Consumption of a Taiwanese cafeteria diet induces metabolic disorders and fecal flora changes in obese rats.

OBJECTIVES: Among diet-induced obesity animal models, the cafeteria diet, which contains human junk food and processed foods, is a popular experimental animal diets in Western countries. Consumption of a cafeteria diet can lead to the development of obesity and non-alcoholic liver disease in as soon as 2 mo, which more accurately reflects human eating patterns. The aim of this study was to establish a Taiwanese cafeteria diet and compare it with a traditional lard-based, 60% high-fat diet in a 12-wk animal model. METHODS: Six-wk-old male Wistar rats were assigned to the following three groups: control diet (C; LabDiet 5001); high-fat diet (HFD; 60% HFD); and the Taiwanese cafeteria diet (CAF). RESULTS: At the end of the study, weight gain and steatosis were observed in the HF and CAF groups. Compared with the HFD group, rats in the CAF group showed significantly higher plasma triacylglycerol concentrations and insulin resistance, which may have been correlated with increased inflammatory responses. Significantly lower hepatic sterol regulatory element-binding protein-1c and insulin receptor substrate-1 protein expressions were observed in the CAF group compared with the HFD group. Additionally, disruption of the microbiotic composition followed by increased obesity-related bacteria was observed in the CAF group. CONCLUSIONS: The present study confirmed that the Taiwanese cafeteria diet-induced rat model provided a potential platform for investigating obesity-related diseases.

Overexpression of zinc-finger protein 677 inhibits proliferation and invasion by and induces apoptosis in clear cell renal cell carcinoma.

Recent studies have demonstrated that zinc-finger protein 677 (ZNF677) acts as a tumor suppressor gene in cancer. However, the expression and function of ZNF677 in clear cell renal cell carcinoma (ccRCC) are still unclear. In this study, we used bioinformatics analysis and in vitro experiments to investigate the expression of ZNF677 in ccRCC tissues and the malignant biological behavior of ZNF677 in 786-0 cells. We demonstrated that ZNF677 is hypermethylated in ccRCC and is associated with clinicopathological features. The results of the functional assays indicate that ZNF677 inhibits tumor cell proliferation and invasion and induces apoptosis. Further prognostic analysis indicated that low expression of ZNF677 is associated with shorter overall survival. Additionally, ZNF677 overexpression suppressed the invasion and epithelial-mesenchymal transition of 786-0 cells by inactivating the PI3K/AKT signaling pathway. This is the first report to evaluate the influence of ZNF677 on ccRCC cells malignant biological behavior. The results indicate that high expression of ZNF677 could be considered as a favorable prognostic indicator for ccRCC.

Higher frequency electrical stimulation enhanced myloglossus satellite cell differentiation by upregulating expression of Pax7 mRNA, MyoD, myogenin and MyHC protein.

OBJECTIVE: We investigated the effect of electrical stimulation (ES) of varying pulse frequency on differentiation and proliferation of canine myloglossus satellite cells in vitro. MATERIALS AND METHODS: Cellular viability and proliferation were assayed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay and flow cytometry fluorescence-activated cell sorting analysis. Cellular differentiation and expression of mark molecule were assayed by Real Time-PCR and Western blot. RESULTS: With increasing frequency ES, we found a significant increase in Myod (r=0.988, p<0.0001), myogenin (r=0.988, p<0.0001), MyHC-slow (r=0.988, p<0.0001), MyHC-fast (r=0.875, p<0.0001) protein expression, and Pax7 mRNA expression (r=0.712, p=0.001). CONCLUSIONS: Pax7 mRNA expression and MyoD, myogenin, and MyHC protein expression were increased with increment of electrical stimulation frequency in myloglossus muscle satellite. Higher frequency ES enhanced myloglossus satellite cell differentiation, not proliferation and viability.

[shRNA-Mediated Suppression of γ-Synuclein Leading to Downregulation of p38/ERK/JNK Phosphorylation and Cell Cycle Arrest in Endometrial Cancer Cells].

In this study, we explored the effects of treating human endometrial cancer cells with γ-synuclein-specific short hairpin RNA (shRNA) and elucidated the associated mechanisms in vitro and in vivo through the p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) signaling pathways. Cell proliferation and migration were assessed using CCK8, Transwell, and scratch wound healing assays. Flow cytometry and laser scanning confocal microscopy were used to detect cell cycle changes. Relative levels of phosphorylated and non-phosphorylated (p) p38, ERK1/2 and JNK1/2/3 were determined in vitro and in vivo using simple western blotting assays. Cell proliferation in the experimental group decreased significantly and cells transfected with shRNA showed reduced migration rates (P < 0.05). p-p38, p-ERK1/2, and p-JNK1/2/3 levels were downregulated in the experimental group in vitro and in vivo. Tumor volumes and weights in the experimental group were significantly lower (P < 0.05). Tumor formation time in the negative control group was significantly shorter (P < 0.05). Flow cytometry showed that the number of cells in the G1 and mitotic phases increased and that in the S phase decreased after SNCG silencing (P < 0.05). Confocal microscopy showed that the percentage of cells in the mitotic phase increased after SNCG gene silencing (P < 0.05). We conclude that shRNA-mediated suppression of γ-synuclein decreased the proliferation, migration, and tumorigenicity of endometrial cancer cells via downregulation of p38, ERK, and JNK phosphorylation. High SNCG expression is closely related to the growth cycle of endometrial cancer cells.

i-SATA: A MATLAB based toolbox to estimate current density generated by transcranial direct current stimulation in an individual brain.

OBJECTIVE: Transcranial Direct Current Stimulation (tDCS) is a technique where a weak current is passed through the electrodes placed on the scalp. The distribution of the electric current induced in the brain due to tDCS is provided by simulation toolbox like Realistic volumetric Approach based Simulator for Transcranial electric stimulation (ROAST). However, the procedure to estimate the total current density induced at the target and the intermediary region of the cortex is complex. The Systematic-Approach-for-tDCS-Analysis (SATA) was developed to overcome this problem. However, SATA is limited to standardized (MNI152) headspace only. Here we develop individual-SATA (i-SATA) to extend it to individual head. APPROACH: T1-weighted images of 15 subjects were taken from two Magnetic Resonance Imaging scanners of different strengths. Across the subjects, the montages were simulated in ROAST. i-SATA converts the ROAST output to Talairach space. The x, y and z coordinates of the anterior commissure (AC), posterior commissure (PC), and Mid-Sagittal (MS) points are necessary for the conversion. AC and PC are detected using the acpcdetect toolbox. We developed a method to determine the MS in the image and cross-verified its location manually using BrainSight®. MAIN RESULTS: Determination of points with i-SATA is fast and accurate. The i-SATA provided estimates of the current-density induced across an individual's cortical lobes and gyri as tested on images from two different scanners. SIGNIFICANCE: Researchers can use i-SATA for customizing tDCS-montages. With i-SATA it is also easier to compute the inter-individual variation in current-density across the target and intermediary regions of the brain. The software is publicly available.

Characterization of hsa_circ_0000594 as a new biomarker and therapeutic target for hepatoblastoma.

OBJECTIVE: Various studies have shown that aberrant expression of circular RNAs (circRNAs) has a pivotal role in multifarious cancers. However, the role of circRNAs in hepatoblastoma (HB) is not clearly understood. In the present study, we attempted to explore the underlying mechanism of hsa_cric_0000594 in HB along with its clinical importance. PATIENTS AND METHODS: In our research, the expression pattern of hsa_circ_0000594 in HB tissues and matched normal liver tissues was determined by in situ hybridization and RT-qPCR. Proliferation, viability, migration, and apoptosis of HB cell lines were detected via Cell Counting Kit-8 (CCK-8), colony formation, transwell, and flow cytometry assays. The interaction of hsa_circ_0000594 with miR-217 was investigated by Dual-Luciferase reporter assay. RESULTS: Expression levels of hsa_circ_0000594 were significantly upregulated in HB tissues compared with those in paired normal liver tissues and showed a clear association with the subtype of HB. The knockdown of hsa_circ_0000594 inhibited the malignant phenotype of HB. Bioinformatics analysis suggests that sirtuin 1 (SIRT1) may serve as a target gene of miR-217. CONCLUSIONS: Mechanically, hsa_circ_0000594 was identified to have a critical role in HB development through the hsa_circ_0000594/mir-217/SIRT1 regulatory axis, which might become a novel diagnostic marker and potential therapeutic target in HB.

LKB1 deficiency promotes proliferation and invasion of glioblastoma through activation of mTOR and focal adhesion kinase signaling pathways.

Liver kinase B1 (LKB1), a serine/threonine kinase, is frequently inactivated in several types of human cancers. To date, inactivation of LKB1 tumor suppressor has rarely been reported in glioblastoma. In this study, we investigated LKB1 status, biological significance, and therapeutic implications in glioblastoma. Loss of LKB1 immunostaining was identified in 8.6% (5/58), while decrease of LKB1 immunostaining was found in 29.3% (17/58) of glioblastoma tissues. Notably, mining TCGA database of LKB1 expression in glioblastoma revealed that lower mRNA level of LKB1 was associated with shorter survival in glioblastoma. We found that knockdown of LKB1 significantly promoted in vitro proliferation, adhesion, invasion, and metformin-induced apoptosis, and simultaneously enhanced activation of ERK and mammalian-target of rapamycin (mTOR) signaling pathways in LKB1-compenent U87 and T98 glioblastoma cells. Moreover, global transcriptional profiling revealed that adhesion and cytoskeletal proteins such as Vinculin, Talin and signaling pathways including focal adhesion kinase (FAK), extracellular martrix (ECM) receptor interaction, and cellular motility were significantly enriched in U87 and T98 glioblastoma cells upon LKB1 knockdown. Additionally, we demonstrated that the enhanced activation of FAK by LKB1 knockdown was dependent on differentially expressed cytoskeletal proteins in these glioblastoma cells. Importantly, we further found that mTOR1 inhibitor rapamycin dominantly inhibited in vitro cellular proliferation, while FAK inhibitor PF-573288 drastically decreased invasion of LKB1-attenuated glioblastoma cells. Therefore, downregulation of LKB1 may contribute to the pathogenesis and malignancy of glioblastoma and may have potential implications for stratification and treatment of glioblastoma patients.

Analysis on the correlations of ENOS and ET-2 gene polymorphisms with eclampsia.

OBJECTIVE: To explore the correlations of endothelial nitric oxide synthase (eNOS) G894T and endothelin-2 (ET-2) A985G gene polymorphisms with eclampsia. PATIENTS AND METHODS: A total of 110 eclampsia patients in our hospital from July 2014 to August 2017 were enrolled as the observation group and 100 healthy pregnant women in the same period as the control group. The polymorphisms of eNOS G894T and ET-2 A985G genes in the two groups were analyzed via polymerase chain reaction (PCR), and their correlations with eclampsia risk were investigated. RESULTS: The distribution frequency of eNOS G894T genotype TT and GT and T allele, as well as the ET-2 A985G genotype GG and AG and G allele, were evidently higher in the observation group than in the control group (p<0.05). ENOS G894T genotype TT and ET-2 A985G genotype GG were significantly associated with the occurrence of eclampsia. CONCLUSIONS: The polymorphisms of eNOS G894T and ET-2 A985G genes are correlated with the occurrence of eclampsia.

Heteronemin Induces Anti-Proliferation in Cholangiocarcinoma Cells via Inhibiting TGF-ß Pathway.

A marine sesterterpenoid-type natural product, heteronemin, retains anticancer effects. In the current study, we investigate the antitumor mechanism of heteronemin in cholangiocarcinoma cells and further explore its molecular targets. Initially, heteronemin exhibited potent cytotoxic effects against cholangiocarcinoma HuccT1 and SSP-25 cells. In vitro, heteronemin altered the abilities of cell adhesion and cell migration in HuccT1 and SSP-25 cell lines. It repressed messenger ribonucleic acid (mRNA) expression levels of transforming growth factor (TGF)-ß, mothers against decapentaplegic homolog (SMAD) and Myc, whose protein products play important roles in regulating cell growth, angiogenesis, and metastasis. In addition, heteronemin altered several signaling pathways. The results indicate that heteronemin was able to modulate cell adhesion, the expression of extracellular matrix (ECM) receptors, the TGF-ß pathway, cell motility, the membrane integration, metastasis response, matrix metalloproteinase (MMP) remodeling, the regulation of metabolism, sprouting angiogenesis, transcription factors, and vasculogenesis in cholangiocarcinoma cell lines. The results also suggest that it activated multiple signal transduction pathways to induce an anti-proliferation effect and anti-metastasis in cholangiocarcinoma. In conclusion, heteronemin may be used as a potential medicine for anticancer therapy.

Enhancement by Nano-Diamino-Tetrac of Antiproliferative Action of Gefitinib on Colorectal Cancer Cells: Mediation by EGFR Sialylation and PI3K Activation.

Drug resistance complicates the clinical use of gefitinib. Tetraiodothyroacetic acid (tetrac) and nano-diamino-tetrac (NDAT) have been shown in vitro and in xenografts to have antiproliferative/angiogenic properties and to potentiate antiproliferative activity of other anticancer agents. In the current study, we investigated the effects of NDAT on the anticancer activities of gefitinib in human colorectal cancer cells. ß-Galactoside α-2,6-sialyltransferase 1 (ST6Gal1) catalyzes EGFR sialylation that is associated with gefitinib resistance in colorectal cancers, and this was also investigated. Gefitinib inhibited cell proliferation of HT-29 cells (K-ras wild-type), and NDAT significantly enhanced the antiproliferative action of gefitinib. Gefitinib inhibited cell proliferation of HCT116 cells (K-ras mutant) only in high concentration, and this was further enhanced by NDAT. NDAT enhancedd gefitinib-induced antiproliferation in gefitinib-resistant colorectal cancer cells by inhibiting ST6Gal1 activity and PI3K activation. Furthermore, NDAT enhanced gefitinib-induced anticancer activity additively in colorectal cancer HCT116 cell xenograft-bearing nude mice. Results suggest that NDAT may have an application with gefitinib as combination colorectal cancer therapy.

Nano-Diamino-Tetrac (NDAT) Enhances Resveratrol-Induced Antiproliferation by Action on the RRM2 Pathway in Colorectal Cancers.

Cancer resistance to chemotherapeutic agents is a major issue in the management of cancer patients. Overexpression of the ribonucleotide reductase regulatory subunit M2 (RRM2) has been associated with aggressive cancer behavior and chemoresistance. Nano-diamino-tetrac (NDAT) is a nanoparticulate derivative of tetraiodothyroacetic acid (tetrac), which exerts anticancer properties via several mechanisms and downregulates RRM2 gene expression in cancer cells. Resveratrol is a stilbenoid phytoalexin which binds to a specific site on the cell surface integrin αvß3 to trigger cancer cell death via nuclear translocation of COX-2. Here we report that resveratrol paradoxically activates RRM2 gene expression and protein translation in colon cancer cells. This unanticipated effect inhibits resveratrol-induced COX-2 nuclear accumulation. RRM2 downregulation, whether achieved by RNA interference or treatment with NDAT, enhanced resveratrol-induced COX-2 gene expression and nuclear uptake which is essential to integrin αvß3-mediated-resveratrol-induced antiproliferation in cancer cells. Elsewhere, NDAT downregulated resveratrol-induced RRM2 expression in vivo but potentiated the anticancer effect of the stilbene. These findings suggest that RRM2 appears as a cancer cell defense mechanism which can hinder the anticancer effect of the stilbene via the integrin αvß3 axis. Furthermore, the antagonistic effect of RRM2 against resveratrol is counteracted by the administration of NDAT.

A simulation impact evaluation of a cigarette excise tax increase on licit and illicit cigarette consumption and tax revenue in 36 European countries.

OBJECTIVES: To assess the impact of a simulated 10% tax-induced cigarette price increase on licit and illicit consumption and tax revenues in 36 European countries. METHODS: Employing panel data for licit and illicit cigarette consumption, fixed effects regression models were applied for different income clusters. RESULTS: Total cigarette consumption dropped by about 3.1% as a result of the simulated tax-induced price increase. Annual illicit cigarette consumption increased by 1.52%, (95% confidence interval: 0.21, 2.83), while annual licit cigarette consumption decreased by 4.61% (95% confidence interval: -6.51, -2.72) in the observed 36 European countries. With total consumption decreasing by about 8%, the Czech Republic, Latvia, Lithuania, Poland and Slovakia were affected the most by the price hike. More specifically, licit consumption in these countries decreased by 18.43% (95% confidence interval: -19.91, -16.95) while illicit use increased by 10.99% (95% confidence interval: 6.01, 15.96). Moreover, the overall annual tobacco tax revenue increased by US$14.69 billion in the simulation. CONCLUSION: Results of the study suggest that European policy makers continue to implement tobacco taxation policies to control smoking prevalence and national health care expenditures. At the same time, efforts to kerb contraband activities along EU Eastern borders should be intensified.

Increased expression of miR-330-3p: a novel independent indicator of poor prognosis in human breast cancer.

OBJECTIVE: Previous study has reported that miR-330-3p was highly expressed in breast cancer (BC) patients. However, the effect of miR-330-3p in BC progression remains largely unclear. The purpose of this study was to investigate the clinical significance of miR-330-3p expression in BC. PATIENTS AND METHODS: The expression of miR-330-3p was detected by quantitative Real-time PCR in BC tissues and matched normal breast tissues. The association of miR-330-3p expression with clinicopathological factors of BC patients was also analyzed by x2-test. Prognosis value of patients with BC was assessed by Kaplan-Meier method and Cox proportional hazards model, respectively. RESULTS: Quantitative real-time PCR analysis showed that the expression level of miR-330-3p was significantly higher in BC specimens than that in corresponding noncancerous tissues (p < 0.01). The levels of miR-330-3p were positively correlated with the status of TNM stage (p = 0.011) and lymph node metastasis (p = 0.006). Kaplan-Meier analysis revealed that 5-year overall survival of BC patients with high miR-330-3p expression was shorter compared to those patients with low miR-330-3p expression (p < 0.0001). Moreover, univariate and multivariate regression analysis demonstrated that miR-330-3p was an independent prognostic factor in BC. CONCLUSIONS: Our data suggest that miR-330-3p upregulation maybe concurrently associated with prognosis in patients with BC, suggesting that miR-330-3p may be a potential prognostic biomarker and therapeutic target for patients with BC.

Thyroxine inhibits resveratrol-caused apoptosis by PD-L1 in ovarian cancer cells.

Thyroid hormone, l-thyroxine (T4), has been shown to promote ovarian cancer cell proliferation via a receptor on plasma membrane integrin αvß3 and to induce the activation of ERK1/2 and expression of programmed death-ligand 1 (PD-L1) in cancer cells. In contrast, resveratrol binds to integrin αvß3 at a discrete site and induces p53-dependent antiproliferation in malignant neoplastic cells. The mechanism of resveratrol action requires nuclear accumulation of inducible cyclooxygenase (COX)-2 and its complexation with phosphorylated ERK1/2. In this study, we examined the mechanism by which T4 impairs resveratrol-induced antiproliferation in human ovarian cancer cells and found that T4 inhibited resveratrol-induced nuclear accumulation of COX-2. Furthermore, T4 increased expression and cytoplasmic accumulation of PD-L1, which in turn acted to retain inducible COX-2 in the cytoplasm. Knockdown of PD-L1 by small hairpin RNA (shRNA) relieved the inhibitory effect of T4 on resveratrol-induced nuclear accumulation of COX-2- and COX-2/p53-dependent gene expression. Thus, T4 inhibits COX-2-dependent apoptosis in ovarian cancer cells by retaining inducible COX-2 with PD-L1 in the cytoplasm. These findings provide new insights into the antagonizing effect of T4 on resveratrol's anticancer properties.

Working memory, age and education: A lifespan fMRI study.

Ageing is associated with grey matter atrophy and changes in task-related neural activations. This study investigated the effects of age and education on neural activation during a spatial working memory task in 189 participants aged between 20-80 years old, whilst controlling for grey matter density. Age was related to linear decreases in neural activation in task activated areas, and this effect was no longer significant when adjusting for education or accuracy. Age was also related to cubic increases in neural activation in non-task related areas, such as the temporal gyrus, cuneus and cerebellum when adjusting for accuracy and education. These findings support previous lifespan datasets indicating linear age-related decreases in task activation, but non-linear increases in non-task related areas during episodic memory tasks. The findings also support past studies indicating education offers a form of cognitive reserve through providing a form of neural compensation and highlights the need to consider education in ageing studies.

Blood-derived amyloid-ß protein induces Alzheimer's disease pathologies.

The amyloid-ß protein (Aß) protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD). It is believed that Aß deposited in the brain originates from the brain tissue itself. However, Aß is generated in both brain and peripheral tissues. Whether circulating Aß contributes to brain AD-type pathologies remains largely unknown. In this study, using a model of parabiosis between APPswe/PS1dE9 transgenic AD mice and their wild-type littermates, we observed that the human Aß originated from transgenic AD model mice entered the circulation and accumulated in the brains of wild-type mice, and formed cerebral amyloid angiopathy and Aß plaques after a 12-month period of parabiosis. AD-type pathologies related to the Aß accumulation including tau hyperphosphorylation, neurodegeneration, neuroinflammation and microhemorrhage were found in the brains of the parabiotic wild-type mice. More importantly, hippocampal CA1 long-term potentiation was markedly impaired in parabiotic wild-type mice. To the best of our knowledge, our study is the first to reveal that blood-derived Aß can enter the brain, form the Aß-related pathologies and induce functional deficits of neurons. Our study provides novel insight into AD pathogenesis and provides evidence that supports the development of therapies for AD by targeting Aß metabolism in both the brain and the periphery.

RAF inhibitor LY3009120 sensitizes RAS or BRAF mutant cancer to CDK4/6 inhibition by abemaciclib via superior inhibition of phospho-RB and suppression of cyclin D1.

KRAS, NRAS and BRAF mutations are among the most important oncogenic drivers in many major cancer types, such as melanoma, lung, colorectal and pancreatic cancer. There is currently no effective therapy for the treatment of RAS mutant cancers. LY3009120, a pan-RAF and RAF dimer inhibitor advanced to clinical study has been shown to inhibit both RAS and BRAF mutant cell proliferation in vitro and xenograft tumor growth in vivo. Abemaciclib, a CDK4/6-selective inhibitor, is currently in phase III studies for ER-positive breast cancer and KRAS mutant lung cancer. In this study, we found that combinatory treatment with LY3009120 and abemaciclib synergistically inhibited proliferation of tumor cells in vitro and led to tumor growth regression in xenograft models with a KRAS, NRAS or BRAF mutation at the doses of two drugs that were well tolerated in combination. Further in vitro screen in 328 tumor cell lines revealed that tumor cells with KRAS, NRAS or BRAF mutation, or cyclin D activation are more sensitive, whereas tumor cells with PTEN, PIK3CA, PIK3R1 or retinoblastoma (Rb) mutation are more resistant to this combination treatment. Molecular analysis revealed that abemaciclib alone inhibited Rb phosphorylation partially and caused an increase of cyclin D1. The combinatory treatment cooperatively demonstrated more complete inhibition of Rb phosphorylation, and LY3009120 suppressed the cyclin D1 upregulation mediated by abemaciclib. These results were further verified by CDK4/6 siRNA knockdown. Importantly, the more complete phospho-Rb inhibition and cyclin D1 suppression by LY3009120 and abemaciclib combination led to more significant cell cycle G0/G1 arrest of tumor cells. These preclinical findings suggest that combined inhibition of RAF and d-cyclin-dependent kinases might provide an effective approach to treat patients with tumors harboring mutations in RAS or RAF genes.

Evaluation of NASA Deep Blue/SOAR aerosol retrieval algorithms applied to AVHRR measurements.

The Deep Blue (DB) and Satellite Ocean Aerosol Retrieval (SOAR) algorithms have previously been applied to observations from sen-sors like the Moderate Resolution Imaging Spectroradiometers (MODIS) and Sea-viewing Wide Field-of-view Sensor (SeaWiFS) to provide records of mid-visible aerosol optical depth (AOD) and related quantities over land and ocean surfaces respectively. Recently, DB and SOAR have also been applied to Ad-vanced Very High Resolution Radiometer (AVHRR) observations from several platforms (NOAA11, NOAA14, and NOAA18), to demonstrate the potential for extending the DB and SOAR AOD records. This study provides an evaluation of the initial version (V001) of the resulting AVHRR-based AOD data set, including validation against Aerosol Robotic Network (AERONET) and ship-borne observations, and comparison against both other AVHRR AOD Research (GESTAR), Universities Space Research Association. records and MODIS/SeaWiFS products at select long-term AERONET sites. Although it is difficult to distil error characteristics into a simple expression, the results suggest that one standard deviation confidence intervals on retrieved AOD of ±(0.03+15%) over water and ±(0.05+25%) over land represent the typical level of uncertainty, with a tendency towards negative biases in high-AOD conditions, caused by a combination of algorithmic assumptions and sensor calibration issues. Most of the available validation data are for NOAA18 AVHRR, although performance appears to be similar for the NOAA11 and NOAA14 sensors as well.