SLC22A17 as a Cell Death-Linked Regulator of Tight Junctions in Cerebral Ischemia.

BACKGROUND: Beyond neuronal injury, cell death pathways may also contribute to vascular injury after stroke. We examined protein networks linked to major cell death pathways and identified SLC22A17 (solute carrier family 22 member 17) as a novel mediator that regulates endothelial tight junctions after ischemia and inflammatory stress. METHODS: Protein-protein interactions and brain enrichment analyses were performed using STRING, Cytoscape, and a human tissue-specific expression RNA-seq database. In vivo experiments were performed using mouse models of transient focal cerebral ischemia. Human stroke brain tissues were used to detect SLC22A17 by immunostaining. In vitro experiments were performed using human brain endothelial cultures subjected to inflammatory stress. Immunostaining and Western blot were used to assess responses in SLC22A17 and endothelial tight junctional proteins. Water content, dextran permeability, and electrical resistance assays were used to assess edema and blood-brain barrier (BBB) integrity. Gain and loss-of-function studies were performed using lentiviral overexpression of SLC22A17 or short interfering RNA against SLC22A17, respectively. RESULTS: Protein-protein interaction analysis showed that core proteins from apoptosis, necroptosis, ferroptosis, and autophagy cell death pathways were closely linked. Among the 20 proteins identified in the network, the iron-handling solute carrier SLC22A17 emerged as the mediator enriched in the brain. After cerebral ischemia in vivo, endothelial expression of SLC22A17 increases in both human and mouse brains along with BBB leakage. In human brain endothelial cultures, short interfering RNA against SLC22A17 prevents TNF-α (tumor necrosis factor alpha)-induced ferroptosis and downregulation in tight junction proteins and disruption in transcellular permeability. Notably, SLC22A17 could repress the transcription of tight junctional genes. Finally, short interfering RNA against SLC22A17 ameliorates BBB leakage in a mouse model of focal cerebral ischemia. CONCLUSIONS: Using a combination of cell culture, human stroke samples, and mouse models, our data suggest that SLC22A17 may play a role in the control of BBB function after cerebral ischemia. These findings may offer a novel mechanism and target for ameliorating BBB injury and edema after stroke.

Number of positive lymph nodes is superior to neck stage of the 8th AJCC in predicting prognosis in parotid mucoepidermoid carcinoma.

BACKGROUND: To clarify the impact of the number of positive lymph nodes (LNs) on the prognosis of parotid mucoepidermoid carcinoma (MEC). METHODS: Patients who underwent neck dissection for parotid MEC were retrospectively enrolled. The primary outcome variable was overall survival (OS). Associations between OS and LN factors, including the AJCC N stage, intraparotid LN metastasis, number of positive LNs, LN size, and extranodal extension (ENE), were evaluated using Cox proportional hazard regression analyses. RESULTS: A total of 720 patients were included with a mean age of 56 ± 16 years. There was no additional survival compromise until two positive LNs were presented. After adjusting for the number of positive LNs, intraparotid LN metastasis, ENE, and LN size were not related to prognosis. Our proposed N stage based on the number of metastatic LNs (0/1 vs. 2-4 vs. 5+) showed a superior C-index to the AJCC N stage in OS prediction. CONCLUSION: Quantitative LN burden was an important determinant of prognosis, and the proposed N stage provided better OS stratification than the AJCC N stage.

Single cell profiling of female breast fibroadenoma reveals distinct epithelial cell compositions and therapeutic targets.

Fibroadenomas (FAs) are the most common breast tumors in women. No pharmacological agents are currently approved for FA intervention owing to its unclear mechanisms and a shortage of reproducible human models. Here, using single-cell RNA sequencing of human FAs and normal breast tissues, we observe distinct cellular composition and epithelial structural changes in FAs. Interestingly, epithelial cells exhibit hormone-responsive functional signatures and synchronous activation of estrogen-sensitive and hormone-resistant mechanisms (ERBB2, BCL2 and CCND1 pathways). We develop a human expandable FA organoid system and observe that most organoids seem to be resistant to tamoxifen. Individualized combinations of tamoxifen with ERBB2, BCL2 or CCND1 inhibitors could significantly suppress the viability of tamoxifen-resistant organoids. Thus, our study presents an overview of human FA at single-cell resolution that outlines the structural and functional differences between FA and normal breast epithelium and, in particular, provides a potential therapeutic strategy for breast FAs.

Clinical parameters predictors of malignant transformation of recurrent parotid pleomorphic adenoma.

Malignant transformation (MT) in recurrent parotid pleomorphic adenomas (PAs) is rare; therefore its occurrence lacks reliable predictive factors. Our goal was to clarify the predictors for MT of recurrent parotid PAs based on preoperative clinical parameters. Patients with a clinical diagnosis of recurrent parotid PA were retrospectively enrolled. The association between clinicopathologic variables and MT of PA was assessed using univariate and multivariate analyses. MT occurred in 11.8% of the 467 patients. In univariate analysis, three or more previous recurrences, newly developed facial nerve paralysis, difficulty in mouth opening, tumors with the largest tumor diameter ≥ 2.4 cm, and abnormal neck lymph node enlargement were associated with MT occurrence. Further, multivariate analysis showed that three or more previous recurrences, newly developed facial nerve paralysis, difficulty in mouth opening, and abnormal neck lymph node enlargement were independently related to MT. MT of recurrent PA was not uncommon. Clinical signs of malignancy included newly developed facial nerve paralysis, difficulty in mouth opening, three or more previous recurrences, and abnormal neck lymph node enlargement.

FUT8-AS1/miR-944/Fused in Sarcoma/Transcription Factor 4 Feedback Loop Participates in the Development of Oral Squamous Cell Carcinoma through Activation of Wnt/ß-Catenin Signaling Pathway.

As a common type of head and neck squamous cell carcinoma, oral squamous cell carcinoma (OSCC) is a lethal and deforming disease. Long noncoding RNAs have emerged as critical modulators in different malignancies. However, the role of fucosyltransferase 8 antisense RNA 1 (FUT8-AS1) in OSCC still remains elusive. In this study, quantitative RT-PCR and Western blot were used for the measurement of RNAs and proteins. Mechanism assays explored the putative correlation among genes. In vitro assays evaluated the changes in OSCC cell malignant phenotype, whereas in vivo assays highlighted the influence of FUT8-AS1 on tumor growth. FUT8-AS1, aberrantly up-regulated in OSCC tissues and cells, could exacerbate OSCC cell malignant behaviors. The cancerogenic property of FUT8-AS1 in OSCC was further confirmed via animal experiments. Furthermore, FUT8-AS1 enhanced the expression of transcription factor 4 (TCF4) via sponging miR-944 and recruiting fused in sarcoma (FUS), thus affecting OSCC cell biological behaviors via modulation on Wnt/ß-catenin signaling activity. In addition, TCF4 was validated as the transcriptional activator of FUT8-AS1. To conclude, TCF4-mediated FUT8-AS1 could exacerbate OSCC cell malignant behaviors and facilitate tumor growth via modulation on miR-944/FUS/TCF4.

Annexin A2 promotes angiogenesis after ischemic stroke via annexin A2 receptor - AKT/ERK pathways.

Promoting angiogenesis to restore circulation to the ischemic tissue is still an important therapeutic target in stroke. Our group and others previously reported that the Ca2+-regulated, phospholipid-and membrane-binding protein-Annexin A2 (ANXA2) functions in cerebrovascular integrity and retinal neoangiogenesis. Here, we hypothesized that ANXA2 may regulate angiogenesis after stroke, ultimately improve neurological outcomes. Compared with wild type (WT) mice, the density of microvessels in brain and the number of new vessels sprouting from aortic ring were significantly increased in Anxa2 knock-in (Anxa2 KI) mice. After focal cerebral ischemia, proliferation of brain endothelial cells in Anxa2 KI mice was significantly elevated at 7 days post-stroke, which further improved behavioral recovery. To assess the pro-angiogenic mechanisms of ANXA2, we used brain endothelial cells cultures to investigate its effects on cell tube-numbers and migration. Recombinant ANXA2 increased tube-numbers and migration of brain endothelial cells either under normal condition or after oxygen glucose deprivation (OGD) injury. Co-immunoprecipitation experiments demonstrated that these protective effects of recombinant ANXA2 were regulated by interaction with ANXA2 receptor (A2R), a protein found in cancer cells that can interact with ANXA2 to promote cell migration and proliferation, and the ability of ANXA2-A2R to activate AKT/ERK pathways. Inhibition of AKT/ERK diminished recombinant ANXA2-induced angiogenesis in vitro. Taken together, our study indicates that ANXA2 might be involved in angiogenesis after ischemic stroke. Further investigation of ANXA2-A2R will provide a new therapeutic target for stroke.

Occult neck metastases risk factors and the role of elective neck dissection in cT3-4N0 adenoid cystic carcinoma of the parotid gland.

Objectives: To determine the predictor for occult neck metastases and the role of elective neck dissection (END) in cT3-4N0 parotid adenoid cystic carcinoma (ACC). Methods: Patients with surgically treated parotid ACC were retrospectively enrolled. Predictors of occult neck metastases and the effect of END on disease specific survival (DSS), overall survival (OS), locoregional control survival (LRC), and distant metastasis free survival (DMS) were analyzed. Results: Occult neck metastases occurred in 35 (19.7%) of the 178 patients undergoing an END. The tumor stage [p=0.011, 4.215 (1.387-10.435)] and intra-parotid lymph node metastasis [p=0.032, 3.671 (1.693-8.775)] were related to the possibility of occult neck metastases independently. The END group had better 10-year LRC than the observation group (56% vs. 43%, p=0.002) and also better 10-year DMS than the observation group (43% vs. 32%, p<0.001). The two groups had similar 10-year DSS (40% vs. 33%, p=0.230) and OS (31% vs. 23%, p=0.094) rates. Furthermore, the Cox model confirmed that END was independently associated with better LRC rate [p=0.022, 2.576 (1.338-6.476)] and better DMS [p=0.011, 2.343 (1.274-7.462)]. Conclusions: Occult neck metastases in cT3-4N0 parotid ACC was not common. A T4 tumor with intra-parotid lymph node metastasis had the highest possibility of occult neck metastases. END had no effect on DSS or OS but significantly decreased the risk of locoregional recurrence and distant metastasis.

A novel cuproptosis-related LncRNA signature: Prognostic and therapeutic value for acute myeloid leukemia.

Background: Cuproptosis is a type of programmed cell death that is involved in multiple physiological and pathological processes, including cancer. We constructed a prognostic cuproptosis-related long non-coding RNA (lncRNA) signature for acute myeloid leukemia (AML). Methods: RNA-seq and clinical data for AML patients were acquired from The Cancer Genome Atlas (TCGA) database. The cuproptosis-related prognostic lncRNAs were identified by co-expression and univariate Cox regression analysis. The least absolute shrinkage and selection operator (LASSO) was performed to construct a cuproptosis-related lncRNA signature, after which the AML patients were classified into two risk groups based on the risk model. Kaplan-Meier, ROC, univariate and multivariate Cox regression, nomogram, and calibration curves analyses were used to evaluate the prognostic value of the model. Then, expression levels of the lncRNAs in the signature were investigated in AML samples by quantitative polymerase chain reaction (qPCR). KEGG functional analysis, single-sample GSEA (ssGSEA), and the ESTIMATE algorithm were used to analyze the mechanisms and immune status between the different risk groups. The sensitivities for potential therapeutic drugs for AML were also investigated. Results: Five hundred and three lncRNAs related to 19 CRGs in AML samples from the TCGA database were obtained, and 21 differentially expressed lncRNAs were identified based on the 2-year overall survival (OS) outcomes of AML patients. A 4-cuproptosis-related lncRNA signature for survival was constructed by LASSO Cox regression. High-risk AML patients exhibited worse outcomes. Univariate and multivariate Cox regression analyses demonstrated the independent prognostic value of the model. ROC, nomogram, and calibration curves analyses revealed the predictive power of the signature. KEGG pathway and ssGSEA analyses showed that the high-risk group had higher immune activities. Lastly, AML patients from different risk groups showed differential responses to various agents. Conclusion: A cuproptosis-related lncRNA signature was established to predict the prognosis and inform on potential therapeutic strategies for AML patients.

Predictors predisposing to orocutaneous fistula occurrence following free flap reconstruction.

Objectives: To explore the possible risk factors of orocutaneous fistula (OCF) development in free flap reconstruction of the tongue/floor of the mouth (TFOM). Methods: Data of patients who underwent free flap reconstruction of the TFOM were retrospectively analyzed. The association between clinicopathologic variables and OCF occurrence was analyzed using univariate and multivariate analyses. Results: Altogether, 469 patients were enrolled. OCF occurred in 43 patients with a rate of 9.2%. The univariate analysis revealed the negative effects of smoking, preoperative albumin level, cachexia, T4 stage, neck dissection, entire resection of the floor of the mouth (FOM), segmental mandibulectomy, and surgical site infection on OCF occurrence. The multivariate analysis confirmed the independence of cachexia (p<0.001, 4.386[1.883-9.472]), tumor stage (p<0.001, 2.738[1.482-6.629]), entire FOM resection (p<0.001, 6.332[2.110-14.432]), and surgical site infection (p<0.001, 5.376[1.998-11.218]) in affecting the OCF development. Conclusions: OCF development following free flap reconstruction of the TFOM was relatively uncommon, but significantly associated with presence of cachexia, T4 stage, entire FOM resection, and surgical site infection.

Impacts of microplastics addition on sediment environmental properties, enzymatic activities and bacterial diversity.

Environmental microplastic accumulation can lead to a range of problems and the potential loss of ecosystem services. However, the impacts of microplastics on sediment environmental properties and microbial ecosystems remain unclear. Therefore, this article aimed to better elucidate the effects of microplastics on sediment physicochemical properties, enzymatic activities and the diversity and composition of sediment microbial communities. We conducted a 60-day sediment-incubation experiment using sediments with three concentrations (2%, 5%, and 10%, w/w) and two types (polyethylene (PE) and polyvinyl chloride (PVC)) of microplastics (550 µm) in a climate-controlled chamber. The addition of both PE and PVC microplastics reduced sediment catalase, polyphenol oxidase (PO), and urease activities, and decreased physicochemical indicators, including total organic carbon (TOC), total nitrogen (TN), and pH value. In addition, microplastics reduced bacterial community diversity and inhibited the recovery of community richness, implying that microplastics may compete with sediment microorganisms for niches. Stronger effects were generally detected under a high microplastic concentration (10%), reflecting the influence of the concentration of microplastic exposure on the bacterial community. The dominant bacterial phyla were Chloroflexi, Proteobacteria, Bacteroidota, Firmicutes, and Actinobacteriota, and the relative abundances of Proteobacteria, and Bacteroidota significantly increased in the microplastic treatments during the late incubation period, indicating that microplastic addition may have improved nutritional conditions later in the incubation process. Structural equation modeling indicated that shifts in PO activity had a significant correlation with changes in Proteobacteria abundance (P < 0.01), and important drivers affecting the dissimilarity of Bacteroidota abundance were the changes of TN content and catalase activity (P < 0.05). These results indicated that microplastics with diverse characteristics affected the environmental properties of the sediment, while the physicochemical properties and enzymatic activity of the sediment could directly or indirectly exert different impacts on the dominant bacteria. This study can provide a theoretical basis for the ecological effects of microplastic contamination.

CircPVT1 facilitates the progression of oral squamous cell carcinoma by regulating miR-143-3p/SLC7A11 axis through MAPK signaling pathway.

Oral squamous cell carcinoma (OSCC) is a common malignant tumor occurring in the oral cavity. Circular RNAs (circRNAs) play a crucial regulatory role in many cancers. This study aimed to investigate the function of circRNA plasmacytoma variant translocation 1 (PVT1) (circPVT1) in OSCC and its potential mechanism. The levels of circPVT1, solute carrier family 7 member 11 (SLC7A11), and microRNA-143-3p (miR-143-3p) were examined by quantitative real-time PCR (qRT-PCR) or western blot assay. Cell proliferation, apoptosis, migration, and invasion were evaluated by Cell Counting Kit-8 (CCK-8), colony formation assay, flow cytometry, and transwell assay. The levels of apoptosis and proliferation-related proteins were examined by western blot. The targeting relationship between miR-143-3p and circPVT1 or SLC7A11 was verified by dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The levels of mitogen-activated protein kinase (MAPK) pathway-related proteins were measured by western blot. Xenograft assay was used to assess tumor growth in vivo. CircPVT1 and SLC7A11 were upregulated, while miR-143-3p was downregulated in OSCC tissues and cells. Silencing of circPVT1 or SLC7A11 suppressed proliferation, migration, and invasion and promoted apoptosis in OSCC cells. CircPVT1 upregulated SLC7A11 expression via sponging miR-143-3p. SLC7A11 upregulation alleviated the effect of circPVT1 knockdown on OSCC cell progression. Besides, circPVT1 modulated MAPK signaling pathway by regulating miR-143-3p. Moreover, circPVT1 knockdown inhibited tumor growth in vivo. Knockdown of circPVT1 impeded OSCC progression via the miR-143-3p/SLC7A11 axis through MAPK signaling pathway.

MiR-770 promotes oral squamous cell carcinoma migration and invasion by regulating the Sirt7/Smad4 pathway.

Oral squamous cell carcinoma (OSCC) is a common malignant cancer with unfavorable prognosis, and the epithelial-to-mesenchymal transition (EMT) is a critical contributor to OSCC metastasis. Recently, we have shown that sirtuin 7 (Sirt7) is associated with EMT and OSCC metastasis by acetylating small mother against decapentaplegic 4 (Smad4). Nonetheless, the mechanism of Sirt7 downregulation in OSCC cells remains unknown. This study analyzed the potential microRNAs that were predicted to regulate Sirt7 expression by online databases. We identified miR-770 as an upstream regulator of Sirt7 that targets its 3'-untranslated region. The expression of miR-770 was observed to be negatively correlated with the mRNA expression of Sirt7 in metastatic OSCC tumors, and higher miR-770 expression was correlated with poorer OSCC patient survival. Our in vitro data indicated that miR-770 promoted OSCC cell migration and invasion, and this process was dependent on Sirt7/Smad4 signaling. Furthermore, in vivo metastasis experiments indicated that miR-770 overexpression led to more prominent OSCC metastasis and downregulated Sirt7 expression. Collectively, our results revealed a new role of Sirt7 downregulation in metastatic OSCC and suggested that miR-770 is a potential target in counteracting OSCC metastasis.

Assessment of Quality of Life of Free Anterolateral Thigh Flap for Reconstruction of Tissue Defects of Total or Near-Total Glossectomy.

BACKGROUND: The aim of this study was to evaluate quality of life of free anterolateral thigh flap (ALTFF) for reconstruction of tissue defects of total or near-total glossectomy. METHODS: Quality of life was assessed by means of the University of Washington Quality of Life (UW-QOL) and the 14-item Oral Health Impact Profile (OHIP-14), after 12 months postoperatively. RESULTS: 65 of 79 questionnaires were returned (82.27%). In the UW-QOL, the best-scoring domain was "shoulder," whereas the lowest scores were for "chewing" and "pain." In the OHIP-14, the lowest-scoring domain was "handicap," followed by "Social disability" and "Psychological disability." CONCLUSION: Free anterolateral thigh perforator flaps for reconstruction of total or near-total glossectomy defects after cancer resection would have significantly influenced the patients' oral functions and quality of life.

HOXC13-AS accelerates cell proliferation and migration in oral squamous cell carcinoma via miR-378g/HOXC13 axis.

Oral squamous cell carcinoma (OSCC) is an aggressive cancer type in head and neck. A number of long non-coding RNAs (lncRNAs) are discovered to serve regulatory roles in OSCC. HOXC13 antisense RNA (HOXC13-AS) has been proved to behave as a tumor-facilitator in nasopharyngeal carcinoma, but its regulatory role in OSCC has never been investigated. In this study, GEPIA indicated that HOXC13-AS and its neighbor gene HOXC13 were upregulated in HNSC samples, and we consistently unveiled their upregulation in OSCC tissues and cell lines. Silencing HOXC13-AS abrogated OSCC cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT). Moreover, HOXC13 overexpression rescued the influences of HOXC13-AS silence on OSCC cellular processes and in vivo tumor growth. Mechanistically, HOXC13-AS upregulated HOXC13 expression in OSCC through sequestering miR-378g, which was proved to exert suppressive functions in the malignant behaviors of OSCC cells. Further, HOXC13 was revealed to be positively correlated with HOXC13-AS and negatively with miR-378g in expression in OSCC samples. In sum, our findings suggested that HOXC13-AS functioned as a ceRNA to accelerate the malignant behaviors of OSCC cells via miR-378g/HOXC13 axis, shedding a new light on the lncRNA-targeted treatment for OSCC.

From in vitro to in vivo reprogramming for neural transdifferentiation: An approach for CNS tissue remodeling using stem cell technology.

Advances in stem cell technology have provided three approaches to address the demanding issue of the treatment of intractable neurological disease. One of the approaches is the screening of compounds attenuating pathological phenotypes in stem-cell based models. A second approach consists of exogenous-targeted cell supplementation to the lesion with stem cell-derived differentiated cells. A third approach involves in vivo direct programming to transdifferentiate endogenous somatic cells and to boost CNS tissue remodeling. In this review, we outline research advances in stem cell technology of direct reprogramming in vitro and in vivo and discuss the future challenge of tissue remodeling by neural transdifferentiation.

Impact of the Body Mass Index on Hemorrhage After Surgery for Thyroid Cancer.

OBJECTIVE: To investigate the effects of different values of the body mass index (BMI) on postoperative hemorrhage (PH) in thyroid cancer (TC) and its clinical management. METHODS: This retrospective cohort study selected 43 patients with hemorrhage after TC surgery in 7413 cases. Patients were divided based on the BMI (kg/m2) into normal (24), overweight group (24 ≤BMl<28) and obese (≥28) groups. Clinical and pathologic data, bleeding cause, bleeding site, treatment and prognosis were assessed. RESULTS: BMI (P=0.038) is an independent risk factor for PH of TC, related to hypertension (P=0.004) and coronary heart disease (P=0.001) in the three groups. Preoperative weight loss was not noted (P=0.477). Hemorrhage in 60.47% of patients occurred between 4 h and 8 h after surgery. The higher the BMI, the longer was the operative time (≥1 h, 65.12%) (P=0.017), which resulted in greater intraoperative blood loss (≥20 mL, 74.42%) (P=0.025), postoperative hypoparathyroidism (P=0.015) and the probability of injury to the recurrent laryngeal nerve (P=0.026). The main causes of bleeding were incomplete vascular ligation (30.23%), severe postoperative cervical activity (16.28%) and long-term use of anticoagulant drugs (11.63%). Overall survival at 5 years in the obese group was poor (P=0.015). Forty patients (93.02%) underwent surgical exploration and hemostasis and two patients (4.65%) underwent tracheotomy. All PH complications disappeared completely after active postoperative treatment, and all patients were discharged from hospital. CONCLUSION: Obesity is closely associated with PH in TC patients. Therefore, in obese patients, active prevention preoperatively, complete hemostasis intraoperatively, early detection and timely treatment postoperatively are the key factors to reduce PH risk.

LncRNA LINC00662 promotes colon cancer tumor growth and metastasis by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.

BACKGROUND: LncRNA LINC00662 is closely related to the occurrence and development of cancer. This study aims to explore the effect of LINC00662 on colon cancer tumor growth and metastasis and its molecular mechanism. METHODS: CCK8, colony formation, transwell, scratch wound, TUNEL, flow cytometry, RT-PCR, western blotting and immunohistochemistry assays were used to detect the proliferation, apoptosis, invasion and migration of colon cancer cell and mRNA and protein expressions. Luciferase reporter and RNA pull down assays were used to detect the combination of LINC00662 and miR-340-5p or IL22 and the combination of miR-340-5p and CLDN8/IL22. Co-immunoprecipitation were used to detect the co-expression of CLDN8 and IL22 in colon cell lines. The targets of LINC00662 were predicated by Starbase v2.0. The target genes of miR-340-5p were predicated by miRDB and TargetScan. GO and KEGG enrichment analysis were performed by DAVID website. RESULTS: LINC00662 was up-regulation in colon cancer tissues and cell lines. Univariate Cox regression analysis showed that the LINC00662 expression level was related to the poor prognosis. LINC00662-WT and miR-340-5p mimics co-transfection depressed luciferase activity and IL22/CLDN8-WT and miR-340-5p inhibitors co-transfection memorably motivated luciferase activity. LINC00662 overexpression promoted cell proliferation, invasion and migration, and inhibited cell apoptosis in colon cancer. In vivo xenograft studies in nude mice manifested that LINC00662 overexpression prominently accelerate tumor growth. There was an opposite reaction in the biological functions of colon cells and tumor growth between LINC00662 overexpression and LINC00662 inhibition in vitro and in vivo. The functions of miR-340-5p mimics regulating the biological functions of colon cells and tumor growth were consistent with those of LINC00662 inhibition. CLDN8 and IL22, as target genes of miR-340-5p, reversed the functions of LINC00662 affecting the biological functions of colon cells and the protein levels of Bax, Bcl-2, XIAP, VEGF, MMP-2, E-cadherin and N-cadherin. Co-immunoprecipitation experiments indicated that CLDN8 directly interact with IL22 in colon cell lines. LINC00662 regulated CLDN8 and IL22 expressions and the activation of ERK signaling pathway via targeting miR-340-5p. CONCLUSION: LINC00662 overexpression promoted the occurrence and development of colon cancer by competitively binding with miR-340-5p to regulate CLDN8/IL22 co-expression and activating ERK signaling pathway.

Correlation Between Endorectal Ultrasound and Magnetic Resonance Imaging for Predicting the Circumferential Resection Margin in Patients With Mid-Low Rectal Cancer Without Preoperative Chemoradiotherapy.

OBJECTIVES: To assess the correlation between endorectal ultrasound (ERUS) and magnetic resonance imaging (MRI) in predicting the circumferential resection margin (CRM) status of patients with mid-low rectal cancer without preoperative chemoradiotherapy. METHODS: Twenty patients with rectal cancer who did not receive preoperative chemoradiotherapy and underwent ERUS and MRI examinations before total mesorectal excision from May 2018 to April 2019 were included in this study. The patient and tumor characteristics, lymph nodes, tumor stages, ERUS and MRI predictors of the CRM status, and postoperative pathologic results were recorded. The closest distance between the deepest portion of lesion invasion and the mesorectal fascia was independently measured on MRI and ERUS images by 2 observers. The observers were blinded to the pathologic results. Measurements from ERUS and MRI were compared. RESULTS: The mean distance between the distal edge of the lesion and the anal verge was 5.7 cm (range, 3.1-8.1 cm). The ERUS and pathologic evaluations of CRM involvement were consistent in 90% of the cases. The MRI and pathologic evaluations of CRM involvement were concordant in 95% of the cases. The Cohen κ coefficient of ERUS and MRI was 0.608 (P = .007). The correlation coefficient of ERUS and MRI for assessing the closest distance from the edge of cancer invasion to the mesorectal fascia was 0.99 (P = .0005). CONCLUSIONS: Endorectal ultrasound and MRI assessments of the preoperative CRM status appear to be highly consistent. Endorectal ultrasound can be used as a complementary tool with MRI to predict the CRM status of patients with mid-low rectal cancer without preoperative chemoradiotherapy.

Vascular Macrophages in Atherosclerosis.

Atherosclerosis is the main pathological basis for the occurrence of most cardiovascular diseases, the leading global health threat, and a great burden for society. It has been well established that atherosclerosis is not only a metabolic disorder but also a chronic, sterile, and maladaptive inflammatory process encompassing both innate and adaptive immunity. Macrophages, the major immune cell population in atherosclerotic lesions, have been shown to play critical roles in all stages of atherosclerosis, including the initiation and progression of advanced atherosclerosis. Macrophages have emerged as a novel potential target for antiatherosclerosis therapy. In addition, the macrophage phenotype is greatly influenced by microenvironmental stimuli in the plaques and presents complex heterogeneity. This article reviews the functions of macrophages in different stages of atherosclerosis, as well as the phenotypes and functions of macrophage subsets. New treatment strategies based on macrophage-related inflammation are also discussed.

Cr(VI) Adsorption on Engineered Iron Oxide Nanoparticles: Exploring Complexation Processes and Water Chemistry.

Surface-functionalized magnetic nanoparticles are promising adsorbents due to their large surface areas and ease of separation after contaminant removal. In this work, the affinity of Cr(VI) adsorption to 8 nm surface-functionalized superparamagnetic magnetite nanoparticles was determined for surface coatings with amine (trimethyloctadecylammonium bromide, CTAB) and carboxyl (stearic acid, SA) functional groups. Cr(VI) adsorbed more strongly to the CTAB-coated nanoparticles than to the SA-coated materials due to electrostatic interactions between positively charged CTAB and anionic Cr(VI) species. The adsorption of Cr(VI) by CTAB- and SA-coated nanoparticles increased with decreasing pH (4.5-10), which could be simulated by a surface complexation model. Cr(VI) removal performance by the nanocomposite was evaluated for two realistic drinking water compositions. The co-occurrence of divalent cations (Ca2+ and Mg2+) and Cr(VI) resulted in decreased Cr(VI) adsorption as particles were destabilized, leading to the aggregation and lower effective surface area, confirming the importance of the overall water composition on the performance of novel engineered nanomaterials for water treatment applications.