Purpose: To characterize retinal capillary complexity by optical coherence tomography angiography in Parkinson disease. Method: Twenty-five Parkinson disease patients and 25 age- and gender-matched healthy controls were recruited. Optical coherence tomography angiography and optical coherence tomography imaged the superficial and deep retinal capillary plexuses and retinal structure. Retinal capillary skeleton density, retinal capillary perfusion density, and fractal dimension analysis of retinal capillary complexity were performed in the total annular zone and quadrant sectors. The thickness of retinal nerve fiber layer, ganglion cell layer and inner plexiform layer, and total retinal thickness were extracted from retinal structural images. Relationships among the retinal capillaries, retinal structure, and clinical parameters were analyzed. Results: The superficial retinal capillary plexus in Parkinson disease patients had lower retinal capillary skeleton and perfusion densities and capillary complexity in the total annular zone and all quadrant sectors compared with healthy control subjects. The deep retinal capillary plexus retinal capillary complexity was decreased in the total annular zone and the superior and inferior quadrants. The retinal capillary complexity in the inferior quadrant was negatively correlated with the best-corrected visual acuity and disease duration (r = −0.61, r = −0.43, respectively, both P < 0.05). Conclusion: As determined by fractal analysis, retinal capillary complexity can be an objective biomarker in Parkinson disease.

Mitochondrial DNA (mtDNA) has been implicated in various human degenerative diseases. However, the role of mtDNA in Osteoarthritis (OA) is less known. To investigate whether mtDNA haplogroups contribute to the prevalence of knee OA, we have carried out a comprehensive case-control study on 187 knee OA patients and 420 geographically matched controls in southern China. OA patients were classified on the Kellgren/Lawrence scale from two to four for the disease severity study and the data were analyzed by adjusting for age and sex. We found that patients with haplogroup G (OR = 3.834; 95% CI 1.139, 12.908; p = 0.03) and T16362C (OR = 1.715; 95% CI 1.174, 2.506; p = 0.005) exhibited an increased risk of OA occurrence. Furthermore, patients carrying haplogroup G had a higher severity progression of knee OA (OR = 10.870; 95% CI 1.307, 90.909; p = 0.007). On the other hand, people with haplogroup B/B4 (OR = 0.503; 95% CI 0.283, 0.893; p = 0.019)/(OR = 0.483; 95% CI 0.245, 0.954; p = 0.036) were less susceptible for OA occurrence. Interestingly, we found OA patients also exhibited a general increase in mtDNA content. Our study indicates that the mtDNA haplogroup plays a role in modulating OA development.

A primary cardiac tumor is a rare clinical entity which was reported an incidence of 0.03% in previous autopsy series. 75% cardiac tumors are cardiac myxoma and cardiac hemangiomas constitute only 1–2% of primary cardiac tumors. With the development of modern medical imaging technology and the enhancement of people’s health awareness, more and more asymptomatic cardiac hemangiomas were found and confirmed eventually. Here, we described a case of a 71-year-old man, who was hospitalized with intermittent palpitation for 1 year and a large mass of the heart was removed successfully via sternotomy which was confirmed as atrial hemangioma by postoperative histopathology. Furthermore, a comprehensive review of atrial hemangioma was conducted to date and a few recommendations for the diagnosis and treatment of this uncommon disorder were provided for clinicians.

Background: Of all malignancies, lung cancer is the leading cause of death, and non-small cell lung cancer (NSCLC) accounts for 80-85% of all lung cancers. In this study, the long non-coding RNA (lncRNA) THUMPD3-AS1 was observed to be highly expressed in NSCLC and correlated with TNM stages and relapse, suggesting that THUMPD3-AS1 is involved in the regulation of NSCLC. Methods: The aim of this study was to investigate the regulatory function and mechanism of THUMPD3-AS1 in NSCLC cells by cellular function and molecular biology experiments. Results: Overexpression and knockdown analysis revealed that THUMPD3-AS1 promoted tumor progression by increasing cell proliferation and self-renewal of NSCLC cells. Moreover, THUMPD3-AS1 may act as an endogenous sponge of microRNA-543 (miR-543) which can regulate the target gene ONECUT2 in NSCLC cells. Conclusion: Our study indicated that THUMPD3-AS1 regulated NSCLC cell self-renewal by regulating the expression of miR-543 and ONECUT2, and THUMPD3-AS1 can potentially act as a biomarker or therapeutic target in NSCLC.

Purpose: This study aimed to characterize the microvascular and structural changes in the macular that occur in white matter hyperintensities (WMH) using optical coherence tomographic angiography. We also aimed to explore the association between macular microvascular and structural changes with focal markers of brain tissue on MRI in WMH using the Fazekas scale. Methods: This study enrolled healthy participants who were stroke- and dementia-free. MRI was used to image the cerebral white matter lesions, and Fazekas scale was used to evaluate the severity of the white matter lesions. Optical coherence tomography angiography (OCT-A) was used to image the radial peripapillary capillaries (RPCs), macular capillary plexuses [superficial capillary plexus (SCP) and deep capillary plexus (DCP)] and thickness around the optic nerve head, peripapillary retinal nerve fiber layer (pRNFL). Results: Seventy-four participants were enrolled and divided into two groups according to their Fazekas score (Fazekas scores ≤ 1 and ≥2). Participants with Fazekas score ≥2 showed significantly reduced RPC density ( P = 0.02) and DCP density ( P = 0.012) when compared with participants with Fazekas score ≤ 1. Participants with Fazekas score ≥2 showed reduced pRNFL ( P = 0.004) when compared to participants with Fazekas score ≤ 1. Fazekas scores were significantly associated with the pRNFL thickness (Rho = −0.389, P = 0.001), RPC density (Rho = −0.248, P = 0.035), and DCP density (Rho = −0.283, P = 0.015), respectively. Conclusions: Microvascular impairment and neuro-axonal damage are associated with the disease cascade in WMH. We have shown that RPC and DCP densities are significantly affected, and these impairments are associated with the severity of the disease and cognitive function. OCT-A could be a useful tool in quantifying the retinal capillary densities in WMH.

Background: Lung adenocarcinoma (LUAD) is a heterogeneous disease with high mortality. Close attention has been paid to immunotherapy in LUAD treatment. However, immunotherapy has produced different therapeutic effects because of immune heterogeneity. Long noncoding RNAs (lncRNAs) are survival prognostic indicators with functions in the immune process. The present study was designed to examine the predictive power of immune-related lncRNAs in LUAD prognosis and investigated potential molecular mechanisms. Methods: Transcriptome profiling and LUAD sample clinical information were retrieved from online database. The immune-related lncRNAs signature was identified by Cox regression. Survival analysis was used to verify the validity of the prognosis model. Then, possible biological functions were predicted and the abundance of infiltrating immune cells in LUAD samples were further analyzed. Results: An immune-associated lncRNAs signature was established by combining six lncRNAs. Patients with LUAD were stratified into high- and low-risk groups using the six lncRNAs signature. Patients in different risk levels had significantly different prognoses (P&lt;0.001), and the immune-associated lncRNAs signature was identified as an independent prognostic factor for LUAD. The functions of the lncRNA signature were confirmed as ubiquitin mediated proteolysis and signal sequence binding. The lncRNA signature negatively correlates with B-cell immune infiltration. Conclusion: A reliable immune-related lncRNAs prognosis model for LUAD was identified. lncRNAs played a vital role in the tumor immune process and were associated with the LUAD prognosis. Research of lncRNAs in B-cell immune infiltration could provide new insight into the immunotherapy of LUAD.

Accurate segmentation of choroidal thickness (CT) and vasculature is important to better analyze and understand the choroid-related ocular diseases. In this paper, we proposed and implemented a novel and practical method based on the deep learning algorithms, residual U-Net, to segment and quantify the CT and vasculature automatically. With limited training data and validation data, the residual U-Net was capable of identifying the choroidal boundaries as precise as the manual segmentation compared with an experienced operator. Then, the trained deep learning algorithms was applied to 217 images and six choroidal relevant parameters were extracted, we found high intraclass correlation coefficients (ICC) of more than 0.964 between manual and automatic segmentation methods. The automatic method also achieved great reproducibility with ICC greater than 0.913, indicating good consistency of the automatic segmentation method. Our results suggested the deep learning algorithms can accurately and efficiently segment choroid boundaries, which will be helpful to quantify the CT and vasculature.

Background Circular RNA (circRNA) has been recently identified as a critical regulator during carcinogenesis. However, the biological function and potential underlying mechanisms of circRNAs in lung cancer remain to be further elucidated. Methods Here, we first evaluated the differentially expressed circRNAs between tumor and the matched adjacent nontumor tissues (3 pairs) of lung cancer patients via circRNA microarray. The expression of top five dysregulated circRNAs were tested in lung cancer cell lines and the circSCAP with concordant alteration in microarray data and cell lines was selected for further investigation. Then we validated the expression level of circSCAP in tumor and corresponding adjacent tissues (161 pairs) from a lung cancer cohort by RT-PCR analysis followed by correlation and prognosis analysis between circSCAP and clinical characteristics. Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer diagnosis (about 80% in the cohort used in this study). Therefore, we focused the role of circSCAP in NSCLC in the present study. In vitro and in vivo assays were performed to study the biological function of circSCAP in NSCLC. Biotin-labeled RNA pulldown and RNA immunoprecipitation (RIP) assays were carried out to identify the proteins directly interacting with circSCAP. The molecular mechanism of circSCAP-driven tumor suppression was demonstrated by immunoblotting, immunoprecipitation and luciferase reporter assays. In vitro and in vivo rescue experiments were conducted to verify the role of the circSCAP/SF3A3/p53 signaling axis in NSCLC. Results We screened the expression profiles of human circRNAs in lung cancer tissues and found that hsa_circ_0065214 (termed as circSCAP) was significantly decreased. Kaplan–Meier analysis showed that patients with low level of circSCAP had a significantly poor prognosis. Gain- and loss-of-function experiments suggested that circSCAP played an important role in NSCLC cell proliferation, cell migration and apoptosis. Mechanistically, circSCAP directly binds to the SF3A3 protein, facilitating the reduction of SF3A3 by promoting its ubiquitin–proteasome-mediated degradation, which enhances the expression of MDM4-S to finally activate its downstream p53 signaling. Conclusion These findings illustrate a novel circSCAP/SF3A3/p53 signaling axis involved in suppressing the malignance of NSCLC and provide a promising target for NSCLC prognosis prediction and treatment.