Online tracking and retargeting with applications to optical biopsy in gastrointestinal endoscopic examinations

With recent advances in biophotonics, techniques such as narrow band imaging, confocal laser endomicroscopy, fluorescence spectroscopy, and optical coherence tomography, can be combined with normal white-light endoscopes to provide in vivo microscopic tissue characterisation, potentially avoiding the need for offline histological analysis. Despite the advantages of these techniques to provide online optical biopsy in situ, it is challenging for gastroenterologists to retarget the optical biopsy sites during endoscopic examinations. This is because optical biopsy does not leave any mark on the tissue. Furthermore, typical endoscopic cameras only have a limited field-of-view and the biopsy sites often enter or exit the camera view as the endoscope moves. In this paper, a framework for online tracking and retargeting is proposed based on the concept of tracking-by-detection. An online detection cascade is proposed where a random binary descriptor using Haar-like features is included as a random forest classifier. For robust retargeting, we have also proposed a RANSAC-based location verification component that incorporates shape context. The proposed detection cascade can be readily integrated with other temporal trackers. Detailed performance evaluation on in vivo gastrointestinal video sequences demonstrates the performance advantage of the proposed method over the current state-of-the-art

Internal transitions of quasi-2D charged magneto-excitons in the presence of purposely introduced weak lateral potential energy variations

Optically detected resonance spectroscopy has been used to investigate effects of weak random lateral potential energy fluctuations on internal transitions of charged magneto-excitons (trions) in quasi two-dimensional GaAs/AlGaAs quantum-well (QW) structures. Resonant changes in the ensemble photoluminescence induced by far-infrared radiation were studied as a function of magnetic field for samples having: 1) no growth interrupts (short range well-width fluctuations), and 2) intentional growth interrupts (long range monolayer well-width differences). Only bound-to-continuum internal transitions of the negatively charged trion are observed for samples of type 1. In contrast, a feature on the high field (low energy) side of electron cyclotron resonance is seen for samples of type 2 with well widths of 14.1 and 8.4 nm. This feature is attributed to a bound-to-bound transition of the spin-triplet with non-zero oscillator strength resulting from breaking of translational symmetry.Comment: 16 pages, 3 figures, submitted to Physical Review

Expression of transforming growth factor beta-1 in gastric cancer and in the gastric mucosa of first-degree relatives of patients with gastric cancer

Transforming growth factors beta (TGF-β) constitute a family of polypeptide growth factors that control cell growth, cell differentiation and migration, as well as the formation of the extracellular matrix. Recent analyses revealed the overexpression of TGF-β1 in human gastric cancers and demonstrated increased cell proliferation in the stomach of patients with gastric cancer and their first-degree relatives. Using human gastric tissues obtained from patients with gastric cancer (n = 19), biopsies from healthy first-degree relatives of gastric cancer patients (n = 18) and healthy individuals (n = 19), we analysed the expression of TGF-β1 using the reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. Fifteen of 19 patients with gastric cancer expressed TGF-β1 in the tumour. In 11 of these 15 cases TGF-β1 mRNA was also detectable in the non-tumourous stomach. Interestingly, all but two individuals with a first-degree relative diagnosed with gastric cancer exhibited TGF-β1 expression in either the antrum or corpus biopsy or both. In contrast, only one of 19 individuals without a family history of gastric cancer expressed TGF-β1 in the stomach (P< 0.0001). TGF-β1 expression is detectable in a large proportion of gastric cancers and in the stomach of healthy first-degree relatives of gastric cancer patients. Since individuals without gastric cancers in their family express TGF-β1 only in one of 19 cases, the induction of TGF-β1 expression in first-degree relatives of patients with gastric cancer points to the presence of specific molecular alterations in a subgroup of individuals with an increased risk of developing gastric cancer that may precede the development of gastric cancers. © 2000 Cancer Research Campaig

Probe-Based Confocal Laser Endomicroscopy to Guide Real-Time Endoscopic Therapy in Barrett's Esophagus with Dysplasia

Probe-based confocal laser endomicroscopy (pCLE) is a novel imaging technique which utilizes a low-power laser light passed through a fiber-optic bundle, within a miniprobe that is advanced into the working channel, to obtain microscopic images of the mucosa. This allows the endoscopist to evaluate the microarchitecture of the gastrointestinal epithelium in real time. At this time pCLE cannot replace histopathology, but it can provide diagnostic information as well as guide therapeutic management in patients with Barrett's esophagus (BE) with high-grade dysplasia (HGD). We describe a retrospective case series in which four patients with BE and biopsy-proven HGD underwent endoscopy with pCLE to direct real-time endoscopic ablation therapy and/or endoscopic mucosal resection (EMR), which was performed in conjunction with pCLE. All four patients had pCLE showing features of HGD. After either EMR or radiofrequency ablation (RFA), pCLE was again used to evaluate the margins after therapy to assure accuracy. In one case, pCLE had features of dysplasia at the margin and further repeat EMR was immediately performed. Another case had a normal-appearing esophagus, but pCLE found features of BE in discrete areas and targeted biopsies were performed, which confirmed BE. This patient subsequently underwent RFA therapy of the residual areas of BE. In conclusion, in patients with BE and dysplasia, pCLE is an effective tool used to target biopsies, guide endoscopic therapy and assess the accuracy of EMR or RFA

Helicobacter pylori cag-Pathogenicity Island-Dependent Early Immunological Response Triggers Later Precancerous Gastric Changes in Mongolian Gerbils

Infection with Helicobacter pylori, carrying a functional cag type IV secretion system (cag-T4SS) to inject the Cytotoxin associated antigen (CagA) into gastric cells, is associated with an increased risk for severe gastric diseases in humans. Here we studied the pathomechanism of H. pylori and the role of the cag-pathogenicity island (cag-PAI) for the induction of gastric ulcer and precancerous conditions over time (2–64 weeks) using the Mongolian gerbil model. Animals were challenged with H. pylori B128 (WT), or an isogenic B128ΔcagY mutant-strain that produces CagA, but is unable to translocate it into gastric cells. H. pylori colonization density was quantified in antrum and corpus mucosa separately. Paraffin sections were graded for inflammation and histological changes verified by immunohistochemistry. Physiological and inflammatory markers were quantitated by RIA and RT-PCR, respectively. An early cag-T4SS-dependent inflammation of the corpus mucosa (4–8 weeks) occurred only in WT-infected animals, resulting in a severe active and chronic gastritis with a significant increase of proinflammatory cytokines, mucous gland metaplasia, and atrophy of the parietal cells. At late time points only WT-infected animals developed hypochlorhydria and hypergastrinemia in parallel to gastric ulcers, gastritis cystica profunda, and focal dysplasia. The early cag-PAI-dependent immunological response triggers later physiological and histopathological alterations towards gastric malignancies

Lack of association between gene polymorphisms of Angiotensin converting enzyme, Nod-like receptor 1, Toll-like receptor 4, FAS/FASL and the presence of Helicobacter pylori-induced premalignant gastric lesions and gastric cancer in Caucasians

<p>Abstract</p> <p>Background</p> <p>Several polymorphisms of genes involved in the immunological recognition of <it>Helicobacter pylori </it>and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding <it>Angiotensin converting enzyme </it>(<it>ACE</it>), <it>Nod-like receptor 1 </it>(<it>NOD1</it>), <it>Toll-like receptor 4 </it>(<it>TLR4</it>) and <it>FAS/FASL</it>.</p> <p>Methods</p> <p>Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. <it>ACE I/D </it>(rs4646994), <it>NOD1 796G>A </it>(rs5743336), <it>TLR4 3725G>C </it>(rs11536889), <it>FAS 1377G>A </it>(rs2234767), <it>FAS 670A>G </it>(rs1800682) and <it>FASL 844T>C </it>(rs763110) were genotyped by different PCR approaches and restriction fragment length polymorphism analysis.</p> <p>Results</p> <p>Frequencies of genotypes in our study are similar to the data reported on subjects of Caucasian ethnicity. There was a tendency for <it>NOD1 796G/G </it>genotype to be associated with increased risk of HRAG (62.4% <it>vs</it>. 54.5% in controls, <it>p </it>= 0.082). <it>FAS 670G/G </it>genotype was more frequent in HRAG when compared to controls, 23.9% and 17.2% respectively, however it failed to reach significance level (<it>p </it>= 0.077). We did not find any significant associations for all polymorphisms in relation to GC or HRAG. <it>NOD1 796G>A </it>and <it>TLR4 3725G>C </it>gene polymorphisms were also not associated with <it>Helicobacter pylori </it>infection.</p> <p>Conclusions</p> <p><it>ACE, NOD1, TRL4 </it>and <it>FAS/FASL </it>gene polymorphisms are not linked with gastric carcinogenesis in Caucasians, and therefore they should not be considered as potential biomarkers for identifying individuals with higher risk for GC.</p