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Background Non‐small cell lung cancer (NSCLC) accounts for 85% of lung cancer which is the most frequently diagnosed malignancy in China. Colon cancer associated transcript 1 (CCAT1) acts as an oncogene in enhancing tumor progression. However, the effects of CCAT1 in NSCLC remain unclear. The purpose of this study was to explore the role of CCAT1 in NSCLC. Methods Wound healing and transwell assays were performed to measure cell migration. RT‐qPCR was employed to calculate the mRNA level of CCAT1 and miR‐490. Results High expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR‐490. CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR‐490 had the opposite effect. CCAT1 could specifically bind to miR‐490 and regulate its expression. MiR‐490 partially reversed the inhibitory effect of CCAT1 on cell proliferation and metastasis. Conclusions The CCAT1/miR‐490 molecular axis has been shown to be important for the treatment of NSCLC., CCAT1 promotes the survival and metastasis of H1299 cells, while miR‐490 has the opposite effect.The CCAT1/miR‐490 molecular axis has been shown to be important for the treatment of non‐small cell lung cancer.

Dickkopf-related protein 1 (DKK1) is essential to gastric cancer as an inhibitor of Wnt signaling. Gastric intestinal metaplasia (GIM) is an important precancerous lesion of gastric cancer that can be activated by bile acid reflux and chronic inflammation. However, the exact mechanism of DKK1 in bile acid-induced GIM has not been completely elucidated. We aimed to explore the epigenetic alterations and biological functions of DKK1 in the development of GIM. In the present study, bile acid was found to induce the expression of intestinal markers in gastric epithelial cells, whereas DKK1 was downregulated in response to bile acid stimulation. The mRNA and protein expression levels of DKK1 were decreased in GIM tissues as evidenced by qRT-PCR and immunohistochemical staining. Surprisingly, the methylation of the DKK1 promoter increased in GIM tissues, and we discovered 28 differential methylation sites of the DKK1 promoter in GIM tissues. Bile acid was able to induce the partial methylation of the DKK1 promoter, while 5-aza could increase DKK1 expression as well as decrease intestinal markers expression in gastric epithelial cells. In conclusion, the promoter methylation and downregulation of DKK1 might play important roles in the development of GIM, especially bile acid-induced GIM.

Objectives This study was designed to test whether serum vitamin D levels affected Helicobacter pylori (H. pylori) infection and eradication rates. Methods A multicenter observational prospective cohort study was conducted. A total of 496 H. pylori − positive (H. pylori +) and 257 H. pylori‐negative (H. pylori −) patients were enrolled from four hospitals in China. Baseline serum vitamin D levels were measured and a 13C‐urea breath test (UBT) was performed for all the participants. The H. pylori + patients were divided into two subgroups based on their serum vitamin D levels (

In this study, the physicochemical properties, pharmacokinetics properties, and drug-likeness of pigments from Monascus-fermented rice (Monascus pigments, MPs) were predicted in silico using SwissADME tool. In silico prediction of physicochemical properties showed that MPs had desirable lipophilic drug-like physicochemical properties including molecular weight (236 to 543), TPSA (44.76 to 179.77), lipophilicity (−0.81 to 4.14), and water solubility (−4.94 to −0.77). The pharmacokinetic properties of MPs (i.e., GIA, P-glycoprotein substrate, and CYP3A4 inhibitor) illustrated that most MPs had high intestinal absorption and bioavailability, but some MPs might cause pharmacokinetics-related drug–drug interactions. Following this, six main well-known MPs (monascin, ankaflavin, rubropunctatin, monascorubrin, rubropunctamine, monascorubramine) were selected for molecular docking with some enzyme receptors. The docking results were shown with the best molecular docking poses, and the interacting residues, number and distance of hydrogen bonds of the MPs and monacolin K (for docking with 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMG-CoA reductase)), or MPs and oleic acid (for docking with lipase). Dissociation constants showed that MPs had lower inhibitory potential for HMGR (compared with Monacolin K), and higher inhibitory potential for lipase. Individual pigments from Monascus-fermented rice, therefore, have the potential to be developed as drug candidates for controlling hyperlipidemia.

Background Non-small cell lung cancer (NSCLC) is a lethal tumor resulting in a large number of cancer-related deaths globally. Long noncoding RNAs (lncRNAs) may modulate tumor initiation and metastasis. Although dysregulation of lncRNA cancer susceptibility 19 (CASC19) is validated in NSCLC, further exploration of the CASC19-regulated mechanism in NSCLC is still needed. Methods CASC19 expression was examined in NSCLC cells by a quantitative reverse transcriptase-polymerase chain reaction. The specific role of CASC19 in NSCLC was analyzed by cell counting kit-8, EdU, Transwell and western blot assays. The interaction between miR-301b-3p and CASC19 or low-density lipoprotein receptor (LDLR) was confirmed by luciferase reporter and RNA immunoprecipitation assays. Results CASC19 is markedly overexpressed in NSCLC. Its deficiency impairs cell proliferation, as well as metastasis in NSCLC. Molecular mechanism experiments indicated that CASC19 negatively modulates the expression of miR-301b-3p and miR-301b-3p can bind with CASC19 in NSCLC. In addition, miR-301b-3p binds to LDLR to impair its expression in NSCLC. Finally, rescue experiments showed that miR-301b-3p inhibition or LDLR overexpression counteracted the CASC19 knockdown-mediated function on cell proliferation and metastasis in NSCLC. Conclusions CASC19 facilitates NSCLC cell proliferation and metastasis by targeting the miR-301b-3p/LDLR axis, offering a possible strategy for lncRNA-targeted treatment in NSCLC.

Azithromycin (AZM) is a widely used antibiotic, with additional antiviral and anti-inflammatory properties that remain poorly understood. Although Zika virus (ZIKV) poses a significant threat to global health, there are currently no vaccines or effective therapeutics against it. Herein, we report that AZM effectively suppresses ZIKV infection in vitro by targeting a late stage in the viral life cycle. Besides that, AZM upregulates the expression of host type I and III interferons and several of their downstream interferon-stimulated genes (ISGs) in response to ZIKV infection. In particular, we found that AZM upregulates the expression of MDA5 and RIG-I, pathogen recognition receptors (PRRs) induced by ZIKV infection, and increases the levels of phosphorylated TBK1 and IRF3. Interestingly, AZM treatment upregulates phosphorylation of TBK1, without inducing phosphorylation of IRF3 by itself. These findings highlight the potential use of AZM as a broad antiviral agent to combat viral infection and prevent ZIKV associated devastating clinical outcomes, such as congenital microcephaly.

Background Intestinal metaplasia (IM) is a premalignant lesion associated with gastric cancer. Both animal and clinical studies have revealed that bile acid reflux and subsequent chronic inflammation are key causal factors of IM. Previous studies indicated that SOX2, the key transcription factor in gastric differentiation, was downregulated during IM development while CDX2, the pivotal intestine-specific transcription factor was upregulated significantly. However, it remains unclear whether the downregulation of SOX2 promotes gastric IM emergence or is merely a concomitant phenomenon. In addition, the underlying mechanisms of SOX2 downregulation during IM development are unclear. Methods Gastric cell lines were treated with deoxycholic acid (DCA) in a dose-dependent manner. The expression of CDX2 and miR-21 in gastric tissue microarray were detected by immunohistochemistry and in situ hybridization. Coimmunoprecipitation and immunofluorescence were performed to ascertain the interaction of SOX2 and CDX2. Luciferase reporter assays were used to detect the transcriptional activity of CDX2, and confirm miR-21 binding to SOX2 3′-UTR. The protein level of SOX2, CDX2 and downstream IM-specific genes were investigated using western blotting. mRNA level of miR-21, SOX2, CDX2 and downstream IM-specific genes were detected by qRT-PCR. Results Bile acid treatment could suppress SOX2 expression and simultaneously induce expression of CDX2 in gastric cell lines. Furthermore, we demonstrated that SOX2 overexpression could significantly inhibit bile acid- and exogenous CDX2-induced IM-specific gene expression, including KLF4, cadherin 17 and HNF4α expression. In contrast, SOX2 knockdown had the opposite effect. A dual-luciferase reporter assay demonstrated that SOX2 overexpression could significantly suppress CDX2 transcriptional activity in HEK293T cells. CDX2 and SOX2 could form protein complexes in the nucleus. In addition, bile acid induced the expression of miR-21. The inhibition of SOX2 in bile acid-treated gastric cell lines was rescued by miR-21 knockdown. Conclusions These findings suggested that SOX2 can interfere with the transcriptional activity of CDX2 in bile acid-induced IM and that miR-21 might play a key role in this process, which shed new lights in the prevention of gastric cancer. Electronic supplementary material The online version of this article (10.1186/s12935-019-0739-8) contains supplementary material, which is available to authorized users.

The imbalance of Th17/Treg cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Caveolin-1 (Cav-1) has been regarded as a potential critical regulatory protein in pathological mechanisms of chronic inflammatory respiratory diseases. Therefore, we investigated whether the loss of Cav-1 is involved in the homeostasis of Th17/Treg cells in COPD. We examined the expressions of plasma Cav-1 and circulating Th17, Treg cells, and the related cytokines in patients with COPD. Enzyme-linked immunosorbent assay (ELISA) analyses showed a significant reduction of plasma Cav-1 levels in patients with stable COPD (SCOPD) and acutely exacerbated COPD (AECOPD) compared to smokers without COPD. This loss was associated with an increase in frequency of Treg and decreased in frequency of Th17 cells. To further identify the role of Cav-1, we studied the effects of Cav-1 overexpression or downregulation on frequencies of Treg and Th17 cells in peripheral blood mononuclear cells (PBMCs) from subjects. Interestingly, small interfering RNA (siRNA) downregulation of Cav-1 was accompanied by an augmentation of Treg and reduction of Th17 expression. Together, our study demonstrated that the loss of Cav-1 contributed to the imbalance of Th17/Treg cells in patients with COPD.

Background Pain caused by oral mucositis (OM) is the main problem in the process of concurrent chemoradiotherapy for the nasopharyngeal carcinoma (NPC). This protocol aims to explore the standardized nursing and therapeutic effect of OxyContin on OM pain in the patients with NPC undergoing the concurrent chemoradiotherapy. Methods The experiment is a randomized clinical research, which was granted through the Research Ethics Committee of Shandong Provincial Third Hospital (No.20200802097). In this research, 90 NPC patients with OM induced by chemotherapy are enrolled, and the score of visual analogue >5 and the grade of OM >1 are evaluated. Patients with known allergy to OxyContin, the opioid abuse history, or major organ dysfunction, for instance, hepatic insufficiency, renal failure, and respiratory and heart failure, as well as a series of severe mental illness are excluded from our research. Patients in study groups receive standardized nursing and oral OxyContin. Patients in control groups only receive oral OxyContin. The analgesic effect could be assessed with the comparison of the visual analogue scale after and before the treatment. Safety evaluations contain the assessment of the vital signs, laboratory tests, as well as adverse events. The Karnofsky performance status standards of the International Cancer Control Union is utilized to evaluate the quality of life. Results The comparison of outcomes after taking OxyContin in both groups will be shown in .(Table is included in full-text article.) CONCLUSION:: The combination of OxyContin and standardized nursing care appears to improve the analgesic efficacy and life quality in NPC patients. Trial registration We registered this protocol in Research Registry (researchregistry6098).

Solitary fibrous tumor of the pleura (SFTP) is a rare disease, and most published case reports are in patients over 40 years old. We report a case of SFTP in a 22-year-old woman. The imaging features were observed using contrast-enhanced computed tomography (CT), and histomorphological features were evaluated using pathology and immunohistochemistry. The CT showed a mass in the pleura inside the ninth rib on the left. Pathological results of percutaneous puncture in the chest suggested the possibility of solitary fibroma. The patient underwent surgical resection, and the tumor measured 2.5 × 1.5 × 1.5 cm with an intact capsule. Pathological examination revealed a spindle cell tumor, and immunohistochemistry showed strong positive staining for CD34 and STAT6, consistent with typical solitary fibroma. Although SFTP is rare in young patients, early diagnosis and intervention are needed to avoid the possibility of future complications.

The present study aimed to investigate the factors associating with the presence of residual thrombosis in patients with acute pulmonary embolism (APE) after at least 3-month anticoagulant therapy. Demographic and clinical data of 180 cases in the affiliated hospital of Qingdao University from January 2005 to June 2015 were retrospectively analyzed. APE in all patients were confirmed by computed tomography pulmonary angiography (CTPA). Patients were then detected for the presence of residual thrombosis according to a second CTPA. After appropriate comparison test, multivariate logistic regression analysis was performed to identify predictors for residual thrombosis. Among 180 patients, complete clearance of thrombosis occurred in 115 (63.9%) patients. Residual thrombosis remained in 65 (36.1%) patients. The independent factors associating with residual thrombosis include unprovoked APE (OR 0.231, 95% CI 0.062-0.861) and fibrinogen level in acute phase (OR 1.958, 95% CI 1.282-2.911). Furthermore, these two variables were both associated with the presence of residual thrombosis in patients receiving different parenteral anticoagulants (unfractionated heparin or low-molecular-weight heparin). Pulmonary thrombosis in some patients with APE are not completely dissolved after at least 3-month treatment. Additionally, unprovoked APE is positive predictor of decreased residual thrombosis and fibrinogen level in acute phase is a risk factor of the presence of residual thrombosis.

Type 2 diabetes mellitus (T2DM) patients treated with metformin are predisposed to develop contrast-induced nephropathy (CIN) after received emergency contrast-enhanced computed tomography (CT) examination. We evaluated the protective effects of alprostadil on CIN in T2DM patients treated with metformin after contrast media (CM) administration.In this single-institution, single-blind, superiority trial, we randomly assigned 451 T2DM patients taking metformin and underwent emergency contrast-enhanced CT examination to either the alprostadil group (227 patients) receiving alprostadil or the control group (224 patients) without alprostadil. All subjects stopped taking metformin and drank 500 ml water within 12 h after CM exposure. In addition, patients in the alprostadil group were injected with alprostadil (10 μg/day, for 3 days) plus 20 ml normal saline (alprostadil hydration) and the control group patients were daily injected with 20 ml normal saline as control for 3 days following CM administration. Serum creatinine (Scr) was measured before and72 h after contrast-enhanced CT examination. CIN was defined as an increase in Scr ≥ 44.2 µmol/l (0.5 mg/dL) or25% over baseline within 3 days of contrast administration.There was a lower incidence of CIN in patients underwent alprostadil hydration than drinking water monohydration after CM administration, who with either normal renal function or chronic kidney disease (baseline eGFR 60 ml·minAlprostadil hydration was superior to drinking water monohydration regarding preventing CIN in T2DM patients treated with metformin after contrast-enhanced CT.