Extraction of Retinal Layers Through Convolution Neural Network (CNN) in an OCT Image for Glaucoma Diagnosis

Glaucoma is a progressive and deteriorating optic neuropathy that leads to visual field defects. The damage occurs as glaucoma is irreversible, so early and timely diagnosis is of significant importance. The proposed system employs the convolution neural network (CNN) for automatic segmentation of the retinal layers. The inner limiting membrane (ILM) and retinal pigmented epithelium (RPE) are used to calculate cup-to-disc ratio (CDR) for glaucoma diagnosis. The proposed system uses structure tensors to extract candidate layer pixels, and a patch across each candidate layer pixel is extracted, which is classified using CNN. The proposed framework is based upon VGG-16 architecture for feature extraction and classification of retinal layer pixels. The output feature map is merged into SoftMax layer for classification and produces probability map for central pixel of each patch and decides whether it is ILM, RPE, or background pixels. Graph search theory refines the extracted layers by interpolating the missing points, and these extracted ILM and RPE are finally used to compute CDR value and diagnose glaucoma. The proposed system is validated using a local dataset of optical coherence tomography images from 196 patients, including normal and glaucoma subjects. The dataset contains manually annotated ILM and RPE layers; manually extracted patches for ILM, RPE, and background pixels; CDR values; and eventually final finding related to glaucoma. The proposed system is able to extract ILM and RPE with a small absolute mean error of 6.03 and 5.56, respectively, and it finds CDR value within average range of ± 0.09 as compared with glaucoma expert. The proposed system achieves average sensitivity, specificity, and accuracies of 94.6, 94.07, and 94.68, respectively.     

Potential of endogenous estrogen receptor beta to influence the selective ER modulator ERbeta complex

The ratio of estrogen receptor beta (ERbeta) to ERalpha can alter the estrogen-like properties of tamoxifen. Transient transfection of ERbeta cDNA into cells can decrease the estrogen-like properties of the ERalpha:tamoxifen complex, whereas an increase in the amount of ERbeta is associated with tamoxifen-resistant breast cancer. We have addressed each of these hypotheses by examining well characterized laboratory models. We determined whether changes in endogenous ERbeta are responsible for the estrogen-like or antiestrogenic properties of tamoxifen or raloxifene in MDA-MB-231 cells transfected with cDNAs for ERalpha or mutants D351G, D351Y. We found that the amount of ERbeta mRNA in separate, stable transfectants of mutant ERalpha cDNA was always < 2% of ERalpha. Since at least a 50:50 mixture of ERalpha:ERbeta is needed to silence the tamoxifen:ERalpha complex, we conclude that insufficient ERbeta mRNA is available for selective ER modulation in stable transfectants of D351G and D351Y ERalpha. Similarly, to test the hypothesis that ERbeta is up-regulated and plays an important role during the development of tamoxifen-stimulated tumor growth, we quantitatively analyzed ERbeta and ERalpha mRNA in tamoxifen-na?ve (MCF-7:E2, ECC1:E2) and tamoxifen-stimulated tumors (MCF-7:TAM, EnCa 101:TAM). We found that ERbeta mRNA levels were not significantly elevated in tamoxifen-stimulated tumors and the ERalpha mRNA remained over 99% out of all ER species for all the tumors tested. The same results were also obtained when mRNA levels of ERbeta and ERalpha in a series of tamoxifen-na?ve and tamoxifen-resistant breast cancer was analyzed. We conclude that endogenous ERbeta may not play a dominant role in the modulation of the tamoxifen ERalpha complex, or in the development of tamoxifen-stimulated resistant tumor growth.     

An aberrant donor pulmonary vein during lung transplant: a surgical challenge

Aberrant pulmonary veins are uncommon. Anastomosis of such a vein during a lung transplant operation may provide a surgical challenge. We report the first case of an aberrant pulmonary vein anastomosed to the left atrial appendage during the implantation of the left lung.     

The risk of post-operative complications associated with infliximab therapy for Crohn's disease: a controlled cohort study

BACKGROUND: By temporarily suppressing the immune response, the anti-tumour necrosis factor agent, infliximab, may increase the risk of peri-operative complications. AIM: To test this hypothesis for intestinal resection in a cohort of 313 Crohn's disease patients treated with infliximab. Forty received one or more infusions prior to intestinal resection (31/40 within 12 weeks). METHODS: The post-operative events of these patients were compared with those of a control group (infliximab naive) of 39 patients adjusted for age, gender and surgical procedure. Early (10 days) and late (3 months) major or minor complications were identified. RESULTS: The incidence of early minor (15.0% vs. 12.8%) and major (12.5% vs. 7.7%) and late minor (2.5% vs. 5.1%) and major (17.5% vs. 12.8%) complications and the mean hospital stay after surgery (10.3 +/- 4.0 days vs. 9.9 +/- 5.5 days) were similar in both groups. A trend towards an increased early infection rate was found in infliximab pre-treated patients (6 vs. 1; P = 0.10), but more patients in this group received corticosteroids and/or immunosuppressives (29 vs. 16 patients; P < 0.05). CONCLUSION: The use of infliximab before intestinal resection does not prolong the hospital stay and does not increase the rate of post-operative complications.     

Correction of fatty acid oxidation in carnitine palmitoyl transferase 2-deficient cultured skin fibroblasts by bezafibrate

Carnitine palmitoyltransferase 2 (CPTII) deficiency is among the most common inborn errors of mitochondrial fatty acid beta-oxidation (FAO). Clinical phenotype varies in relation to the metabolic block, as assessed by studies of FAO in patient fibroblasts. Thus, fibroblasts from patients with mild manifestations have appreciable residual CPTII enzyme activity, in contrast to those from severely affected patients. In the present study, we hypothesized that the hypolipidemic drug bezafibrate, acting as an activator of the peroxisome proliferator-activated receptor alpha might stimulate FAO in CPTII-deficient cells. Data obtained show that bezafibrate treatment of mild-type CPTII-deficient cells resulted in a time- and dose- dependent increase in CPTII mRNA (from +47% to +66%) and residual enzyme activity (from +54% to 135%), and led to normalization of 3H-palmitate and 3H-myristate cellular oxidation rates. Bezafibrate did not correct FAO in fibroblasts from patients with severe phenotype. This study establishes for the first time that peroxisome proliferator-activated receptor activators, acting via stimulation of gene expression, can stimulate CPTII residual activity to a level sufficient to allow normal FAO flux in deficient human fibroblasts, and suggests that this approach should be tested in other inborn errors of mitochondrial beta-oxidation.