The additional value of high-resolution vessel wall imaging in screening suitable chronic internal carotid artery occlusion candidates for endovascular recanalization: comparison with digital subtraction angiography.

BACKGROUND: High-resolution vessel wall imaging (HR-VWI) can provide information about exact occluded length, etiology, and the presence of intraluminal thrombus or residual cavity. PURPOSE: To investigate the extra value of HR-VWI in screening patients with chronic internal carotid artery occlusion (CICAO) for recanalization suitability in comparison with digital subtraction angiography (DSA). MATERIAL AND METHODS: We retrospectively reviewed patients who underwent endovascular recanalization with no internal carotid artery signal on magnetic resonance angiography (MRA) and whose both preoperative DSA and HR-VWI data were available. Patients were classified into type I (focal occlusion distal to ophthalmic artery), type II or III (occlusion proximal or at/distal to clinoid segment), and near-occlusion. Occlusion etiology and suitability for recanalization were analyzed both on preoperative DSA and HR-VWI. Accuracy of occlusion classification and differences in the modified Rankin scale scores between the baseline and follow-up were estimated. RESULTS: A total of 20 patients were included. With intraoperative DSA as the gold standard, we found HR-VWI could additionally show intraluminal thrombi. Preoperative DSA misclassified one near-occlusion, one type I occlusion, and one type II occlusion as type III occlusions, and one near-occlusion as a type II occlusion. Therefore, compared with the preoperative DSA, three additional cases were successfully recanalized based on HR-VWI. The accuracy of HR-VWI was higher than preoperative DSA (100% vs. 80%). Prognosis improvement of type I was significantly better than type II and near-occlusion (P<0.05). CONCLUSION: HR-VWI can identify occluded etiology, extent, and classification of CICAO. This information is potentially useful in screening candidates for endovascular recanalization and helpful to indicate prognosis.

Silencing PRSS1 suppresses the growth and proliferation of gastric carcinoma cells via the ERK pathway.

Background: Gastric carcinoma (GC) is one of the most common malignant tumors and seriously threatens human life and health. Methods: In the present study, 243 differentially expressed proteins in GC were identified using laser capture microdissection (LCM) combined with isotopically labeled quantitative proteomics technology. The expression of serine protease 1 (PRSS1) protein was analyzed by immunohistochemistry and Western blot. MTT and colony formation assays were employed to determine the effect of PRSS1 expression on the growth and proliferation of GC cells. Then, we observed the expression of miR-146a-5p in GC by qRT-PCR. A dual luciferase assay was performed to determine whether PRSS1 is a target gene of miR-146a-5p. We also explored the influence of miR-146a-5p expression on PRSS1 expression and on the growth and proliferation of GC cells. Finally, Western blotting was used to analyze the effect of PRSS1 expression on the activation of the ERK signaling pathway. Results: We confirmed that PRSS1 expression was significantly increased and was positively correlated with the differentiation, tumor size and lymph node metastasis of GC. Subsequently, we found that overexpression of PRSS1 promoted the growth and proliferation of cells, whereas silencing PRSS1 expression inhibited the growth and proliferation of MGC803 cells by inhibiting activation of the ERK signaling pathway via reductions in PAR-2 activation. MiR-146a-5p targets PRSS1 and suppresses the growth and proliferation of MGC803 cells. Conclusions: miR-146a-5p targets PRSS1 and suppresses the growth and proliferation of MGC803 cells. Silencing PRSS1 expression inhibits the ERK signaling pathway by reducing PAR-2 activation, resulting in suppressed growth and proliferation of MGC803 GC cells.

Carboxyl terminal activating region 3 of latent membrane protein 1 encoded by the Epstein­Barr virus regulates cell proliferation and protein expression in NP69 cells.

In the present study, the mechanism by which carboxyl terminal activating region 3 (CTAR3) of latent membrane protein 1 (LMP1), encoded by the Epstein­Barr virus, regulated cell proliferation and protein expression was investigated in the nasopharyngeal epithelial cell line NP69. The deletion mutant LMP1 (LMP1Δ232­351; amino acid residues including 232­351 codons in CTAR3 deleted) was generated by polymerase chain reaction. An NP69­LMP1Δ232­351 cell line was established by retroviral infection. Finally, cell proliferation and protein expression of NP69 cells expressing LMP1Δ232­351 were examined using a cell growth curve and western blot analysis. The results demonstrated: i) The proliferation of NP69­LMP1Δ232­351 cells was significantly decreased compared with cells expressing wild type LMP1 (LMP1WT; n=3; P<0.05); ii) 17 proteins exhibited differential protein expression (>2­fold change) in NP69­LMP1Δ232­351 cells compared with NP69­LMP1WT cells; and iii) LMP1WT was involved in activating the Janus kinase 3 (JAK3) promoter and regulating the expression of JAK3 protein, while LMP1Δ232­351 was almost defective in ability to activate the JAK promoter. These results suggested that LMP1­CTAR3 may be an important functional domain for regulating cell proliferation and protein expression in nasopharyngeal epithelial cells.

Trends in stroke incidence among elderly low-income residents of rural China: a population-based study from 1992 to 2016.

In China, >70% of stroke deaths occur in people aged ≥65 years. However, trends in the stroke incidence among elderly people are unclear. We aimed to determine trends in the stroke incidence among elderly people in rural China. This was a population-based surveillance study conducted in Tianjin, China. Stroke events and all deaths were registered annually. Trends and annual proportion of change in incidence of first-ever stroke were evaluated from 1992 to 2016. The age-standardized incidence of first-ever stroke increased annually by 3.7% overall in elderly people (2.7% for men; 5.0% for women; all P<0.05). However, from 2008 to 2016, there was no significant change in the trends of stroke incidence among elderly people, across gender and subtypes. The proportion of elderly patients with first-ever stroke decreased by 1.1% annually. In contrast to young patients, annual changes in the incidence of stroke tended to be slight in elderly patients (3.7% vs. 9.5%) with greater increase in female patients than those in male patients (2.7% vs. 10.3% for men; 5.0% vs. 8.9% for women). Thus, the control of risk factors for stroke among elderly people is crucial, especially among older women, to reduce the burden of stroke in China.

Identification of differentially expressed proteins in the gastric mucosal atypical hyperplasia tissue microenvironment.

In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differentially expressed GMAH proteins of the NGM and GMAH tissues were identified by quantitative proteomic techniques with isotope labeling. The cross-talk between differentially expressed proteins in NGM and GMAH tissues was then analyzed by bioinformatics. There were 165 differentially expressed proteins identified from the stromata of NGM and GMAH tissues. Among them, 99 proteins were upregulated and 66 were downregulated in GMAH tissue. The present study demonstrated that these proteins in gastric mucosal atypical hyperplasia were involved in cancer-associated signaling pathways, including the p53, mitogen-activated protein kinase (MAPK), cell cycle and apoptosis signaling pathways, and were involved in cellular growth, cellular proliferation, apoptosis and the humoral immune response. The results of the present study suggest that the 165 differentially expressed proteins, including S100 calcium-binding protein A6 (S100A6) and superoxide dismutase 3 (SOD3) in the microenvironment of gastric mucosal atypical hyperplasia, are involved in the p53, MAPK, cell cycle and apoptosis signaling pathways, and serve a function in the pathogenesis of gastric cancer.

Reusable light-emitting-diode induced chemiluminescence aptasensor for highly sensitive and selective detection of riboflavin.

A novel reusable chemiluminescence aptasensor was developed based on aptamer recognition coupled with light-emitting-diode induced chemiluminescence (LED-CL) detection. The sensing approach was based on the design that the model analyte riboflavin (Rf) in sample solutions was captured by the immobilized aptamers and then eluted simply with alkaline luminol solution to catalyze the CL reaction between luminol and dissolved oxygen under high power LED irradiation. This design allowed a very simple (branch-free) flow way for the CL sensing system. The CL intensity versus the Rf concentration was linear in the range from 0.03 to 5ngmL(-1) with a limit of detection (LOD) down low to 8pgmL(-1). Without renewing the aptamer, the relative standard deviation (RSD) for seven consecutive detections is 2.33%; the sensor also showed good stability without performance deterioration after >100 times use. Up to 10000-fold of K(+), Na(+), Ca(2+), Mg(2+), and Fe(3+), 5000-fold for glucose and bovine serum albumin, 1000-fold of uric acid, 1500-fold of ascorbic acid (added with Fe(3+)), 100-fold of flavin mononucleotide and 200-fold of flavin adenine dinucleotide caused no significant interference with the determination of 0.5ngmL(-1) Rf. The sensor was applied for analysis of Rf in urine and food samples with the recovery of 94-103%. The advantages of reusability, simplicity, high sensitivity and selectivity provided by the LED-CL aptasensor will make it a good alternative tool for biological and food analysis.

Regulation of dietary energy level and oil source on leptin and its long form receptor mRNA expression of the adipose tissues in growing pigs.

Two experiments were conducted to evaluate the effects of dietary energy level and source of oil on leptin mRNA and long form leptin receptor (Ob-Rl) mRNA expression in dorsal, abdominal and visceral adipose tissues in young growing pigs. In experiment one, 15 barrows (initial body weight 15.0 kg) were used to examine the effects of dietary energy levels on leptin mRNA and Ob-Rl mRNA expression. The pigs were randomly allotted to one of three dietary treatments (n=5 per treatment) containing 13.4, 15.1 or 16.7 MJ DE/kg diet for 28 days. Based on the results of experiment one, experiment two was designed to examine the effects of oil sources including soybean oil (rich in n-6 polyunsaturated fatty acids) or fish oil (rich in n-3 polyunsaturated fatty acids) on leptin mRNA and Ob-Rl mRNA expression in the same adipose tissues examined in experiment one. The energy content of these diets was 15.1 MJ/kg. Fourteen barrows (initial weight 20.5 kg) were allocated to either of the two dietary treatments (n=7 per treatment), which was supplemented with either soybean or fish oil (both 5.73% of the diet) and fed to the pigs for 21 days. At the end of both experiments, blood samples were collected to determine plasma leptin and insulin concentrations. Adipose tissues were sampled to determine leptin and Ob-Rl mRNA expression using real-time fluorescence quantification PCR. In experiment one, plasma leptin concentrations were enhanced (P=0.02), and insulin concentrations were decreased (P<0.01) in pigs fed the high-energy diet (16.7 MJ DE/kg). Dorsal adipose tissue leptin mRNA expression was increased by feeding the diet containing 15.1 MJ/kg DE compared with the diets containing 13.4 and 16.7 MJ/kg DE. There was no difference in leptin mRNA expression in abdominal and visceral adipose tissue. In experiment two, there were no differences in plasma leptin and insulin concentrations between pigs fed with either fish oil or soybean oil diets. Nevertheless, fish oil decreased both leptin mRNA and Ob-Rl mRNA expression in dorsal adipose tissues compared with soybean oil (P<0.01). These experiments indicate that the source of oil plays a more potent role in regulation of leptin mRNA expression relative to dietary energy levels by an insulin-independent mechanism. Plasma leptin concentrations may also be regulated by a post-transcriptional mechanism.