Bifidobacterium, and g_Lactobacillus. Furthermore, antibiotic interference experiments showed that the gut microbiota was indispensable for preserving the redox state of PSPAE. These results suggested that PSPAE administration could be an opportunity for improving HCD-induced obesity and the redox state related to gut dysbiosis. PRACTICAL APPLICATION: Purple sweet potato anthocyanin has diverse pharmacological properties. It is applicable for individuals to consume extracts (as pills or other forms) from raw purple sweet potato if they want to improve obesity or redox state.

Purple sweet potatoes extract (PSPE) have been used as a natural food antioxidant with high anthocyanin concentrations. Research investigated the lifespan and the mechanisms of PSPE on female Drosophila melanogaster. Supplementation of PSPE extended the lifespan by 16.3% and had a protective effect on injury by oxidative stress. PSPE treatment enhanced the endogenous antioxidant enzyme activity and reduced malondialdehyde (MDA) content. Furthermore, PSPE significantly up-regulated foxo-related genes, inhibited mTOR mRNA expression, and activated autophagy to maintain intestinal homeostasis. Meanwhile, PSPE improved intestinal barrier dysfunction by 22.86%, decelerated the abnormal proliferation rate of intestinal stem cell (ISCs) by 23.77%, and improved intestinal integrity in geriatric D. melanogaster. In conclusion, PSPE may maintain intestinal homeostasis, and improve the antioxidant and stress resistance capacity through the insulin and rapamycin pathway, thereby extending the lifespan. Therefore, it provides active support to the development and application of PSPE in functional food. PRACTICAL APPLICATIONS: In recent years, with the increase of age, age-related complications have generally increased and seriously affected people's healthy life. Purple sweet potato is a nutrient-rich substance, which not only has a unique color but also contains rich anthocyanins, so it has many potential biological and pharmacological functions. Our results showed that the PSPE had a good effect of maintaining the intestinal homeostasis of the older adult, and provided a favorable theoretical basis for the development of PSPE functional products and scientific academic research.

Inhibition the activity of glycosidase is an effective method for the treatment and prevention of diabetes. In this study, enzymatic kinetics, fluorescence spectrum experiment, starch granule digestion, molecular docking studies and animal's studies were used to investigate the interaction mechanism of carnosic acid against two glycosidase (α-amylase and α-glucosidase). Enzymatic kinetics showed that carnosic acid inhibited α-amylase activity in a competitive manner and α-glucosidase activity in a non-competitive manner. The half inhibitory concentrations (IC50) of carnosic acid to α-amylase and α- glucosidase were (1.12 ± 0.31) and (0.08 ± 0.17), respectively. The fluorescence quenching experiments showed that the intrinsic fluorescence of α-amylase or α-glucosidase was quenched by forming a complex with carnosic acid, and there was only one binding site between carnosic acid and glycosidase. The starch granules were no longer hydrolyzed by α-amylase after the addition of carnosic acid, which indicated that carnosic acid inhibited the activity of α-amylase. Molecular docking study showed that carnosic acid binds to the amino acid residues of glycosidase through hydrogen bond and van der Waals force, which leads to the change of the molecular conformation of glycosidase and thus reduces the activity of glycosidase. The experiment on mice showed that carnosic acid could effectively reduce postprandial blood glucose in mice.

Phlorizin is the main active ingredient of apple peel and has potential utilization value. Some recent studies have suggested that phlorizin may have antioxidant capacity and protect the liver. The injection of a low dose of d-galactose can cause some changes that resemble accelerated aging in mice. This study explored the protective effects of phlorizin on d-galactose-induced mice and PC12 cells. In this study, ICR mice were divided into a normal group (NOR), a d-galactose model group (d-gal) and phlorizin treatment groups (100 mg kg-1, 200 mg kg-1 and 400 mg kg-1). In addition to the NOR group, four other groups were injected with d-galactose (120 mg kg-1) for 12 weeks. The results showed that phlorizin reduced the decline of strength, coordination and spatial memory caused by aging, increased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), increased total antioxidant capacity (T-AOC), and reduced the content of malondialdehyde (MDA). On the other hand, phlorizin increased the levels of interleukin-2 (IL-2) and acetylcholine (ACh), reduced the release of interleukin-6 (IL-6), aspartate aminotransferase (AST) and alanine aminotransferase (ALT), and decreased the activity of acetylcholinesterase (AChE) in the brain, improved the expression of antioxidant genes related to the nuclear factor E2-related factor 2 (Nrf2) pathway, and reduced the occurrence of morphological lesions in the hippocampus and liver. In addition, phlorizin improved cell viability and reduced the cytotoxicity of d-galactose-induced oxidative stress in PC12 cells. Meanwhile, the protective effect of phlorizin was abolished in Nrf2 gene knockdown PC12 cells. Furthermore, molecular docking showed that phlorizin could bind Keap1 protein, which can interact with Nrf2 protein. Therefore, these results suggest that phlorizin may delay senescence and enhance antioxidant capacity through the Nrf2 pathway.

We explored the effects of dietary supplementation with phlorizin on redox state-related gut microbiota homeostasis in an obesity mouse model. Mice (C57BL/6J) were grouped as follows for 12 weeks: normal chow diet group (NCD), high-fat and cholesterol diet group (HFD), and treatment groups fed with HFD along with three levels of phlorizin. Phlorizin alleviated the hyperlipidemia and redox status and increased the total ccal SCFA content (1.88 ± 0.25 mg/g). Additionally, phlorizin regulated gene expression related to lipid metabolism, redox status, and cecum barrier and rebuilt gut microbiota homeostasis. After interference by antibiotics, the total phloretin content in the feces was decreased about 4-fold, and most of the health-promoting effects were abolished, indicating that phlorizin might be susceptible to microbial biotransformation and that microecology is indispensable for maintaining the redox state capacities of phlorizin. Phlorizin treatment could be an advantageous option for improving HFD-related obesity and redox states related to gut microbiota homeostasis.

Background:Apoptosis of photoreceptor cells and oxidative stress of RPE in age-related macular degeneration (AMD) could be promoted by photopic oxidative stress. In our study we are aim to study the protective effect of chrysanthemum extract on light damaged retina of mice.Methods:In vitro, ARPE-19 cells are incubated and divided into four groups: the control, the light damaged, the low and high dose-chrysanthemum extract groups. The last three groups were dropped in zero, low and high concentration of chrysanthemum extract separately before exposing to light. Cellular viability and Reactive Oxygen Species(ROS) production were measured by MTT and immunofluorescence. In vivo, C57BL/6J mice were divided into four groups as above mentioned. Low and high concentration of chrysanthemum extract were given by continuous intragastric administration before being exposed to white light. Retinal function was evaluated by electroretinogram. Optical coherence tomography and Fluorescein fundus angiography were used to observe the morphology and vessels. HE staining and TUNEL immunofluorescence for presenting morphology and apoptosis of isolated retina.Results:Viability of ARPE-19 cells decreased and ROS production increased after the light damaged. However, treatment with chrysanthemum extract, viability improved and ROS declined. After light injury, dysfunctional retina, destroyed morphology and increased apoptosis rate were observed in mice especially in RPE and photoreceptor layer. Treatment with chrysanthemum extract, retina function improved as well as structure of RPE and photoreceptor layers. Rate of apoptosis decreased via the raised concentration of anti-oxidative enzyme superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). Conclusions:Preventive administration of chrysanthemum extract reduces the oxidative-stress induced by light damage, which indicating Chrysanthemum have a potential of preventive measure for AMD.

Introduction Purple sweet potato is a nutritive food rich in anthocyanins that possess antioxidant effects. Drosophila melanogaster owns short growth cycle, fast reproduction, less chromosomes, more mutants, small individuals, therefore, which is an appropriate genetic model organism. Objective To investigate the anti-aging activity of Purple Sweet Potato Extract (PSPE) in male Drosophila melanogaster and explore the underlying mechanism. Results PSPE-induced longevity was associated with improvements in climbing ability and tolerance to stressors such as paraquat and hydrogen peroxide (H2O2). Furthermore, PSPE supplementation increased the activity of superoxide dismutase (SOD) and catalase (CAT), as well as expression of SOD and CAT genes, but decreased malondialdehyde (MDA) content. Meanwhile, PSPE decreased the intestinal stem cells (ISCs) proliferation and improved intestinal homeostasis, which was measured by Smurf assay and colony-forming units (CFUs) measurement in aging flies. Additionally, PSPE markedly inhibited the expression of upstream genes AKT-1, PI3K and mTOR and elevated the downstream gene 4E-BP, which further activated the expression of autophagy-related genes (Atg1, Atg5, Atg8a and Atg8b). Moreover, the production of lysosomes increased, indicating that the autophagy pathway was activated. Conclusion The results provided direct evidence of PSPE anti-aging effects on an organism level, indicating PSPE could be developed for use in effective anti-aging products.

Lutein, as a bioactive substance, has the ability to decrease the risk of some chronic diseases, but the poor water solubility, chemical instability, and low bioaccessibility limit its wide application in foods. In this study, an emulsion-based delivery system stabilized by chlorogenic acid (CA)-whey protein isolate (WPI)-dextran (DEX) ternary conjugates was prepared and vitamin E (VE) was added to increase the chemical stability of lutein. Molecular weight and conformational information of ternary conjugates were obtained by sodium dodecyl sulphate-polyacrylamide gel electrophoresis, fluorescence spectroscopy, and Fourier transform infrared spectroscopy. o-Phthalaldehyde results suggested that the extent of glycation was 16.4% and 19.5% for (CA-WPI)-DEX and WPI-DEX conjugates, respectively. The physicochemical stability of lutein-enriched emulsions was evaluated under different environmental stresses and long-term storage. The obtained results showed that compared with emulsions stabilized by WPI alone or binary conjugates, ternary conjugates imparted emulsions high stability under different environmental stress conditions (ionic strength, freeze-thaw, and heat) and long-term storage (within 3 weeks). VE can effectively decrease the degradation rate of lutein without changing the physical stability of emulsions. Additionally, the lutein-enriched emulsions prepared by ternary conjugates and VE exhibited a relatively high bioaccessibility. PRACTICAL APPLICATION: The ternary conjugates constructed in this paper has excellent physicochemical characteristics to stabilize emulsion, and can increase the water solubility of functional factors and reduce their degradation rate. Additionally, this conjugate was prepared by food-grade materials. Therefore, it can be used as emulsion-based delivery systems in food industrials.

The mechanism underlying the effect of ursolic acid (UA) on lipid metabolism remains unclear. This study aimed to explore the mechanisms of UA in reducing lipid accumulation in free fatty acids-cultured HepG2 cells and in high-fat-diet-fed C57BL/6J mice. In vivo, UA effectively alleviated liver steatosis and decreased the size of adipocytes in the epididymis. It also significantly decreased the total cholesterol (TC) and triglyceride (TG) contents in the liver and plasma in C57BL/6 mice. In vitro, UA (20 µM) significantly reduced lipid accumulation; the intracellular TC contents decreased from 0.078 ± 0.0047 to 0.049 ± 0.0064 µmol/mg protein, and TG contents from 0.133 ± 0.005 to 0.066 ± 0.0047 µmol/mg protein, in HepG2 cells. Furthermore, UA reduced the mRNA expression related to fat synthesis, enhanced the mRNA expression related to adipose decomposition, and dramatically upregulated the protein expression of P-AMPK in vivo and in vitro. Of note, these protective effects of UA on a high-fat environment were blocked by the AMPK inhibitor (compound C) in vitro. In addition, the molecular docking results suggested that UA could be docked to the AMPK protein as an AMPK activator. These results indicated that UA lowered the lipid content probably via activating the AMPK signaling pathway, thereby inhibiting lipid synthesis and promoting fat decomposition. PRACTICAL APPLICATION: Ursolic acid (UA) widely exists in vegetables and fruits. This study highlighted a lipid-lowing mechanism of UA in HepG2 cells and C57BL/6J mice. The data indicated that UA might be used in lipid-lowering functional foods.

To investigate the effects of dietary supplementation of WGBR on lipid metabolism, C57BL/6J mice were fed a normal chow diet, a high-fat diet based on corn starch, a high-fat diet based on white rice, and low or high dosage of black rice for 12 weeks. WGBR alleviated high-fat diet-induced increase in body weight and visceral weight; reduced serum TC, TG, and non-HDL-C/HDL-C levels; and increased fecal sterols and fat excretion. Furthermore, WGBR decreased hepatic TG and TC contents through the pathway of AMPK. This, in turn, decreased PPARγ, SREBP-1c, FASN, ACC, and HMGCOR-A and increased LXRα, PPARα, and CPT1α at the gene level. Further, it lowered PPARγ and elevated PPARα, p-ACC/ACC, and p-AMPKα/AMPKα at the protein level. Additionally, WGBR treatment decreased gene expression of NPC1L1, ACAT2, MTTP, which regulated lipid absorption in the intestine and preserved CYP7A1, ABCG5/8 that transported cholesterol from the liver and enterocytes to the intestinal lumen.

Scope This study explores the beneficial effects of dietary supplementation of black rice anthocyanin extract (BRAE) on cholesterol metabolism and gut dysbiosis. Methods and results C57BL/6J mice are grouped into the normal chow diet group (NCD), the high-fat and the cholesterol diet group (HCD), and three treatment groups feeding HCD supplemented with various dosage of BRAE for 12 weeks. Results reveal that BRAE alleviates the increased body weight, serum triglyceride (TG), total cholesterol (TC), non-high-density lipoprotein cholesterol levels (non-HDL-C), and increased fecal sterols excretion and caecal short-chain fatty acids (SCFAs) concentration in HCD-induced hypercholesterolemic mice. Moreover, BRAE decreases hepatic TC content through the fundamental regulation of body energy balance gene, adenosine 5'-monophosphate activated protein kinase α (AMPKα). Meanwhile, BRAE improves the genes expression involved in cholesterol uptake and efflux, and preserves CYP7A1, ATP-binding cassette subfamily G member 5/8 mRNA expression, and the relative abundance of gut microbiota. Additionally, the antibiotic treatment experiment indicates that the beneficial effects of BRAE in reducing hypocholesterolemia risk largely depends on the gut microbiota homeostasis. Conclusion BRAE supplement could be a beneficial treatment option for preventing HCD-induced hypocholesterolemia and related metabolic syndromes.

Metaplasticity, the adaptive changes of long-term potentiation (LTP) and long-term depression (LTD) in response to fluctuations in neural activity is well documented in visual cortex, where dark rearing shifts the frequency threshold for the induction of LTP and LTD. Here we studied metaplasticity affecting spike-timing-dependent plasticity, in which the polarity of plasticity is determined not by the stimulation frequency, but by the temporal relationship between near-coincidental presynaptic and postsynaptic firing. We found that in mouse visual cortex the same regime of deprivation that restricts the frequency range for inducing rate-dependent LTD extends the integration window for inducing timing-dependent LTD, enabling LTD induction with random presynaptic and postsynaptic firing. Notably, the underlying mechanism for the changes in both rate-dependent and time-dependent LTD appears to be an increase of NR2b-containing NMDAR at the synapse. Thus, the rules of metaplasticity might manifest in opposite directions, depending on the plasticity-induction paradigms.

Many forms of synaptic plasticity require NMDA-type glutamate receptors (NMDAR). These tetrameric receptors consist of two obligatory NR1 subunits and two regulatory subunits, usually a combination of NR2A and NR2B. In the neonatal visual cortex NR2B-containing NMDAR predominate, after thatvisual experience facilitates a developmental switch in which NR2A levels increase relative to NR2B. In this review, it puts emphasis on the role and the regulation of this shift as well as the effect on synaptic plasticity.

Visual deprivation during the critical period induces long-lasting changes in cortical circuitry by adaptively modifying neuro-transmission and synaptic connectivity at synapses. Spike timing-dependent plasticity (STDP) is considered a strong candidate for experience-dependent changes. However, the visual deprivation forms that affect timing-dependent long-term potentiation(LTP) and long-term depression(LTD) remain unclear. Here, we demonstrated the temporal window changes of tLTP and tLTD, elicited by coincidental pre- and post-synaptic firing, following different modes of 6-day visual deprivation. Markedly broader temporal windows were found in robust tLTP and tLTD in the V1M of the deprived visual cortex in mice after 6-day MD and DE. The underlying mechanism for the changes seen with visual deprivation in juvenile mice using 6 days of dark exposure or monocular lid suture involves an increased fraction of NR2b-containing NMDAR and the consequent prolongation of NMDAR-mediated response duration. Moreover, a decrease in NR2A protein expression at the synapse is attributable to the reduction of the NR2A/2B ratio in the deprived cortex.

Background Genetic polymorphisms of the Optic atrophy 1 gene have been implicated in altering the risk of primary open angle glaucoma (POAG), especially the susceptibility to normal tension glaucoma (NTG), but the results remain controversial. Methods Multiple electronic databases (up to January 20, 2012) were searched independently by two investigators. A meta-analysis was performed on the association between Optic atrophy 1 polymorphisms (rs 166850 and rs 10451941) and normal tension glaucoma (NTG)/high tension glaucoma (HTG). Summary odds ratios (ORs) and 95% confidence intervals (CI) were estimated. Results Seven studies of 713 cases and 964 controls for NTG and five studies of 1200 cases and 971 controls for HTG on IVS8+4C>T (rs 166850) and IVS8+32T>C (rs10451941) were identified. There were significant associations between the OPA1 rs10451941polymorphism and NTG susceptibility for all genetic models(C vs. T OR = 1.26, 95% CI 1.09–1.47, p = 0.002; CC vs. TT: OR = 1.52, 95% CI 1.04–2.20, p = 0.029; CC vs. CT+TT: OR = 1.64, 95% CI 1.16–2.33, p = 0.005; CC+CT vs. TT: OR = 1.21, 95% CI 1.02–1.44, p = 0.032). However, no evidence of associations was detected between the OPA1 IVS8+32C>T polymorphism and POAG susceptibility to HTG. Similarly, clear associations between the rs 166850 variant and NTG were observed in allelic and dominant models (T vs. C OR = 1.52, 95% CI 1.16–1.99, p = 0.002; TT+TC vs. CC OR = 1.50, 95% CI 1.13–2.01, p = 0.006) but not to HTG. In subgroup analyses by ethnicity, we detected an association between both OPA1 polymorphisms and risk for NTG in Caucasians but not in Asians. By contrast, no significant findings were noted between OPA1 variants for HTG, either in Caucasians or in Asians. Conclusions Both the IVS8+4C>T and IVS8+32T>C variants may affect individual susceptibility to NTG. Moreover, stratified analyses for NTG detecting the effects of both OPA1 polymorphisms seemed to vary with ethnicity. Further investigations are needed to validate the association.

SummaryNeuromodulatory input, acting on G protein-coupled receptors, is essential for the induction of experience-dependent cortical plasticity. Here we report that G-coupled receptors in layer II/III of visual cortex control the polarity of synaptic plasticity through a pull-push regulation of LTP and LTD. In slices, receptors coupled to Gs promote LTP while suppressing LTD; conversely, receptors coupled to Gq11 promote LTD and suppress LTP. In vivo, the selective stimulation of Gs- or Gq11-coupled receptors brings the cortex into LTP-only or LTD-only states, which allows the potentiation or depression of targeted synapses with visual stimulation. The pull-push regulation of LTP/LTD occurs via direct control of the synaptic plasticity machinery and it is independent of changes in NMDAR activation or neuronal excitability. We propose these simple rules governing the pull-push control of LTP/LTD form a general metaplasticity mechanism that may contribute to neuromodulation of plasticity in other cortical circuits.