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Under the influence of novel corona virus pneumonia epidemic, the protection of traditional villages is put forward higher request The spread of the epidemic among villages will make the situation of epidemic prevention and control more difficult As an important part of culture, traditional villages have high historical value In this paper, the traditional village protection method, a new geographical data algorithm IData storage method Compared with the traditional ArcGIS method, it improves the efficiency and accuracy of topographic map entry IData's data factory can use the symbolic technology of skeleton lines to represent all the figures in the national standard mode, and any complex figure can only be represented by one element Idate can quickly load data and render symbols in a drawing With the powerful data processing engine of IData data factory, we can check out the errors that other software can't find and process the data automatically Records of the loss of traditional villages can be recorded quickly The establishment and protection of traditional villages have had a beneficial impact [ABSTRACT FROM AUTHOR] Copyright of Journal of Intelligent & Fuzzy Systems is the property of IOS Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission However, users may print, download, or email articles for individual use This abstract may be abridged No warranty is given about the accuracy of the copy Users should refer to the original published version of the material for the full abstract (Copyright applies to all Abstracts )

Over the years, microRNA-20b-3p (miR-20b-3p) has been found to play an essential role in human diseases; we aimed to investigate the effect of miR-20b-3p on the progression of diabetic retinopathy (DR). The DR rat models were established by streptozotocin injection and treated with miR-20b-3p mimics, silenced, or overexpressed thioredoxin-interacting protein (TXNIP). Afterward, the expression of miR-20b-3p and TXNIP, visual function, inflammatory factors, microvascular injury, vascular permeability, cell apoptosis, and angiogenesis in rats' retinal tissues were assessed. The target relation between miR-20b-3p and TXNIP was confirmed by dual luciferase reporter gene assay. MiR-20b-3p was poorly expressed while TXNIP was highly expressed in DR rats' retinal tissues. Elevated miR-20b-3p and inhibited TXNIP promoted the visual function, and restricted the inflammatory reaction, microvascular injury, vascular permeability, cell apoptosis, and angiogenesis in DR rats, thereby decelerating the development of DR. Furthermore, TXNIP was targeted by miR-20b-3p. We have found in this study that elevated miR-20b-3p could repress the levels of inflammatory factors by inhibiting TXNIP, thus attenuating the pathology of retina in DR rats, which provided new candidates for DR treatment.

It is growingly recognized that messenger RNAs (mRNAs) are important regulators of various cancers. However, there are few reporters about the function of E2F3 in retinoblastoma (RB), which needs more exploration. In addition, the circRNA circ-0075804 was derived from the E2F3 host gene. The purpose of the study is to figure out the role and molecular regulation mechanism of E2F3 and circ-0075804 in RB. The role of E2F3 in RB was determined through E2F3 silencing and loss of expression was evaluated by real-time quantitative polymerase chain reaction (RT-qPCR), Western blot, CCK-8, colony formation, and 5-ethynyl-2'-deoxyuridine assays. The interactions between E2F3 and circ-0075804 were validated through loss and gain function of circ-0075804. Besides, the role of circ-0075804 in RB was determined by several functional assays. And the binding ability between heterogeneous nuclear ribonucleoprotein K and circ-0075804 was verified by RNA pull-down, Western blot, and RT-qPCR assays. The expression of E2F3 was upregulated in RB cell lines. Furthermore, knockdown of E2F3 inhibited cell proliferation and induced cell apoptosis in RB. And circ-0075804 positively regulated the expression of E2F3. Moreover, circ-0075804 facilitated cell proliferation and suppressed cell apoptosis. Besides, HNRNPK could bind with circ-0075804 in RB. Finally, knockdown of E2F3 partly rescued the promoting role of circ-0075804 overexpression in RB. Overall, circ-0075804 promotes the proliferation of RB via combining HNRNPK to improve the stability of E2F3, which brings new light for treating RB.

Wang S, Du S, Lv Y, Zhang F, Wang W. Cancer Management and Research. 2019;11:3111–3123 The Editor and Publisher of Cancer Management and Research wish to retract the published article. Concerns were raised over alleged image duplication in Figures 4D and 8B with similar images from unrelated articles, specifically: Figure 4D, panel WERI-RB-1 si-HMGB1 appears to have been duplicated with a similar image in Figure 2C from Cheng et al, 2020 (https://doi.org/10.2147/OTT.S218876). Figure 8B, panels miR-NC; miR-665 mimics, far left and miR-NC; miR-665 mimics, centre-right appear to have been duplicated with similar images in Figure 8A from Dou et al, 2020 (https://doi.org/10.3389/fphar.2019.01700) and Figure 7B from Jiao et al, 2019 (https://doi.org/10.2147/OTT.S210567), respectively. The authors did not respond to our queries and the Editor determined the findings of the study were no longer valid and advised for the article to be retracted. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. This retraction relates to this paper

Purpose: The excessive secretion of interleukin (IL)-17 contributes to the pathological process of sympathetic ophthalmia (SO). Celastrol is a naturally active product and exhibits an immunosuppressive effect. However, whether the supplementation of celastrol relieves SO remains unclear. Methods: The peripheral blood mononuclear cells (PBMCs) were extracted from the venous blood samples of 20 SO patients and 20 healthy controls, followed by stimulating with various concentrations of celastrol. The levels of IL-23 and IL-17 were measured by enzyme-linked immunosorbent assay and real-time polymerase chain reaction assay. The activation of the signal transducer and activator of transcription 3 (STAT3) in PBMCs of SO patients was detected by Western blot. Results: The levels of IL-23 and IL-17 in PBMCs isolated from SO patients were significantly increased compared with those in PBMCs isolated from healthy controls. Celastrol treatment inhibited the production of both IL-23 and IL-17 in PBMCs of SO patients in a dose-dependent manner. In PBMCs isolated from SO patients and healthy controls, the administration of recombinant human IL-23 (rIL-23) enhanced the production of IL-17, which was then suppressed by co-stimulation with celastrol. Also, celastrol treatment reduced rIL-23-induced phosphorylation of STAT3 in PBMCs isolated from SO patients. Conclusions: Celastrol can reduce the production of IL-17 in PBMCs of SO patients. The mechanism may be related to the reduction of IL-23 secretion, which in turn inhibits the phosphorylation of STAT3.

Background Diabetes is a risk factor for various cancers, but its prognostic role in renal cell carcinoma (RCC) is controversial and understudied. This study investigated the prognostic value of type 2 diabetes (T2D) in RCC patients. Methods The clinicopathological and follow‐up data of 451 RCC patients undergoing radical or partial nephrectomy at the First Hospital of Shanxi Medical University from 2013 to 2018 were reviewed. Associations of T2D with clinicopathological parameters of RCC were evaluated using the Kaplan‐Meier method for survival estimates and Cox regression univariate and multivariate analyses. Results Of 451 patients, 74 (16.4%) had T2D. These patients were older, had a higher body mass index, higher incidence rates of hypertension and cardiovascular morbidity, a higher rate of laparoscopic surgery, and smaller neoplasms (all P, Highlights Type 2 diabetes (T2D) is an independent predictor of survival and recurrence after surgery in patients with renal cell carcinoma (RCC).This finding reveals the importance of T2D in determining the prognosis of patients with RCC.

Xanthomonas oryzae pv. oryzicola (Xoc) causes bacterial leaf streak in rice. To promote disease development, bacteria deliver effectors such as transcription activator-like (TAL) effectors into plant cells to modulate host defense and promote bacterial growth. In this study, we constructed a Tn5 transposon-mediated mutation library of GD41, which possesses 30 TAL effectors. A TalI gene deficient mutant GD21 was obtained. GD21 demonstrated compromised bacterial virulence and growth. Sequence analysis showed that TalI is a typical TAL effector gene with 14.5 repeats and RVDs identical to Tal3 in Xoc BXOR1. Expression of TalI in Xo strains resulted in enhanced bacterial growth in rice and medium. Target gene screening results suggest that TalI does not target the rice gene OsSULTR3;6 and Os09g29100. Orthology analysis showed that TalI does not belong to the 13 conserved TAL ortholog families crossing Xoc strains. Next, the role of TalI in SA, JA, and ET hormone pathways was tested, and our results showed that TalI has an effect on the expression of PR1a, PR1b, and PR5 but not on other marker genes. The HR suppression ability of TalI was then evaluated by introducing avrXa10 and avrXa7 into GD41 and GD21. The transformed strains displayed similar HR eliciting pattern on rice lines IRBB10 and IRBB7, which suggests that TalI does not interfere with effector mediated defense directly.

Background/Aims: Age-related macular degeneration (AMD) is the primary cause of senior blindness in developed countries. Mechanisms underlying initiation and development of AMD remained known. Methods: We examined the CD4+ T cell compartments and their functions in AMD patients. Results: AMD patients presented significantly higher frequencies of interferon (IFN)-γ-expressing and interleukin (IL)-17-expressing CD4+ T cells than healthy controls. The levels of IFN-γ and IL-17 expression by CD4+ T cells were significantly higher in AMD patients. These IFN-γ-expressing Th1 cells and IL-17-expressing Th17 cells could be selectively enriched by surface CCR3+ and CCR4+CCR6+ expression, respectively. Th1 and Th17 cells from AMD patients promoted the differentiation of monocytes toward M1 macrophages, which were previously associated with retinal damage. Th1 and Th17 cells also increased the level of MHC class I expression in human retinal pigment epithelial (RPE)-1 cells, while Th1 cells increased the frequency of MHC class II-expressing RPE-1 cells. These proinflammatory effects were partly, but not entirely, induced by the secretion of IFN-γ and IL-17. Conclusions: This study demonstrated an enrichment of Th1 cells and Th17 cells in AMD patients. These Th1 and Th17 cells possessed proinflammatory roles in an IFN-γ- and IL-17-dependent fashion, and could potentially serve as therapeutic targets.

We analyzed the effects of anti-vascular endothelial growth factor (VEGF) drugs combined with photodynamic therapy (PDT) in the treatment of age-related macular degeneration (AMD). Ninety-six cases (192 eyes) of AMD were included in this study and randomly divided into the observation group and control group (n=48 cases per group). The control group was administered the treatment of Lucentis intravitreal injection alone and the observation group was administered Lucentis combined with PDT. The therapeutic effects were compared. The best corrected visual acuity of patients in the two groups increased gradually after treatment. Patients in the observation group had a significantly higher visual acuity when compared to the control group 1 and 6 months post-operation. The differences were statistically significant (P

Type-III (T3) effectors PthXo1 and AvrXa10 of Xanthomonas oryzae pv. oryzae are translocated into rice cells to induce virulence and avirulence on susceptible- and resistant-rice varieties Nipponbare and IRBB10, respectively. The translocation needs the bacterial T3 translocator Hpa1 and rice Oryza sativa plasma membrane protein OsPIP1;3. Here, we employed the beta-lactamase (BlaM) reporter system to observe PthXo1 and AvrXa10 translocation. The system was established to monitor effectors of animal-pathogenic bacteria by quantifying the BlaM hydrolysis product [P] and fluorescence resonance energy transfer (FRET) of the substrate. The feasibility of the BlaM reporter in rice protoplasts was evaluated by three criteria. The first criterion indicated differences between both [P] and FRET levels among wild types and OsPIP1;3-overexpressing and OsPIP1;3-silenced lines of both Nipponbare and IRBB10. The second criterion indicated differences between [P] and FRET levels in the presence and absence of Hpa1. The last criterion elucidated the coincidence of PthXo1 translocation with induced expression of the PthXo1 target gene in protoplasts of Nipponbare and the coincidence of AvrXa10 translocation with induced expression of the AvrXa10 target gene in protoplasts of IRBB10. These results provide an experimental avenue for real-time monitoring of bacterial T3 effector translocation into plant cells with a pathological consequence.

Type-III (T3) effectors PthXo1 and AvrXa10 of Xanthomonas oryzae pv. oryzae are translocated into rice cells to induce virulence and avirulence on susceptible- and resistant-rice varieties Nipponbare and IRBB10, respectively. The translocation needs the bacterial T3 translocator Hpa1 and rice Oryza sativa plasma membrane protein OsPIP1;3. Here, we employed the β-lactamase (BlaM) reporter system to observe PthXo1 and AvrXa10 translocation. The system was established to monitor effectors of animal-pathogenic bacteria by quantifying the BlaM hydrolysis product [P] and fluorescence resonance energy transfer (FRET) of the substrate. The feasibility of the BlaM reporter in rice protoplasts was evaluated by three criteria. The first criterion indicated differences between both [P] and FRET levels among wild types and OsPIP1;3-overexpressing and OsPIP1;3-silenced lines of both Nipponbare and IRBB10. The second criterion indicated differences between [P] and FRET levels in the presence and absence of Hpa1. The last criterion elucidated the coincidence of PthXo1 translocation with induced expression of the PthXo1 target gene in protoplasts of Nipponbare and the coincidence of AvrXa10 translocation with induced expression of the AvrXa10 target gene in protoplasts of IRBB10. These results provide an experimental avenue for real-time monitoring of bacterial T3 effector translocation into plant cells with a pathological consequence.

Shuai Wang, Shanshan Du, Yong Lv, Fengyan Zhang, Wenzhan WangDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, People’s Republic of ChinaPurpose: Previous studies have revealed that microRNA-665 (miR-665) is dysregulated in a variety of human cancers. However, little is known regarding its expression profiles and functions in retinoblastoma (RB). Therefore, the aims of our study were to evaluate miR-665 expression in RB and determine the precise roles of miR-665 in the progression of RB.Patients and methods: Herein, RT-qPCR was used to determine miR-665 expression levels in RB tissues and cell lines, and a series of functional experiments were performed to explore the influence of miR-665 on RB cell proliferation, colony formation, apoptosis, migration, and invasion as well as tumor growth. The molecular mechanisms underlying the tumor-suppressive action of miR-665 in RB were also explored.Results: We found that miR-665 was markedly reduced in RB tissues and cell lines and that lower miR-665 expression was strongly associated with tumor size, TNM stage, and differentiation in patients with RB. Exogenous expression of miR-665 suppressed cell proliferation, colony formation, migration, and invasion, and induced cell apoptosis in RB cells, while silencing miR-665 expression had the opposite effects. In addition, upregulation of miR-665 decreased the tumor growth of RB cells in vivo. High-mobility group box 1 (HMGB1) was identified as a direct target of miR-665 in RB cells, and decreasing the expression of HMGB1 simulated the regulatory effects of miR-665 overexpression in RB cells, while knockdown of HMGB1 expression counteracted the miR-665-mediated antitumor effects in RB cells. Moreover, miR-665 was shown to regulate the Wnt/β-catenin signaling pathway by targeting HMGB1 in vitro and in vivo.Conclusion: Taken together, our in vitro and in vivo results suggest that miR-665 acts as a tumor-suppressive miRNA in RB by directly targeting HMGB1 and inactivating the Wnt/β-catenin pathway. Hence, this miRNA is a candidate prognostic biomarker and therapeutic target in patients with RB.Keywords: microRNA-665, retinoblastoma, high-mobility group box 1, Wnt/β-catenin pathway, oncogenicity

Background Optic nerve injury is a severe complication of traumatic brain injury, which may lead to permanent and potentially loss of vision. Arbutin (ARB) is a natural hydroquinone glycoside, has been widely utilized to treat pigmented disorders. However, the role of ARB in optic nerve injury is still unclear. The study attempted to explore the effect of ARB on H2O2-induced oxidative injury in RGCs. Methods RGCs were treated with different concentrations of H2O2 to construct a cell oxidative injury model. Subsequently, the effects of ARB on these injured cells were examined through testing cell viability, apoptosis and their associated factors. MicroRNA-29a (miR-29a) inhibitor was transfected into RGCs, and the regulatory effect of miR-29a inhibition on H2O2-injured cells was detected. Further, the important signaling pathways of MEK/ERK and p38MAPK were determined to uncover the underlying mechanism. Results We firstly used H2O2 to induce RGCs injury, and subsequent experiments found that ARB significantly alleviated H2O2-induced cell injury in RGCs by promoting cell viability, reducing apoptosis, and regulating the protein levels of cell growth-associated factors. Increasing expression of miR-29a was observed in ARB and H2O2 treated cells. Moreover, miR-29a inhibition significantly abrogated the protective effect of ARB on H2O2-injured RGCs. NRAS was predicated as a direct target gene of miR-29a. Mechanistically, ARB blocked MEK/ERK and p38MAPK pathways by up-regulating miR-29a. Conclusions These data demonstrated that ARB protected RGCs against oxidative injury induced by H2O2 through blocking MEK/ERK and p38MAPK signaling pathways by up-regulation of miR-29a.

Panshi Yan, Cheng Qian, Wenzhan Wang, Yi Dong, Guangming Wan, Yue Chen Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China Background: This study was designed to examine the clinical effects of treating diabetic macular edema with an intravitreal injection of ranibizumab in combination with retinal photocoagulation.Methods: Sixty-two cases (75 eyes) with confirmed severe proliferative diabetic retinopathy or proliferative diabetic retinopathy in combination with macular edema were randomly divided into the observation group (37 eyes were given an intravitreal injection of ranibizumab combined with retinal photocoagulation) and the control group (38 eyes received retinal photocoagulation only). Vision, fundus condition, central macular thickness, and the macular leakage area were recorded before and after treatment.Results: The best-corrected visual acuity and macular leakage area were similar between the observation and control groups (P>0.05). The best-corrected visual acuity in the observation group was higher than that in the control group 3 and 6 months after treatment (P0.05). The central macular thickness of the observation group was lower than that in the control group 1, 3, and 6 months after treatment (P