Network analysis of autism traits and problematic mobile phone use and their associations with depression among Chinese college students

The current study employed network analysis to examine the relationship between symptoms from factor level about autism traits and problematic mobile phone use (PMPU) and to explore their associations with depression. We measured the above three variables in 949 college students in China with Autism Spectrum Quotient (AQ), Smartphone Addiction Scale (SAS), Center for Epidemiological Studies Depression Scale (CES-D). Central and bridge symptoms were pinpointed through the examination of centrality index. In the AQ and PMPU network, results revealed that WD (“Withdrawal”), COR (“Cyberspace-oriented relationship”) and OU (“Overuse”) emerged as the core symptoms. AS (“Attention switching”), CO (“Communication”) and COR (“Cyberspace-oriented relationship”) were the most symptoms bridging the AQ and PMPU communities, suggesting that these symptoms could serve as focal points for interventions aimed at college students with concurrent autism traits and PMPU. SK (“Social skills”), COR (“Cyberspace-oriented relationship”), CO (“Communication”), and DLD (“Daily-life disturbance”) were most strongly associated with depression. In addition, future research should consider various measurement tools and methods to investigate the location of AD (“Attention to detail”), because AD was an isolated symptom in the flow network of depression

CPT1 deficiency blocks autophagic flux to promote lipid accumulation induced by co-exposure to polystyrene microplastic and cadmium

IntroductionCadmium (Cd) and polystyrene microplastics (PS-MPs), two ubiquitous environmental contaminants, produce unique synergistic toxicity when co-existing. Key unanswered questions include specific effects on liver function and potential mechanisms.MethodsIn this study, C57BL/6 mice and AML12 cells were used to establish in vivo and in vitro models to elucidate the effects of combined exposure to PS-MPs and Cd on the liver and their mechanisms.ResultsThe results showed that the combined effects of PS-MPs and Cd caused significantly more liver damage than exposure alone. As observed by transmission electron microscopy (TEM), the number of autophagosomes was significantly increased in the PS-MPs and Cd co-treated group. In addition, autophagic flux was assayed by RFP-GFP-LC3, a reporter system expressing dual fluorescent proteins, which showed an overwhelming enhancement of autophagic flux damage by co-exposure to PS-MPs and Cd compared to exposure alone. To further investigate the involvement of carnitine palmitoyltransferase1(CPT1) in liver injury induced by co-exposure to Cd and PS-MPs, we co-exposed Baicalin, an activator of CPT1, with PS-MPs and Cd, and showed that activation of CPT1 alleviated the impairment of autophagic fluxes induced by co-exposure of Cd and PS-MPs and further alleviated the changes in lipid accumulation and associated protein levels.DiscussionIn conclusion, the concurrent exposure of PS-MPs and Cd resulted in the blockage of hepatic lipid accumulation and autophagic pathway and further aggravated the toxic damage to the liver. Activation of CPT1 could alleviate the PS-MPs and Cd-induced lipid accumulation and autophagy pathway blockage thus reducing liver injury

Microscopic and endoscopic “chopstick” technique removal of choroid plexus papilloma in the third ventricle of an infant: a case report with systematic review of literature

BackgroundChoroid plexus papilloma (CPP) is rare and even rarer in infants and young children, and it usually occurs in the ventricles. Due to the physical peculiarities of infants, tumor removal by microscopic or endoscopic surgery alone is difficult.Case PresentationA 3-month-old patient was found to have an abnormally enlarged head circumference for 7 days. Cranial magnetic resonance imaging (MRI) examination revealed a lesion in the third ventricle. The patient underwent combined microscopic and endoscopic “chopstick” technique to remove the tumor. He recovered well after the surgery. Postoperative pathological examination revealed CPP. Postoperative MRI suggested total resection of the tumor. Follow-up for 1 month showed no recurrence or distant metastasis.ConclusionsCombined microscopic and endoscopic “chopstick” technique may be a suitable approach to remove tumors in infant ventricles

Research progress on the mechanism of food-derived antihypertensive peptides

In this review, several mechanisms of antihypertensive peptides derived from food and its by-products were summarized. Mechanisms based on the RAAS system such as ACE/Ang Ⅱ/AT1R signaling pathways and ACE2/Ang (1-7)/MasR signaling pathways were included. Mechanisms targeting at KNOS system including PI3K/Akt/eNOS signaling pathway, PPAR-γ/caspase3/MAPK/eNOS signaling pathway and L-type Ca2+ channel were also discussed. In addition, the pathways of reducing blood pressure by inhibiting endothelin-converting enzyme (ECE) activity discovered in recent years were also introduced

Pathological demand avoidance: my thoughts on looping effects and commodification of autism

Hacking suggests autism is a human kind, and has used autism to discuss their evolution over time. Looping effects caused the autism human kind to evolve since 1995, with people identifying with the autism human kind, and the commodification of the autism human kind by the autism industry. Pathological demand avoidance (PDA) was created from the looping effects controlled by the autism industry. This has undermined autism self-advocacy by supporting the medical paradigm of the autism human kind. By refusing to engage with PDA, people of the autism human kind limit the commodification of autism; creating greater emancipation

Zearalenone Promotes Cell Proliferation or Causes Cell Death?

Citation: Zheng, W.; Wang, B.; Li, X.; Wang, T.; Zou, H.; Gu, J.; Yuan, Y.; Liu, X.; Bai, J.; Bian, J.; Liu, Z. Zearalenone Promotes Cell Proliferation or Causes Cell Death? Toxins 2018, 10, 184.Zearalenone (ZEA), one of the mycotoxins, exerts different mechanisms of toxicity in different cell types at different doses. It can not only stimulate cell proliferation but also inhibit cell viability, induce cell apoptosis, and cause cell death. Thus, the objective of this review is to summarize the available mechanisms and current evidence of what is known about the cell proliferation or cell death induced by ZEA. An increasing number of studies have suggested that ZEA promoted cell proliferation attributing to its estrogen-like effects and carcinogenic properties. What’s more, many studies have indicated that ZEA caused cell death via affecting the distribution of the cell cycle, stimulating oxidative stress and inducing apoptosis. In addition, several studies have revealed that autophagy and some antioxidants can reverse the damage or cell death induced by ZEA. This review thoroughly summarized the metabolic process of ZEA and the molecular mechanisms of ZEA stimulating cell proliferation and cell death. It concluded that a low dose of ZEA can exert estrogen-like effects and carcinogenic properties, which can stimulate the proliferation of cells. While, in addition, a high dose of ZEA can cause cell death through inducing cell cycle arrest, oxidative stress, DNA damage, mitochondrial damage, and apoptosis