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Background: Early detection of ophthalmic conditions such as diabetic retinopathy (DR) and glaucoma is crucial to preventing vision loss. Previous studies have evaluated teleretinal screening programs for DR in well-insured populations. The purpose of this retrospective study was to evaluate a teleretinal screening program in a population of uninsured and underinsured patients seen in a Federally Qualified Health Center (FQHC). Methods: We conducted a retrospective chart review of patients (age ≥ 18) who underwent teleretinal imaging (TRI) at a FQHC between January 2015 and September 2019. TRI gradings and patient demographic and clinical information were abstracted. Factors associated with referral for a dilated eye exam by an ophthalmologist, adherence to recommended follow-up dilated eye exam, and ophthalmology visit attendance were examined. Results: 3130 TRIs were graded in 2216 eyes (1107 patients). 65.2% (N = 722) self-identified as Hispanic and 56.3% (N = 623) required interpreter services. Follow-up dilated fundus examination (DFE) was recommended for 388 TRIs, 49% (N = 190) of which were completed within 1 year. Adherence to the recommended ophthalmology exam was not associated with any baseline clinical or demographic characteristics (p > 0.05). Older age, male sex, hypertension, proteinuria, and higher A1c were significantly associated with greater odds of ophthalmology referral based on TRI (all p < 0.05), after adjusting for covariates. Less severe diabetic retinopathy, no insurance coverage, and Hispanic ethnicity were associated with lower odds of attending an ophthalmology visit, regardless of follow-up recommendations based on TRI (all p < 0.05). Conclusion: In an FQHC serving predominantly uninsured and underinsured patients, only 49% of recommended DFE were completed within one year. Less severe diabetic retinopathy, lack of insurance coverage, and Hispanic ethnicity were associated with a lower likelihood of having a DFE regardless of recommendation. These results suggest that greater system-level efforts are needed to increase adherence to follow-up eye exams after TRI to ensure sight-saving care for underserved populations. [ABSTRACT FROM AUTHOR]

This study uses organosilane waste, a byproduct of the organosilane industry, to produce SiC particles through an accessible and effective method. Thermodynamic analysis was adopted to provide evidence of this route followed by exploring the effects of carbon content, time and temperature on SiC purity, crystallinity of, and the Si recovery ratio. The maximum purity of SiC of 88.4% and Si recovery of 95% was achieved at a temperature of 1750 °C, time of 45 min, and sludge waste: petroleum coke ratio of 2.8:1. The mechanism of the associated reaction is explained in three parts: phase separation of SiOC, nucleation in Si melt and carbothermal reduction of SiO 2. This sustainable approach repurposes sludge waste, which contributes to environmental preservation and resource efficiency. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a neurodegenerative disease that causes dementia. While molecular basis of AD is not fully understood, genetic factors are expected to participate in the development and progression of the disease. Our goal was to uncover novel genetic underpinnings of Alzheimer's disease with a bioinformatics approach that accounts for tissue specificity. Findings: We performed genome-wide association studies (GWAS) for hippocampal volume in two Alzheimer's Disease Neuroimaging Initiative (ADNI) cohorts. We used these GWAS in a subsequent tissue-specific network-wide association study (NetWAS), which applied nominally significant associations in the initial GWAS to identify disease relevant patterns in a functional network for the hippocampus. We compared prioritized gene lists from NetWAS and GWAS with literature curated AD-associated genes from the Online Mendelian Inheritance in Man (OMIM) database. In the ADNI-1 GWAS, where we also observed an enrichment of low p-values, NetWAS prioritized disease-gene associations in accordance with OMIM annotations. This was not observed in the ADNI-2 dataset. We provide source code to replicate these analyses as well as complete results under permissive licenses. Conclusions: We performed the first analysis of hippocampal volume using NetWAS, which uses machine learning algorithms applied to tissue-specific functional interaction network to prioritize GWAS results. Our findings support the idea that tissue-specific networks may provide helpful context for understanding the etiology of common human diseases and reveal challenges that network-based approaches encounter in some datasets. Our source code and intermediate results files can facilitate the development of methods to address these challenges. [ABSTRACT FROM AUTHOR]

Preparation of cow dung briquette • Cow dung briquette (CDB) was prepared by the cold-press briquetting technology. • The co-combustion behavior of cow dung and coal was investigated by a TG-DTG. • The effect of acidified CaO as desulphurizer on the combustion was determined. • Cow dung briquette has lower smokes, higher desulphurization and easier flaming. Transformation of agricultural wastes into biomass energy is a strategy towards the development of alternative energy sources. In this study, the effect of the additives on combustion performance of cow dung briquette was investigated. Cow dung briquette (CDB) was prepared using the cold-press briquetting technology by mixing of coal and cow dung as raw materials, composite of potassium nitrate, manganese dioxide and citric acid as combustion promoter, mixture of calmogastrin and molybdenum as smoking suppressor, sodium humate and red clay as binder and acidified calcium oxide as desulphurizer. The comprehensive combustion characteristic index (S N), the stable burning characteristic index (D W) and the burnout index (C b) of CDB were calculated by thermogravimetric analysis. The desulphurizing property of CDB was examined. When the mass ratio of cow dung to coal is 1:3-4, the mass content of binder, combustion promoter, smoke suppressor and desulphurizer are 17.0%, 6.0%, 4.5% and 6.5%, respectively, the calorific value of CDB is 19.1 MJ/kg, ash content is 29.5%, volatile matter is 13.0% and desulphurization rate can be reached to 70.02%. [ABSTRACT FROM AUTHOR]

Central retinal artery occlusion (CRAO; retinal stroke or eye stroke) is an under-recognized, disabling form of acute ischemic stroke which causes severe visual loss in one eye. The classical risk factor for CRAO is ipsilateral carotid stenosis; however, nearly half of patients with CRAO do not have high-grade carotid stenosis, suggesting that other cardiovascular risk factors may exist for CRAO. Specifically, prior studies have suggested that cardioembolism, driven by underlying atrial fibrillation, may predispose patients to CRAO. We describe the design of an observational, population-based study in this protocol. We evaluate two specific objectives: 1) To determine if atrial fibrillation is an independent risk factor for CRAO after adjusting for medical and cardiovascular risk; 2) To determine if use of oral anticoagulation can modify the risk of CRAO for patients with atrial fibrillation. This protocol lays out our strategy for cohort definition, case and control definition, comorbidity ascertainment, and statistical methods. [ABSTRACT FROM AUTHOR]

Recently, increasing evidence has indicated lncRNAs are powerful regulators in the progression of multiple tumors. Dysregulation of lncRNA NEAT1 has been recognized in many cancer types. Meanwhile, the studies on NEAT1 function have suggested that NEAT1 can serve as a crucial oncogene. Nevertheless, the investigation of NEAT1 in colon cancer is still few. In our study, the function of NEAT1 was studied in colon cancer. As we observed, NEAT1 level was obviously elevated in colon cancer cells. Then, HCT‐116 and SW620 cells were stably infected with shRNA‐NEAT1 for 48 hr. As exhibited, silence of NEAT1 could greatly repress colon cancer cell progression. Apoptosis of colon cancer cells was triggered and the cell cycle progression was remarkably inhibited by downregulation of NEAT1. Interestingly, as exhibited, miR‐495‐3p was obviously decreased in colon cancer cells and it significantly suppressed colon cancer progression. Subsequently, miR‐495‐3p was predicted as a target of NEAT1. CDK6 was speculated as the target of miR‐495‐3p and miR‐495‐3p modulated its expression negatively. Finally, it was indicated that NEAT1 promoted colon cancer development through modulating miR‐495‐3p and CDK6 in vivo. Taken these together, we reported that NEAT1 could sponge miR‐495‐3p to contribute to colon cancer progression through activating CDK6. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the third leading cause of cancer-associated mortality worldwide. Ginsenoside Rh1 (Rh1) is a traditional medicine monomer with antitumor activity; however, the effects of Rh1 in CRC remain to be determined. In the present study, SW620 cells were treated with different concentrations of Rh1. Cell Counting Kit-8, wound healing and Transwell assays were performed to measure cell viability and proliferation, migration and invasion, respectively. Subsequently, the mRNA expression levels of matrix metallopeptidase (MMP)1, MMP3 and tissue inhibitor of metalloproteinases 3 (TIMP3) were detected by reverse transcription-quantitative PCR analysis. In addition, the protein expression levels of MMP1, MMP3, TIMP3, and total or phosphorylated (p-)ERK1/2, P38, JNK were detected by western blotting. Furthermore, tumor growth was examined in a nude mouse xenograft model. The results of the present study indicated that Rh1 was not toxic to CRC cells at various concentrations (0, 50 or 100 µM) and treatment durations (24 or 48 h). However, cell proliferation was suppressed by Rh1 in a dose-dependent manner. Rh1 (100 µM) significantly inhibited cell migration and invasion in vitro. Additionally, Rh1 suppressed the mRNA and protein expression of MMP1 and MMP3, and promoted TIMP3 expression. Rh1 decreased the ratios of p-P38/P38, p-ERK1/2/ERK1-2 and p-JNK/JNK in vitro and in vivo, which suggested that Rh1 inactivated the mitogen-activated protein kinase (MAPK) signaling pathway. Notably, Rh1 markedly decreased tumor volume and weight in vivo. In conclusion, the present study demonstrated that Rh1 inhibited the proliferation, migration and invasion of CRC cells in vitro and tumor growth in vivo. This inhibition was at least partially due to the inhibition of MMP1 and MMP3 expression, the increase in TIMP3 expression level and the MAPK signaling pathway inactivation. Therefore, Rh1 may effectively inhibit the development of CRC as an anticancer drug, and may have a supporting effect during CRC treatment. [ABSTRACT FROM AUTHOR]

This study aimed to identify potential biomarkers and the therapeutic targets for colorectal adenocarcinoma by systematically evaluate a large scale of long noncoding RNAs (lncRNAs) expression data from TCGA. The algorithm t‐distributed stochastic neighbor embedding and hierarchical clustering were utilized to group the samples into three clusters that showed a different prognosis. To identify the relationship between the clustered groups and different histoclinical features, different statistical methods were used. The functions of LINC01234 and MIR210HG were investigated with the help of the public database. The results showed that the expression levels of lncRNAs were able to distinguish the tumor samples from the normal tissues and in further they were able to predict the prognosis of the patients. We proposed two potential lncRNAs, which might serve as a biomarker or therapeutic targets. LINC01234 can be a good biomarker. In contrast, MIR210HG participated in the progression of colorectal adenocarcinoma by regulating hypoxia. It might function through an lncRNA–microRNA–messenger RNA regulatory network with MIR210 and RASSF7. [ABSTRACT FROM AUTHOR]

• MiR-150 was down-regulated in colorectal cancer. • Overexpression of miR-150 repressed colorectal cancer in vitro and in vivo. • β-catenin was the target of miR-150. Colorectal cancer remains as a serious global cause of morbidity and mortality. The current therapies for colorectal cancer treatment are still unsatisfactory and thus, identification of novel targets is an urgent requisite. Recent evidence has reported miRNAs are closely correlated with colorectal cancer development. miR-150 has been identified in tumor progression in various cancers. Nevertheless, its roles in colorectal cancer remain poorly known. In our study, a decreased miR-150 expression in colorectal cancer tissues and cells was observed. Meanwhile, we reported a negative correlation between miR-150 and β-catenin in colorectal cancer. β-catenin can participate in the physiological mechanism of many types of cancers. Then, miR-150 was overexpression in SW480 and HT-29 cells and it was show that miR-150 repressed SW480 and HT-29 cell viability, proliferation and colony formation capacity. Moreover, colorectal cancer cell progression was triggered by the inhibition of miR-150 via negatively regulating β-catenin. Subsequently, the direct binding correlation between miR-150 and β-catenin was demonstrated. β-catenin, c-myc and CyclinD1 level was significantly restrained by the up-regulation of miR-150 in SW480 and HT-29 cells. Finally, it was proved that miR-150 depressed colorectal cancer growth through modulating β-catenin in vivo. Overall, it was implied that miR-150 could inhibit colorectal cancer progression and serve as a tumor suppressor via inactivating β-catenin pathway. [ABSTRACT FROM AUTHOR]

Breast cancer is one of the most prevalent malignancies and the leading cause of cancer‑associated mortality in women worldwide and in China. Everolimus (C53H83NO14) is an efficient anti‑cancer drug for breast cancer which targets mammalian target of rapamycin (mTOR). The present study investigated the inhibitory effects of everolimus on breast cancer cells and an MCF‑7‑bearing mouse model. The potential mechanism of the everolimus‑mediated decrease in growth and aggressiveness of breast cancer cells was reported. Results demonstrated that everolimus significantly inhibited breast cancer cell growth, migration and invasion. It was demonstrated that everolimus induced apoptosis through decreasing B cell lymphoma (Bcl)‑2 and Bcl‑w and increasing caspase‑3 and caspase‑8 expression levels in breast cancer cells. It was observed that everolimus decreased phosphoinositide 3‑kinase (PI3K), protein kinase B (AKT) and mTOR expression levels in breast cancer cells. Results additionally demonstrated that PI3 K overexpression prevented that everolimus‑mediated inhibition of growth and aggressiveness in MCF‑7 cells. In vivo assays demonstrated that everolimus treatment markedly inhibited tumor growth in the MCF‑7 bearing mouse model. Overall, these data indicate that everolimus inhibits growth and aggressiveness of breast cancer cells through the PI3K/AKT/mTOR signaling pathways, suggesting the PI3K/AKT/mTOR signaling pathway may act as a therapeutic target for the treatment of human cancer. [ABSTRACT FROM AUTHOR]