Understanding the epidemic of chronic kidney disease of uncertain etiology may be critical for health policies and public health responses. Recent studies have shown that microplastics (MPs) ...contaminate our food chain and accumulate in the gut, liver, kidney, muscle, and so on. Humans manufacture many plastics-related products. Previous studies have indicated that particles of these products have several effects on the gut and liver. Polystyrene (PS)-MPs (PS-MPs) induce several responses, such as oxidative stress, and affect living organisms.
The aim of this study was to investigate the effects of PS-MPs in kidney cells
and
.
PS-MPs were evaluated in human kidney proximal tubular epithelial cells (HK-2 cells) and male C57BL/6 mice. Mitochondrial reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, inflammation, and autophagy were analyzed in kidney cells.
, we evaluated biomarkers of kidney function, kidney ultrastructure, muscle mass, and grip strength, and urine protein levels, as well as the accumulation of PS-MPs in the kidney tissue.
Uptake of PS-MPs at different concentrations by HK-2 cells resulted in higher levels of mitochondrial ROS and the mitochondrial protein Bad. Cells exposed to PS-MPs had higher ER stress and markers of inflammation. MitoTEMPO, which is a mitochondrial ROS antioxidant, mitigated the higher levels of mitochondrial ROS, Bad, ER stress, and specific autophagy-related proteins seen with PS-MP exposure. Furthermore, cells exposed to PS-MPs had higher protein levels of LC3 and Beclin 1. PS-MPs also had changes in phosphorylation of mitogen-activated protein kinase (MAPK) and protein kinase B (AKT)/mitogen-activated protein kinase (mTOR) signaling pathways. In an
study, PS-MPs accumulated and the treated mice had more histopathological lesions in the kidneys and higher levels of ER stress, inflammatory markers, and autophagy-related proteins in the kidneys after PS-MPs treatment by oral gavage.
The results suggest that PS-MPs caused mitochondrial dysfunction, ER stress, inflammation, and autophagy in kidney cells and accumulated in HK-2 cells and in the kidneys of mice. These results suggest that long-term PS-MPs exposure may be a risk factor for kidney health. https://doi.org/10.1289/EHP7612.
Celotno besedilo
Dostopno za:
CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
Quantum dots (QDs) have shown great potential for next generation displays owing to their fascinating optoelectronic characteristics. In this work, we present a novel full-color display based on blue ...organic light emitting diodes (BOLEDs) and patterned red and green QD color conversion layers (CCLs). To enable efficient blue-to-green or blue-to-red photoconversion, micrometer-thick QD films with a uniform surface morphology are obtained by utilizing UV-induced polymerization. The uniform QD layers are directly inkjet printed on red and green color filters to further eliminate the residual blue emissions. Based on this QD-BOLED architecture, a 6.6-inch full-color display with 95% Broadcasting Service Television 2020 (BT.2020) color gamut and wide viewing-angles is successfully demonstrated. The inkjet printing method introduced in this work provides a cost-effective way to extend the applications of QDs for full-color displays.
We proposed a new full-color display framework QD-OLEDs, where blue OLEDs are used as pump light, and red and green QDs are printed on color filters as color conversion layers.
Oral submucous fibrosis (OSF) stands as a progressive oral ailment, designated as a potentially malignant disorder. OSF has gained widespread recognition as a significant precursor to malignant ...transformation. In the pursuit of dependable, straightforward, and non-invasive diagnostic measures for the early detection of oral malignant progression, research has delved into potential diagnostic biomarkers of OSF. This comprehensive review delves into current investigations that explore the correlation between various biomarkers and OSF. The molecular biomarkers of OSF are categorized based on cytology and sampling methods. Moreover, this review encompasses pertinent studies detailing how these biomarkers are acquired and processed. Within this scope, we scrutinize four potential biomarkers that hold the promise of facilitating the development of diagnostic tools for detecting early-stage OSF.
Identification of patients at risk of death from cancer surgery should aid in preoperative preparation. The purpose of this study is to assess and adjust the age-adjusted Charlson comorbidity index ...(ACCI) to identify cancer patients with increased risk of perioperative mortality.
We identified 156,151 patients undergoing surgery for one of the ten common cancers between 2007 and 2011 in the Taiwan National Health Insurance Research Database. Half of the patients were randomly selected, and a multivariate logistic regression analysis was used to develop an adjusted-ACCI score for estimating the risk of 90-day mortality by variables from the original ACCI. The score was validated. The association between the score and perioperative mortality was analyzed.
The adjusted-ACCI score yield a better discrimination on mortality after cancer surgery than the original ACCI score, with c-statics of 0.75 versus 0.71. Over 80 years of age, 70-80 years, and renal disease had the strongest impact on mortality, hazard ratios 8.40, 3.63, and 3.09 (P < 0.001), respectively. The overall 90-day mortality rates in the entire cohort varied from 0.9%, 2.9%, 7.0%, and 13.2% in four risk groups stratifying by the adjusted-ACCI score; the adjusted hazard ratio for score 4-7, 8-11, and ≥ 12 was 2.84, 6.07, and 11.17 (P < 0.001), respectively, in 90-day mortality compared to score 0-3.
The adjusted-ACCI score helps to identify patients with a higher risk of 90-day mortality after cancer surgery. It might be particularly helpful for preoperative evaluation of patients over 80 years of age.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Chronic obstructive pulmonary disease (COPD) is a progressive, life-threatening lung disease with increasing prevalence and incidence worldwide. Increasing evidence suggests that lung microbiomes ...might play a physiological role in acute exacerbations of COPD. The objective of this study was to characterize the association of the microbiota and exacerbation risk or airflow limitation in stable COPD patients.
The sputum microbiota from 78 COPD outpatients during periods of clinical stability was investigated using 16S rRNA V3-V4 amplicon sequencing. The microbiome profiles were compared between patients with different risks of exacerbation, i.e., the low risk exacerbator (LRE) or high risk exacerbator (HRE) groups, and with different airflow limitation severity, i.e., mild to moderate (FEV1 ≥ 50; PFT I) or severe to very severe (FEV1 < 50; PFT II).
The bacterial diversity (Chao1 and observed OTUs) was significantly decreased in the HRE group compared to that in the LRE group. The top 3 dominant phyla in sputum were Firmicutes, Actinobacteria, and Proteobacteria, which were similar in the HRE and LRE groups. At the genus level, compared to that in the LRE group (41.24%), the proportion of Streptococcus was slightly decreased in the HRE group (28.68%) (p = 0.007). However, the bacterial diversity and the proportion of dominant bacteria at the phylum and genus levels were similar between the PFT I and PFT II groups. Furthermore, the relative abundances of Gemella morbillorum, Prevotella histicola, and Streptococcus gordonii were decreased in the HRE group compared to those in the LRE group according to linear discriminant analysis effect size (LEfSe). Microbiome network analysis suggested altered bacterial cooperative regulation in different exacerbation phenotypes. The proportions of Proteobacteria and Neisseria were negatively correlated with the FEV1/FVC value. According to functional prediction of sputum bacterial communities through Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) analysis, genes involved in lipopolysaccharide biosynthesis and energy metabolism were enriched in the HRE group.
The present study revealed that the sputum microbiome changed in COPD patients with different risks of exacerbation. Additionally, the bacterial cooperative networks were altered in the HRE patients and may contribute to disease exacerbation. Our results provide evidence that sputum microbiome community dysbiosis is associated with different COPD phenotypes, and we hope that by understanding the lung microbiome, a potentially modifiable clinical factor, further targets for improved COPD therapies during the clinically stable state may be elucidated.
Objectives
To determine whether periodontitis is a modifiable risk factor for dementia.
Design
Prospective cohort study.
Setting
National Health Insurance Research Database in Taiwan.
Participants
...Individuals aged 65 and older with periodontitis (n = 3,028) and an age‐ and sex‐matched control group (n = 3,028).
Measurements
Individuals with periodontitis were compared age‐ and sex‐matched controls with for incidence density and hazard ratio (HR) of new‐onset dementia. Periodontitis was defined according to International Classification of Diseases, Ninth Revision, Clinical Modification (ICD‐9‐CM) codes 523.3–5 diagnosed by dentists. To ensure diagnostic validity, only those who had concurrently received antibiotic therapies, periodontal treatment other than scaling, or scaling more than twice per year performed by certified dentists were included. Dementia was defined according to ICD‐9‐CM codes 290.0–290.4, 294.1, 331.0–331.2.
Results
After adjustment for confounding factors, the risk of developing dementia was calculated to be higher for participants with periodontitis (HR = 1.16, 95% confidence interval = 1.01–1.32, P = .03) than for those without.
Conclusion
Periodontitis is associated with greater risk of developing dementia. Periodontal infection is treatable, so it might be a modifiable risk factor for dementia. Clinicians must devote greater attention to this potential association in an effort to develop new preventive and therapeutic strategies for dementia.
IMPORTANCE: The benefits and risks associated with intensive low-density lipoprotein cholesterol (LDL-C)–lowering statin-based therapies to lessen the risk of recurrent stroke have not been ...established. OBJECTIVE: To conduct a meta-analysis of randomized clinical trials to evaluate the association of more intensive vs less intensive LDL-C–lowering statin-based therapies with outcomes for patients with ischemic stroke. DATA SOURCES: PubMed, Embase, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov were searched from January 1, 1970, to July 31, 2021. STUDY SELECTION: This meta-analysis included randomized clinical trials that compared more intensive vs less intensive LDL-C–lowering statin-based therapies and recorded the outcome of recurrent stroke among patients with stroke. DATA EXTRACTION AND SYNTHESIS: The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline was used for abstracting data and assessing data quality and validity. Relative risk (RR) with 95% CI was used as a measure of the association of more intensive vs less intensive LDL-C lowering with primary and secondary outcomes. MAIN OUTCOMES AND MEASURES: The primary outcome was recurrent stroke, and the secondary outcomes were major cardiovascular events and hemorrhagic stroke. RESULTS: The final analysis included 11 randomized clinical trials with 20 163 patients (13 518 men 67.0%; mean SD age, 64.9 3.7 years) with stroke. The mean follow-up was 4 years (range, 1-6.1 years). Pooled results showed that more intensive LDL-C–lowering statin-based therapies were associated with a reduced risk of recurrent stroke compared with less intensive LDL-C–lowering statin-based therapies (absolute risk, 8.1% vs 9.3%; RR, 0.88; 95% CI, 0.80-0.96) and that the benefit associated with these LDL-C–lowering therapies was not different among LDL-C–lowering strategies (statins vs no statins: RR, 0.90; 95% CI, 0.81-1.01; more statins or ezetimibe vs less statins or ezetimibe: RR, 0.77; 95% CI, 0.62-0.96; and proprotein convertase subtilisin/kexin type 9 inhibitors plus statins vs placebo plus statins: RR, 0.90; 95% CI, 0.71-1.15; P = .42 for interaction). More intensive LDL-C–lowering statin-based therapies were associated with a reduced risk of major cardiovascular events, but with an increased risk of hemorrhagic stroke, compared with less intensive LDL-C–lowering statin-based therapies. More intensive LDL-C–lowering statin-based therapies were associated with a reduced risk of recurrent stroke in trials with all patients having evidence of atherosclerosis (RR, 0.79; 95% CI, 0.69-0.91), but not in trials with most patients not having evidence of atherosclerosis (RR, 0.95; 95% CI, 0.85-1.07; P = .04 for interaction), compared with less intensive LDL-C–lowering statin-based therapies. CONCLUSIONS AND RELEVANCE: This study suggests that the benefits and risks of more intensive LDL-C–lowering statin-based therapies for recurrent stroke risk reduction might be more favorable than the benefits and risks of less intensive LDL-C–lowering statin-based therapies, especially for patients with evidence of atherosclerosis.
Background
The aim of this systematic review and meta‐analysis was to compare the clinical efficacy of the early dental implant placement protocol with immediate and delayed dental implant placement ...protocols.
Methods
An electronic and manual search of literature was made to identify clinical studies comparing early implant placement with immediate or delayed placement. Data from the included studies were pooled and quantitative analyses were performed for the implant outcomes reported as the number of failed implants (primary outcome variable) and for changes in peri‐implant marginal bone level, peri‐implant probing depth, and peri‐implant soft tissue level (secondary outcome variables).
Results
Twelve studies met the inclusion criteria. Significant difference in risk of implant failure was found neither between the early and immediate placement protocols (risk difference = −0.018; 95% confidence interval CI = −0.06, 0.025; P = 0.416) nor between early and delayed placement protocols (risk difference = −0.008; 95% CI = –0.044, 0.028; P = 0.670). Pooled data of changes in peri‐implant marginal bone level demonstrated significantly less marginal bone loss for implants placed using the early placement protocol compared with those placed in fresh extraction sockets (P = 0.001; weighted mean difference = −0.14 mm; 95% CI = −0.22, −0.05). No significant differences were found between the protocols for the other variables.
Conclusions
The available evidence supports the clinical efficacy of the early implant placement protocol. Present findings indicate that the early implant placement protocol results in implant outcomes similar to immediate and delayed placement protocols and a superior stability of peri‐implant hard tissue compared with immediate implant placement.
•Decreased systolic blood pressure and heart rate are observed with time.•Increased vigor and decreased negative emotions are observed in forest settings.•Increased fatigue and decreased self-esteem ...were reported in urban settings.•Greater benefits were found when immersing in forest settings.
Previous studies used pictures or movies to investigate the impact of virtual nature environments on physiological and psychological health, providing inferior immersive experiences. The latest virtual reality (VR), launched in 2016, allows users to be fully immersed in simulated surroundings. However, the effects of the simulated environments created by the latest VR technology on health were not yet known. This study employed both cross-over and pretest-posttest design to examine the influence of forest and urban VR environments on restoration (N = 30). Both physiological and psychological responses were collected. The results show that participants’ systolic blood pressure and heart rate decreased with time, regardless of environmental differences. About psychological responses, an increased level of fatigue and a decreased level of self-esteem were reported in simulated urban environments. In contrast, an increased level of vigor and a decreased level of negative emotions (i.e., confusion, fatigue, anger-hostility, tension, and depression) were observed in simulated forest environments. In sum, greater benefits were found when immersing in forest settings. The latest VR technology can serve as an alternative way to access nature environments for restoration.
An increasing amount of evidence emphasizes the role of metabolic reprogramming in immune cells to fight infections. However, little is known about the regulation of metabolite transporters that ...facilitate and support metabolic demands. In this study, we found that the expression of equilibrative nucleoside transporter 3 (ENT3, encoded by solute carrier family 29 member 3, Slc29a3) is part of the innate immune response, which is rapidly upregulated upon pathogen invasion. The transcription of Slc29a3 is directly regulated by type I interferon‐induced signaling, demonstrating that this metabolite transporter is an interferon‐stimulated gene (ISG). Suprisingly, we unveil that several viruses, including SARS‐CoV‐2, require ENT3 to facilitate their entry into the cytoplasm. The removal or suppression of Slc29a3 expression is sufficient to significantly decrease viral replication in vitro and in vivo. Our study reveals that ENT3 is a pro‐viral ISG co‐opted by some viruses to gain a survival advantage.
Synopsis
ENT3 is an IFN‐stimulated metabolite transporter in macrophages that facilitates viral genome release. Suppression of ENT3 expression is sufficient to decrease viral replication both in vitro and in vivo.
ENT3 is a fast‐responding metabolite transporter upon pathogen insults.
ENT3 is an interferon‐stimulated gene whose expression is regulated by the type I IFN‐IFNAR axis.
Viruses have co‐evolved with the host and take advantage of ENT3 for their genome release and their replication.
ENT3 is an IFN‐stimulated metabolite transporter in macrophages that facilitates viral genome release. Suppression of ENT3 expression is sufficient to decrease viral replication both in vitro and in vivo.
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