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Abstract: An electrostatic self-assembly approach was employed to prepare Fe3O4/graphene oxide nanocomposites, and their application in the magnetic solid-phase extraction of polycyclic aromatic hydrocarbons from environmental samples was investigated. With the highly hydrophilic graphene oxide sheets and positively charged surface of the Fe3O4 nanoparticles, the nanocomposites were synthesized through electrostatic interaction in aqueous solution. Simultaneously, the different loading amounts of Fe3O4 onto the graphene oxide were easily controlled by changing the proportion of the initial precursors. The identity of the hybrid materials was confirmed using transmission electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy and a vibrating sample magnetometer. Five polycyclic aromatic hydrocarbons were selected as model analytes to validate the extraction performance of the Fe3O4/GO nanocomposite as a MSPE sorbent. The excellent adsorption property was attributed to the dominant roles of π–π stacking interaction and hydrophobic interaction. After optimizing the conditions, the results indicated that the recoveries of these compounds were in the range of 76.8–103.2%, with relative standard deviations ranging between 1.7% and 11.7%; the limits of detection were in the range of 0.09–0.19ngmL−1. [Copyright &y& Elsevier]

Objective: To conduct a literature survey of COVID-19-related chronic diseases to inform future research., Methods: Publications on COVID-19 and chronic disease were retrieved from PubMed using MeSH Major Topic, including the terms COVID-19, SARS-CoV-2, Chronic Disease and Noncommunicable Diseases. Bibliometric features, journals, research areas, countries, funding agencies and citation reports, were extracted from Web of Science and highly cited papers identified and summarized. Fisher's exact probability test was used to associate highly cited papers with countries., Results: A total of 1034 English-language publications were included. Urology/nephrology was the most active research area (n=230), PLOS ONE the most frequently involved journal (n=29) and the United States of America (USA) had the greatest research output (n=223). A medium number of publications were in the areas of hematology and immunology and these papers had a high citation rate. No statistically significant difference was found in the ratio of highly cited papers: total papers across high-output countries (P=0.668). The USA, Europe and China were the sources of the most highly cited articles and productive funding agencies., Conclusions: The influence of COVID-19 on chronic disease has received considerable attention. Hematology and immunology may continue to be productive research fields. Much research remains to be done to characterize the emerging chronic effects of COVID-19 on human health., Competing Interests: None., (AJTR Copyright © 2023.)

Recent evidence suggests the commensal microbiome regulates host immunity and influences brain function; findings that have ramifications for neurodegenerative diseases. In the context of Alzheimer's disease (AD), we previously reported that perturbations in microbial diversity induced by life-long combinatorial antibiotic (ABX) selection pressure in the APP SWE /PS1 ΔE9 mouse model of amyloidosis is commensurate with reductions in amyloid-β (Aβ) plaque pathology and plaque-localised gliosis. Considering microbiota-host interactions, specifically during early post-natal development, are critical for immune- and neuro-development we now examine the impact of microbial community perturbations induced by acute ABX exposure exclusively during this period in APP SWE /PS1 ΔE9 mice. We show that early post-natal (P) ABX treatment (P14-P21) results in long-term alterations of gut microbial genera (predominantly Lachnospiraceae and S24-7) and reduction in brain Aβ deposition in aged APP SWE /PS1 ΔE9 mice. These mice exhibit elevated levels of blood- and brain-resident Foxp3 + T-regulatory cells and display an alteration in the inflammatory milieu of the serum and cerebrospinal fluid. Finally, we confirm that plaque-localised microglia and astrocytes are reduced in ABX-exposed mice. These findings suggest that ABX-induced microbial diversity perturbations during post-natal stages of development coincide with altered host immunity mechanisms and amyloidosis in a murine model of AD.

Objective: To assess the advantages and nursing experience of foley catheter for nephrostomy tube after minimally invasive percutaneous nephrolithotomy (mPCNL).
 Methods: From October 2015 to April 2016, the clinical data of 137 patients, who were diagnosed with upper urinary tract calculi and need to perform mPCNL, were collected and randomized into 2 groups: a foley catheter group (research group, n=69) and a normal nephrostomy tube group (control group, n=68). The patients in research group used foley catheter for nephrostomy tube, while those in the control group used normal nephrostomy tube. Bleeding volume, the days of bleeding, pipes shedding and pain degree were compared, and the experience of the nursing process was summarized.
 Results: The bleeding volume, the days of bleeding in the research group were significantly lower than those in the control group (both P<0.01). The pipes shedding rate in the research group were lower than that in the control group (P<0.05). There was no significant difference in postoperative pain scores between the 2 groups (P>0.05). There was no other complications and discomfortable symptoms in the experimental group.
 Conclusion: The use of foley catheter for nephrostomy tube after mPCNL is safe, and it can decrease the bleeding volume and pipes shedding rate. It doesn't increase the patient's postoperative pain and can reduce the difficulty and risk for postoperative nursing.

Rare, familial, early-onset autosomal dominant forms of familial Alzheimer's disease (FAD) are caused by mutations in genes encoding β-amyloid (Aβ) precursor protein (APP), presenilin-1 (PS1), and presenilin-2. Each of these genes is expressed ubiquitously throughout the CNS, but a widely held view is that excitatory neurons are the primary (or sole) source of the Aβ peptides that promote synaptic dysfunction and neurodegeneration. These efforts notwithstanding, APP and the enzymes required for Aβ production are synthesized by many additional cell types, and the degree to which those cells contribute to the production of Aβ that drives deposition in the CNS has not been tested. We generated transgenic mice in which expression of an ubiquitously expressed, FAD-linked mutant PSEN1 gene was selectively inactivated within postnatal forebrain excitatory neurons, with continued synthesis in all other cells in the CNS. When combined with an additional transgene encoding an FAD-linked APP "Swedish" variant that is synthesized broadly within the CNS, cerebral Aβ deposition during aging was found to be unaffected relative to mice with continued mutant PS1 synthesis in excitatory neurons. Thus, Aβ accumulation is non-cell autonomous, with the primary age-dependent contribution to cerebral Aβ deposition arising from mutant PS1-dependent cleavage of APP within cells other than excitatory neurons.

The vast majority of pedigrees with familial Alzheimer's disease (FAD) are caused by inheritance of mutations in the PSEN1 1 gene. While genetic ablation studies have revealed a role for presenilin 1 (PS1) in embryonic neurogenesis, little information has emerged regarding the potential effects of FAD-linked PS1 variants on proliferation, self-renewal and differentiation, key events that control cell fate commitment of adult brain neural progenitors (NPCs). We used adult brain subventricular zone (SVZ)-derived NPC cultures transduced with recombinant lentivirus as a means to investigate the effects of various PS1 mutants on self-renewal and differentiation properties. We now show that viral expression of several PS1 mutants in NPCs leads to impaired self-renewal and altered differentiation toward neuronal lineage, in vitro. In line with these observations, diminished constitutive proliferation and steady-state SVZ progenitor pool size was observed in vivo in transgenic mice expressing the PS1DeltaE9 variant. Moreover, NPC cultures established from the SVZ of adult mice expressing PS1DeltaE9 exhibit reduced self-renewal capacity and premature exit toward neuronal fates. To these findings, we show that both the levels of endogenous Notch/CBF-1-transcriptional activity and transcripts encoding Notch target genes are diminished in SVZ NPCs expressing PS1DeltaE9. The deficits in self-renewal and multipotency are restored by expression of Notch1-ICD or a downstream target of the Notch pathway, Hes1. Hence, we argue that a partial reduction in PS-dependent gamma-secretase processing of the Notch, at least in part, accounts for the impairments observed in SVZ NPCs expressing the FAD-linked PS1DeltaE9 variant.