SARS-CoV-2 Infection Impairs Oculomotor Functions: A Longitudinal Eye-tracking Study.

Although Severe Acute Respiratory Syndrome Coronavirus 2 infection (SARS-CoV-2) is primarily recognized as a respiratory disease, mounting evidence suggests that it may lead to neurological and cognitive impairments. The current study used three eye-tracking tasks (free-viewing, fixation, and smooth pursuit) to assess the oculomotor functions of mild infected cases over six months with symptomatic SARS-CoV-2 infected volunteers. Fifty symptomatic SARS-CoV-2 infected, and 24 self-reported healthy controls completed the eye-tracking tasks in an initial assessment. Then, 45, and 40 symptomatic SARS-CoV-2 infected completed the tasks at 2- and 6-months post-infection, respectively. In the initial assessment, symptomatic SARS-CoV-2 infected exhibited impairments in diverse eye movement metrics. Over the six months following infection, the infected reported overall improvement in health condition, except for self-perceived mental health. The eye movement patterns in the free-viewing task shifted toward a more focal processing mode and there was no significant improvement in fixation stability among the infected. A linear discriminant analysis shows that eye movement metrics could differentiate the infected from healthy controls with an accuracy of approximately 62%, even 6 months post-infection. These findings suggest that symptomatic SARSCoV- 2 infection may result in persistent impairments in oculomotor functions, and the employment of eye-tracking technology can offer valuable insights into both the immediate and long-term effects of SARS-CoV-2 infections. Future studies should employ a more balanced research design and leverage advanced machine-learning methods to comprehensively investigate the impact of SARSCoV- 2 infection on oculomotor functions.

Assessing the data quality of AdHawk MindLink eye-tracking glasses.

Most commercially available eye-tracking devices rely on video cameras and image processing algorithms to track gaze. Despite this, emerging technologies are entering the field, making high-speed, cameraless eye-tracking more accessible. In this study, a series of tests were conducted to compare the data quality of MEMS-based eye-tracking glasses (AdHawk MindLink) with three widely used camera-based eye-tracking devices (EyeLink Portable Duo, Tobii Pro Glasses 2, and SMI Eye Tracking Glasses 2). The data quality measures assessed in these tests included accuracy, precision, data loss, and system latency. The results suggest that, overall, the data quality of the eye-tracking glasses was lower compared to that of a desktop EyeLink Portable Duo eye-tracker. Among the eye-tracking glasses, the accuracy and precision of the MindLink eye-tracking glasses were either higher or on par with those of Tobii Pro Glasses 2 and SMI Eye Tracking Glasses 2. The system latency of MindLink was approximately 9 ms, significantly lower than that of camera-based eye-tracking devices found in VR goggles. These results suggest that the MindLink eye-tracking glasses show promise for research applications where high sampling rates and low latency are preferred.

Transgelin-2 as an Early Detection for Diabetic Nephropathy Through Inflammation, Periostin and E-cadherin by STAT3 Signaling Through ANXA2.

BACKGROUND: Diabetic nephropathy (hereinafter referred to as DN) is one of the important causes of chronic renal failure, with great harm. We aimed to elucidate the role of transgelin-2, a key early detection for diabetic ne-phropathy. METHOD: The serum samples of 12 DN patients and 12 normal volunteers were collected for this experiment. Mice of the model group were injected intraperitoneally with streptozotocin following a high fat diet. Mouse podocyte (MPC5) cells were induced with 20 mmol/L d-glucose. RESULT: Transgelin-2 was highly expressed in DN patients with diabetic nephropathy both at the expression levels of mRNA and protein. Transgelin-2 expression was correlated with blood sugar in patients with DN. Transgelin-2 gene up-regulation enhanced inflammation and periostin levels, and reduced E-cadherin activity level in mice with DN. Over-expression of transgelin-2 increased inflammation and periostin levels, and reduced E-cadherin activity level in the in vitro model. Down-regulation of Transgelin-2 reduced inflammation and periostin levels and induced E-cadherin activity level in the in vitro model. Transgelin-2 induced ANXA2/ STAT3 signaling in a mouse model or an in vitro model. ANXA2 was one of the regulatory factors for the effects of transgelin-2 with inflammation, periostin, and E-cadherin in a model of DN. CONCLUSIONS: Taken together, these findings demonstrated that transgelin-2 promoted inflammation and periostin levels, and suppressed E-cadherin levels in DN by STAT3 signaling through ANXA2.

Interference of periostin attenuates pathological changes, proinflammatory markers and renal fibrosis in diabetic kidney injury.

BACKGROUND: Diabetic nephropathy (DN) is a prevalent complication of diabetes, in which inflammation and fibrosis are the significant pathogenesis. Periostin is a matricellular protein that functions on stabilizing the extracellular matrix by binding to integrins during development. This study aimed to explored the role of periostin in DN. METHODS: The animal and cell models of DN were constructed in streptozocin (STZ)-induced mice and high glucose-challenged human mesangial cells (HMCs). The role of periostin in pathological changes, inflammation and fibrosis in DN was investigated through biochemical detection, HE and Masson staining and scores, western blot, enzyme­linked immunosorbent assay (ELISA) and real-time quantitative PCR (RT-qPCR) assays. RESULTS: Knockdown of periostin counteracted the STZ-induced the ratio of kidney weight and body weight, and the concentrations of urine albumin excretion (UAE), serum creatinine (Scr), urine albumin/creatinine ratio (UACR) and blood urea nitrogen (BUN) in mice. Moreover, silencing of periostin alleviated the pathological manifestations and reduced the concentrations of IL-6, TNF-α and IL-1ß in mice kidney tissues and sera. Also, downregulation of periostin decreased the relative protein expression of fibronectin, collagen IV and α-SMA in kidney tissues. Meanwhile, interference of periostin attenuated the levels of pro-inflammation factors and the expressions of fibrosis markers in HG-induced HMCs. CONCLUSION: Interference of periostin resisted DN via attenuating the pro-inflammatory cytokines release and renal fibrosis in diabetic kidney injury. Our study establishes a basis for its further study and underlying application in clinical practice in diagnosing and treating diabetic kidney injury or other relevant diseases.

A CNN-Based Wearable System for Driver Drowsiness Detection.

Drowsiness poses a serious challenge to road safety and various in-cabin sensing technologies have been experimented with to monitor driver alertness. Cameras offer a convenient means for contactless sensing, but they may violate user privacy and require complex algorithms to accommodate user (e.g., sunglasses) and environmental (e.g., lighting conditions) constraints. This paper presents a lightweight convolution neural network that measures eye closure based on eye images captured by a wearable glass prototype, which features a hot mirror-based design that allows the camera to be installed on the glass temples. The experimental results showed that the wearable glass prototype, with the neural network in its core, was highly effective in detecting eye blinks. The blink rate derived from the glass output was highly consistent with an industrial gold standard EyeLink eye-tracker. As eye blink characteristics are sensitive measures of driver drowsiness, the glass prototype and the lightweight neural network presented in this paper would provide a computationally efficient yet viable solution for real-world applications.

LncTUG1 ameliorates renal tubular fibrosis in experimental diabetic nephropathy through the miR-145-5p/dual-specificity phosphatase 6 axis.

The renal interstitial fibrosis contributes to the progression and deterioration of diabetic nephropathy (DN). Long noncoding RNA taurine-up-regulated gene 1 (TUG1) in kidneys may be down-regulated by hyperglycemia. We aim to explore its role in tubular fibrosis caused by high glucose and the possible target genes of TUG1. In this study, a streptozocin-induced accelerated DN mouse model and a high glucose-stimulated HK-2 cells model was established to evaluate TUG1 expression. Potential targets of TUG1 were analyzed by online tools and confirmed by luciferase assay. A rescue experiment and gene silencing assay were used to investigate whether TUG1 plays its regulation role via miR-145-5p/dual-specificity phosphatase 6 (DUSP6) in HK2 cells. The effects of TUG1 on inflammation and fibrosis in high glucose treated tubular cells were evaluated by in vitro study, as well as in vivo DN mice model through AAV-TUG1 delivery. Results showed TUG1was downregulated in HK2 cells incubated with high glucose while miR-145-5p was upregulated. Overexpression of TUG1 alleviated renal injury by suppressing inflammation and fibrosis in vivo. Overexpression of TUG1 inhibited HK-2 cell fibrosis and relieved the inflammation. A mechanism study demonstrated that TUG1 directly sponged to miR-145-5p, and DUSP6 was identified as a target downstream of miR-145-5p. In addition, miR-145-5 overexpression and DUSP6 inhibition countervailed the impacts of TUG1. Our findings revealed that TUG1 overexpression alleviates kidney injury in DN mice and decreases the inflammatory response and fibrosis of high glucose-stimulated HK-2 cells via miR-145-5p/DUSP6 axis.

Natural Deterioration Processes of Salix psammophila Sand Barriers in Atmospheric Exposure Section.

The atmospheric conditions of desert environments are important for the protection of Salix psammophila Sand Barrier, and these conditions can affect and change the structure and performance of the sand barrier, causing them to lose their wind proofing and sand fixing benefits. In this study, we have first examined the key environmental factors that affect the exposure of S. psammophila sand barrier. Then, we assessed how key factors in the desert atmospheric environment affect structural aging and performance. The relative crystallinity and chemical composition changes in the sand barrier were measured by X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), and X-ray photoelectron spectroscopy (XPS), and the main degradation factors and processes were discussed. The results showed that the degradation degree of the exposed S. psammophila sand barrier was mainly affected by moisture and ultraviolet radiation. Lignin was the main component and the source of photodegradation and photodiscoloration observed in the sand barrier. However, other polysaccharides, such as cellulose and hemicellulose, were less affected by photodegradation. The stress generated by alternating desorption-absorption was the main cause of the expansion and contraction, deformation, cracking, and warping observed in S. psammophila sand barrier. We also found a series of irreversible changes and losses that occurred, which affected the natural material properties of S. psammophila sand barrier exposed to atmospheric conditions for several years. Exposure times between 5 and 7 years were the most important turning point in time for determining the deterioration of the S. psammophila sand barrier. Our results highlighted the importance of the interactions between atmospheric factors and the exposed atmospheric sections of the S. psammophila sand barrier from the perspective of environmental effects. However, the exact mechanisms of the sand barrier deterioration still need further investigation. Nevertheless, our overall findings advanced the current understanding of the environmental effects of S. psammophila sand barrier for ecological restoration and desertification reversal, especially in stressful desert environments.

The clinical efficacy and safety of TACE combined with apatinib for advanced hepatocellular carcinoma: A propensity score matching analysis.

Background: The combined treatment of transcatheter arterial chemoembolization (TACE) and apatinib had beneficial effects on the survival of patients with advanced hepatocellular carcinoma (HCC), but the efficacy of this regimen is still controversial and needs further investigation. Materials and Methods: The clinical records of advanced HCC patients between May 2015 and December 2016 were collected from our hospital. They were categorized into the TACE monotherapy group and the combination of TACE and apatinib group. After propensity score matching (PSM) analysis, the disease control rate (DCR), objective response rate (ORR), progression-free survival (PFS), and occurrence of adverse events were compared between the two treatments. Results: There were 115 HCC patients included in the study. Among them, 53 received TACE monotherapy and 62 were treated with TACE plus apatinib. After PSM analysis, 50 pairs of patients were compared. The DCR of the TACE group was significantly lower than that of the combination of TACE and apatinib group (35 [70%] versus 45 [90%], P < 0.05). The ORR of the TACE group was also significantly lower than that of the combination of TACE and apatinib group (22 [44%] versus 34 [68%], P < 0.05). Patients who received the combined treatment of TACE and apatinib had longer PFS compared with those in the TACE monotherapy group (P < 0.001). Moreover, hypertension, hand-foot syndrome, and albuminuria were more common in the combination of TACE and apatinib group (P < 0.05), although all adverse events were well tolerated. Conclusions: The combined treatment of TACE and apatinib showed beneficial effects on tumor response, survival outcomes, and tolerance to treatment, which may be used as a routine regimen for advanced HCC patients.

Long non-coding RNA TMCC1-AS1 predicts poor prognosis and accelerates epithelial-mesenchymal transition in liver cancer.

Long non-coding RNA transmembrane and coiled-coil domain family 1 antisense RNA 1 (TMCC1-AS1) has been frequently reported to be associated with prognosis in patients with liver cancer (LC). However, the biological role of TMCC1-AS1 in LC in vitro remains unclear. The expression levels of TMCC1-AS1 in primary tumor tissues and LC cell lines were determined using reverse transcription-quantitative PCR. The associations between TMCC1-AS1 expression and the clinicopathological factors of patients with LC were statistically analyzed using the χ2 test. The role of TMCC1-AS1 in LC prognosis was assessed using Kaplan-Meier curves and proportional hazards model (Cox) analysis. Cell proliferation was determined by Cell Counting Kit-8 and colony formation assays. Transwell assays were performed to determine migration and invasion. TMCC1-AS1 expression was found to be significantly upregulated in LC tissues and cell lines compared with the corresponding controls. High TMCC1-AS1 expression was associated with advanced TNM stage and lymph node metastasis. Furthermore, high TMCC1-AS1 expression predicted poor survival in patients with LC. Knockdown of TMCC1-AS1 significantly inhibited the proliferation, migration and invasion of HepG2 and SNU-182 cells, while overexpression of TMCC1-AS1 had the opposite effect in HepG2 and SNU-182 cells. At the molecular level, downregulation of TMCC1-AS1 expression resulted in increased E-cadherin expression and decreased proliferating cell nuclear antigen, Ki67, N-cadherin and Vimentin expression in HepG2 cells. Overexpression of TMCC1-AS1 had the opposite effects on these factors in SNU-182 cells. In conclusion, the present findings indicated that TMCC1-AS1 might be considered as a novel oncogene, which promotes cell proliferation and migration, and may be a potential therapeutic target for LC.

Knockout of NGAL aggravates tubulointerstitial injury in a mouse model of diabetic nephropathy by enhancing oxidative stress and fibrosis.

Neutrophil gelatinase-associated lipocalin (NGAL), also called lipocalin 2, is considered a promising biomarker for acute and chronic kidney injuries. Several studies have demonstrated that its levels increase in plasma and urine in diabetic nephropathy (DN), and its urine concentration increases upon kidney function deterioration. However, its role in DN progression remains unclear. The current study used in vitro gene expression knockdown in human proximal tubular cell line human kidney (HK)2 to investigate the role of NGAL in oxidation and extracellular matrix secretion under high-glucose (HG) incubation. In addition, type 1 diabetes was induced in vivo in knockout NGAL-/- and wild-type mice in order to investigate role of NGAL in the progression of DN. The results demonstrated that NGAL knockdown in HK2 cells significantly increased oxidative stress under HG stimulation tested by flow cytometry, and increased the secretion of interleukin-6, fibronectin (FN) and collagen IV examined by ELISA. Western blotting demonstrated that the phosphorylation of Smad2/3 also increased in HK2 cells under transforming growth factor-ß1 stimulation. In vivo experiments demonstrated that diabetic NGAL-/- mice showed deteriorated renal function compared with that of diabetic wild-type mice. Histopathological analysis suggests that diabetic NGAL-/- mice had more serious glomerulosclerosis and tubular vascular degeneration than wild-type mice. Immunohistochemistry suggested that the absence of NGAL lead to increased FN deposition in glomeruli in a mouse model of DN. In conclusion, NGAL appears to have renal protective effects by slowing down the progression of DN, and its effect may be associated with a reduction in oxidation, fibrosis and inflammation.