Comprehensive assessment of soil and dust heavy metal(loid)s exposure scenarios at residential playgrounds in Beijing, China.

Small playgrounds situated within residential communities are popular recreational areas. However, heavy metal(loid)s (HMs) in soil or equipment dust may pose a public health risk. This study provides a comprehensive assessment of the health risk associated with HMs exposure at residential playgrounds in cities, a field that has not been thoroughly investigated previously. 70 soil and 70 equipment dust samples were collected from 30 urban and 40 suburban playgrounds in Beijing. Results indicated significant enrichment of Cu, As, and Ni in the soil with Enrichment Factors (EFs) >5 from both anthropogenic and lithogenic sources. Correlation analyses showed that the levels of Be, Cr, Mn, Co, Ni in soil and Be, Mn, As, Cd in dust were positively correlated with the distance to the nearest highway, with p-values < 0.01. Enrichment and correlation analyses contributed to a better understanding of the sources and transport pathways of HMs in urban environment. Based on a site-specific Conceptual Site Model (CSM), the carcinogenic risks (CRs) and Hazard Quotients (HQs) were quantified for residents as the ratio of HMs exposure to reference doses. Risk assessment indicated the mean predicted CR for children and adults exposed to soil was 3.75 × 10-6 and 5.29 × 10-6, respectively, while that at dust exposure scenarios was lower, at 2.47 × 10-6 and 3.49 × 10-6, respectively, all of which were at the upper end of U.S. EPA's acceptable criteria of 1 × 10-6 to 1 × 10-4. Among the HMs, As and Ni were identified as the priority control contaminants due to significant contribution to CRs. Furthermore, the spatial distribution revealed an increasing trend in health risk from the urban center to the suburbs. This study emphasizes the need for effective measures to mitigate potential health risk and enhance the safety of recreational areas, particularly for susceptible individuals.

Myeloidcells in the immunosuppressive microenvironment in glioblastoma: The characteristics and therapeutic strategies.

Glioblastoma (GBM) is the most common and lethal malignant tumor of the central nervous system in adults. Conventional therapies, including surgery, radiotherapy, and chemotherapy, have limited success in ameliorating patient survival. The immunosuppressive tumor microenvironment, which is infiltrated by a variety of myeloid cells, has been considered a crucial obstacle to current treatment. Recently, immunotherapy, which has achieved great success in hematological malignancies and some solid cancers, has garnered extensive attention for the treatment of GBM. In this review, we will present evidence on the features and functions of different populations of myeloid cells, and on current clinical advances in immunotherapies for glioblastoma.

Highly selective colorimetric determination of catechol based on the aggregation-induced oxidase-mimic activity decrease of δ-MnO2.

Multiple enzyme-like activities of manganese oxides (MnO2) have been reported and applied in catalysis, biosensors, and cancer therapy. Here, we report that catechol can be determined colorimetrically based on the 3,3',5,5'-tetramethylbenzidine (TMB) oxidase-like activity of δ-MnO2. The detection was based on pre-incubation of catechol containing water samples with δ-MnO2, and then the residual TMB oxidase-like activity of reacted δ-MnO2 was linearly dependent on the catechol concentration in the range of 0.5 to 10 µM. This determination method was stable at pH 3.73-6.00 and was not affected by ion strength up to 200 µM. Common co-solutes in water bodies (50 µM) have negligible effects and excellent selectivity of catechol among various phenolic compounds (15 µM) was facilitated. Both reduction and aggregation of δ-MnO2 were observed during the incubation process with catechol, and aggregation-induced TMB oxidase-mimic activity decrease was the main factor for this colorimetric determination.

Ginsenoside compound K attenuates cognitive deficits in vascular dementia rats by reducing the Aß deposition.

Ginsenoside compound K (CK) is the main metabolite of protopanaxadiol-type ginsenosides and has been demonstrated to exert neuroprotective and cognition-enhancing effects. The effects of CK on cognitive function in vascular dementia (VD) has not been elucidated. Therefore, the present study aims to elucidate the effects of CK on memory function as well as its potential mechanism in VD rats. Sprague-Dawley rats were subjected to Chronic Cerebral Hypoperfusion (CCH) by permanent bilateral common carotid artery occlusion (2VO). CCH induced neuronal damage and aggravated the aggregation of Amyloid-ß1-42 peptides (Aß1-42), which plays a critical role in the neurotoxicity and cognitive impairment. CK treatment attenuated CCH-induced Aß1-42 deposition and ameliorated cognition impairment. Furthermore, CK enhanced the activity of the pSer9-Glycogen synthase kinase 3ß (pSer9-GSK3ß) and the insulin degrading enzyme (IDE), which mainly involved the production and clearance of Aß1-42. Moreover, CK treatment enhanced the activity of protein kinase B (PKB/Akt), a key kinase in phosphatidylinositol 3 kinase (PI3K)/Akt pathway that can regulate the activity of GSK-3ß and IDE. In short, our findings provide the first evidence that CK might attenuate cognitive deficits and Aß1-42 deposition in the hippocampus via enhancing the expression of pSer9-GSK-3ß and IDE.

Aucubin Alleviates Seizures Activity in Li-Pilocarpine-Induced Epileptic Mice: Involvement of Inhibition of Neuroinflammation and Regulation of Neurotransmission.

Neuroinflammation and imbalance of neurotransmitters play pivotal roles in seizures and epileptogenesis. Aucubin (AU) is an iridoid glycoside derived from Eucommia ulmoides that possesses anti-inflammatory and neuroprotective effects. However, the anti-seizure effects of AU have not been reported so far. The present study was designed to investigate the effects of AU on pilocarpine (PILO) induced seizures and its role in the regulation of neuroinflammation and neurotransmission. We found that AU reduced seizure intensity and prolonged the latency of seizures. AU significantly attenuated the activation of astrocytes and microglia and reduced the levels of interleukine-1 beta (IL-1ß), high mobility group box 1 (HMGB1), tumor necrosis factor-α (TNF-α). Furthermore, the contents of γ-aminobutyric acid (GABA) were increased while the levels of glutamate were decreased in the hippocampus with AU treatment. The expression of γ-aminobutyric acid type A receptor subunit α1 (GABAARα1) and glutamate transporter-1 (GLT-1) protein were up-regulated in AU treatment group. However, AU had no significant effect on N-methyl-d-aspartate receptor subunit 2B (NR2B) expression in status epilepticus (SE). In conclusion, our findings provide the first evidence that AU can exert anti-seizure effects by attenuating gliosis and regulating neurotransmission. The results suggest that AU may be developed as a drug candidate for the treatment of epilepsy.

Nonalcoholic Fatty Liver Disease in Pediatrics.

A 16-year-old Hispanic girl with an elevated body mass index in an otherwise normal state of health presented for her well-child examination. She had signs of metabolic syndrome and insulin resistance including increased waist circumference and acanthosis nigricans. Laboratory results revealed elevated transaminases with otherwise normal hepatic function. Based on the physical examination and laboratory results, she was diagnosed with nonalcoholic fatty liver disease (NAFLD). After further evaluation, she eventually underwent a liver biopsy. The biopsy revealed nonalcoholic steatohepatitis (NASH) with stage 2 fibrosis. This article reviews the definition of NAFLD and NASH, an increasingly prevalent cause of pediatric chronic liver disease associated with obesity and metabolic syndrome. The article also outlines the epidemiology, risk factors, and natural history of NAFLD, which may help identify and prevent high-risk pediatric patients from progressing to irreversible liver disease. Understanding the diagnostic and treatment options offers the best chance at preventing and reversing the early stages of this disease.