Current and future role of magnetically assisted gastric capsule endoscopy in the upper gastrointestinal tract

Capsule endoscopy first captivated the medical world when it provided a means to visualize the small bowel, which was previously out of endoscopic reach. In the subsequent decade and a half we continue to learn of the true potential that capsule endoscopy has to offer. Of particular current interest is whether capsule endoscopy has any reliable investigative role in the upper gastrointestinal tract. Much research has already been dedicated to enhancing the diagnostic and indeed therapeutic properties of capsule endoscopy. Specific modifications to tackle the challenges of the gut have already been described in the current literature. In the upper gastrointestinal tract, the capacious anatomy of the stomach represents one of many challenges that capsule endoscopy must overcome. One solution to improving diagnostic yield is to utilize external magnetic steering of a magnetically receptive capsule endoscope. Notionally this would provide a navigation system to direct the capsule to different areas of the stomach and allow complete gastric mucosal examination. To date, several studies have presented promising data to support the feasibility of this endeavour. However the jury is still out as to whether this system will surpass conventional gastroscopy, which remains the gold standard diagnostic tool in the foregut. Nevertheless, a minimally invasive and patient-friendly alternative to gastroscopy remains irresistibly appealing, warranting further studies to test the potential of magnetically assisted capsule endoscopy. In this article the authors would like to share the current state of magnetically assisted capsule endoscopy and anticipate what is yet to come

Haplotype Analysis and Linkage Disequilibrium at Five Loci in Eragrostis tef

Eragrostis tef (Zucc.), a member of the Chloridoideae subfamily of grasses, is one of the most important food crops in Ethiopia. Lodging is the most important production problem in tef. The rht1 and sd1 dwarfing genes have been useful for improving lodging resistance in wheat and rice, respectively, in what has been known as the “Green Revolution.” All homologs of rht1 and sd1 were cloned and sequenced from 31 tef accessions collected from across Ethiopia. The allotetraploid tef genome was found to carry two rht1 homologs. From sequence variation between these two putative homologs, an approximate ancestral divergence date of 6.4 million years ago was calculated for the two genomes within tef. Three sd1 homologs were identified in tef, with unknown orthologous/paralogous relationships. The genetic diversity in the 31 studied accessions was organized into a relatively small number of haplotypes (2−4) for four of these genes, whereas one rht1 homeologue exhibited 10 haplotypes. A low level of nucleotide diversity was observed at all loci. Linkage disequilibrium analysis demonstrated strong linkage disequilibrium, extending the length of the five genes investigated (2−4 kb), with no significant decline. There was no significant correlation between haplotypes of any of these genes and their recorded site of origin

Upregulation of Endocan by Epstein-Barr Virus Latent Membrane Protein 1 and Its Clinical Significance in Nasopharyngeal Carcinoma

<div><p>Endocan (or called Esm-1) has been shown to have tumorigenic activities and its expression is associated with poor prognosis in various cancers. Latent membrane protein 1 (LMP1) is an Epstein-Barr virus (EBV)-encoded oncoprotein and has been shown to play an important role in the pathogenesis of EBV-associated nasopharyngeal carcinoma (NPC). To further understand the role of LMP1 in the pathogenesis of NPC, microarray analysis of LMP1-regulated genes in epithelial cells was performed. We found that endocan was one of the major cellular genes upregulated by LMP1. This induction of endocan by LMP1 was confirmed in several epithelial cell lines including an NPC cell line. Upregulation of endocan by LMP1 was found to be mediated through the CTAR1 and CTAR2 domains of LMP1 and through the LMP1-activated NF-κB, MEK-ERK and JNK signaling pathways. To study whether endocan was expressed in NPC and whether endocan expression was associated with LMP1 expression in NPC, the expression of endocan and LMP1 in tumor tissues from 42 NPC patients was evaluated by immunohistochemistry. Expression of endocan was found in 52% of NPC specimens. Significant correlation between LMP1 and endocan expression was observed (<i>p</i><0.0001). Moreover, NPC patients with endocan expression were found to have a shorter survival than NPC patients without endocan expression (<i>p</i>=0.0104, log-rank test). Univariate and Multivariate analyses revealed that endocan was a potential prognostic factor for NPC. Finally, we demonstrated that endocan could stimulate the migration and invasion ability of endothelial cells and this activity of endocan was dependent on the glycan moiety and the phenylalanine-rich region of endocan. Together, these studies not only identify a new molecular marker that may predict the survival of NPC patients but also provide a new insight to the pathogenesis of NPC. </p> </div

Endocan is overexpressed in NPC tissues and its expression is correlated with LMP1 expression.

<p>(<b>A</b>) Immunohistochemical staining of endocan in NPC tissues. Panel a, H&E staining (original magnification, ×100). Panel b, Endocan was expressed in NPC tumor cells but not in adjacent normal epithelial cells (original magnification, ×100). Panel c, The tumor part (marked as square c) in Panel b was photographed at higher magnification (original magnification, ×400). Panel d, Square d in Panel b was photographed at higher magnification (original magnification, ×400). Endocan expression was found in vascular endothelial cells adjacent to the tumor. Arrowhead indicates vascular endothelial cells. T, tumor cells; N, normal epithelial cells. The brown color represents endocan staining. (<b>B</b>) Immunohistochemical staining of endocan and LMP1 in NPC tissues. Case I shows the representative result with high endocan and LMP1 expression in consecutive sections. Case II shows the representative result with negative staining of endocan and LMP1 in consecutive sections. The brown color represents endocan or LMP1 staining. T, tumor cells. (<b>C</b>) Association between endocan and LMP1 protein expressions in 42 NPC cases. Statistical relationships between endocan and LMP1 expressions were analyzed by χ² test.</p

Endocan stimulates the migration and invasion ability of endothelial cells.

<p>(<b>A</b>) Western blot analysis shows the amount of endocan in the concentrated CM of RHEK-1, RHEK-Vec, and RHEK-endocan cells. (<b>B</b>) Effect of the CM from RHEK-1, RHEK-Vec, and RHEK-endocan cells on HMEC-1 cell migration. Upper panel, images of migrated HMEC-1 endothelial cells in the presence of CM from RHEK-1, RHEK-Vec, and RHEK-endocan cells. Lower panel, quantitation of migrated HMEC-1 endothelial cells. The migrated cells were counted in six randomly selected microscopic fields (x 200 magnification). Values represent means ± SD. ** <i>P</i> < 0.005 versus CM from RHEK-Vec cells. (<b>C</b>) Effect of the CM from RHEK-Vec and RHEK-endocan cells on HUVEC cell migration. The migrated cells were counted in six randomly selected microscopic fields. Values represent means ± SD. ** <i>P</i> < 0.005 versus CM from RHEK-Vec cells. (<b>D</b>) Pretreatment of CM from RHEK-endocan cells with anti-endocan antibody reduces its ability to induce HMEC-1 cell migration. CM from RHEK-Vec or RHEK-endocan cells was pre-treated with 200 ng/mL control or anti-endocan monoclonal antibody (Abnova) before using them for transmigration assays. The migrated cells were counted in six randomly selected microscopic fields. Values represent means ± SD. * <i>P</i> < 0.05 versus control antibody-pretreated CM. (<b>E</b>) Effect of endocan on the invasion ability of HMEC-1 endothelial cells. The cells that invaded and migrated to the lower chamber were counted in six randomly selected microscopic fields. Values represent means ± SD. * <i>P</i> < 0.05, ** <i>P</i> < 0.005. RHEK-V, RHEK-Vec cells; RHEK-E, RHEK-endocan cells.</p

Relationship between survival and endocan expression or LMP1 expression in NPC patients.

<p>(<b>A</b>) Overall survival curve of endocan-positive (n=21; dotted line) and endocan-negative (n=20; solid line) NPC patients. A statistically significant difference was found between these two groups of patients (<i>P</i> = 0.0104, log-rank test). (<b>B</b>) Overall survival curve of LMP1-positive (n=19; dotted line) and LMP1-negative (n=22; solid line) NPC patients. A statistically significant difference was found between these two groups of patients (<i>P</i> = 0.0166, log-rank test).</p

Validation of LMP1-regulated genes by quantitative real-time RT-PCR.

<p>Total RNA from doxycycline-treated and untreated RHEK/Tet-LMP1 cells was extracted and subjected to quantitative real-time RT-PCR. The level of respective mRNA expressed in the untreated RHEK/Tet-LMP1 cells was set as 1. Values represent means ± SD. </p