FoodNet: Recognizing Foods Using Ensemble of Deep Networks

In this work we propose a methodology for an automatic food classification system which recognizes the contents of the meal from the images of the food. We developed a multi-layered deep convolutional neural network (CNN) architecture that takes advantages of the features from other deep networks and improves the efficiency. Numerous classical handcrafted features and approaches are explored, among which CNNs are chosen as the best performing features. Networks are trained and fine-tuned using preprocessed images and the filter outputs are fused to achieve higher accuracy. Experimental results on the largest real-world food recognition database ETH Food-101 and newly contributed Indian food image database demonstrate the effectiveness of the proposed methodology as compared to many other benchmark deep learned CNN frameworks.Comment: 5 pages, 3 figures, 3 tables, IEEE Signal Processing Letter

Interlayer-engineered high remnant polarization (2Pr_r > 70μ\muC/cm2^2) in Hf0.5_{0.5}Zr0.5_{0.5}O2_2 thin films

In this letter, we report a high remnant polarization, 2P$_r$ > 70$\mu$C/cm$^2$ in thermally processed atomic layer deposited Hf$_{0.5}$Zr$_{0.5}$O$_2$ (HZO) film on Silicon with NH$_3$ plasma exposed thin TiN interlayer and Tungsten (W) as a top electrode. The effect of interlayer on the ferroelectric properties of HZO is compared with standard Metal-Ferroelectric-Metal and Metal-Ferroelectric-Semiconductor structures. The x-ray diffraction confirms that the thickness of the interlayer plays an important role to enhance the orthorhombic ferroelectric phase. The HRTEM images reveal that TiN acts as a seed layer for the local epitaxy in HZO and hence a 2X improvement in remnant polarization. Finally, the HZO devices are shown to be wake-up free, and exhibit endurance $>10^6$ cycles. This study opens a pathway to achieve epitaxial ferroelectric HZO films on Si with improved memory performance.Comment: 4 pages, 4 figure

PBEF1/NAmPRTase/Visfatin: a potential malignant astrocytoma/glioblastoma serum marker with prognostic value

Malignant astrocytomas comprise anaplastic astrocytoma (AA; grade III) and Glioblastoma (GBM; grade IV). GBM is the most malignant with a median survival of 10-12 months in patients. Using cDNA microarray based expression profiling of different grades of astrocytomas, we identified several fold increased levels of PBEF1 transcripts in GBM samples. Pre-B-cell colony enhancing factor 1 gene (PBEF1) encodes Nicotinamide phosphoribosyltransferase (NAmPRTase), which catalyses the rate limiting step in the salvage pathway of NAD metabolism in mammalian cells. Further validation using real time RT-qPCR on an independent set of tumor samples (n=91) and normal brain samples (n=9), GBM specific higher expression of PBEF1 was confirmed. Immunohistochemical staining for PBEF1 on a subset of the above samples largely reinforced our finding. We carried out ELISA analysis on serum samples of astrocytoma patients to determine whether this protein levels would correlate with the presence of tumor and tumor grade. PBEF1 serum levels were substantially elevated in many of the AA and GBM patients. Statistical analysis of these data indicates that in patients with astrocytoma, serum PBEF1 levels correlate with tumor grade and is highest in GBM. Immunohistochemical analysis of an independent set of 51 retrospective GBM cases with known survival data revealed that PBEF1 expression in the tumor tissue along with its co-expression with p53 was associated with poor survival. Thus, we have identified PBEF1 as a potential malignant astrocytoma serum marker and prognostic indicator among GBMs

Novel glioblastoma markers with diagnostic and prognostic value identified through transcriptome analysis

Purpose: Current methods of classification of astrocytoma based on histopathologic methods are often subjective and less accurate. Although patients with glioblastoma have grave prognosis, significant variability in patient outcome is observed. Therefore, the aim of this study was to identify glioblastoma diagnostic and prognostic markers through microarray analysis. Experimental Design: We carried out transcriptome analysis of 25 diffusely infiltrating astrocytoma samples [WHO grade II - diffuse astrocytoma, grade III - anaplastic astrocytoma, and grade IV - glioblastoma (GBM)] using cDNA microarrays containing 18,981 genes. Several of the markers identified were also validated by real-time reverse transcription quantitative PCR and immunohistochemical analysis on an independent set of tumor samples (n = 100). Survival analysis was carried out for two markers on another independent set of retrospective cases (n = 51). Results: We identified several differentially regulated grade-specific genes. Independent validation by real-time reverse transcription quantitative PCR analysis found growth arrest and DNA-damage-inducible α (GADD45α) and follistatin-like 1 (FSTL1) to be up-regulated in most GBMs (both primary and secondary), whereas superoxide dismutase 2 and adipocyte enhancer binding protein 1 were up-regulated in the majority of primary GBM. Further, identification of the grade-specific expression of GADD45α and FSTL1 by immunohistochemical staining reinforced our findings. Analysis of retrospective GBM cases with known survival data revealed that cytoplasmic overexpression of GADD45α conferred better survival while the coexpression of FSTL1 with p53 was associated with poor survival. Conclusions: Our study reveals that GADD45α and FSTLI are GBM-specific whereas superoxide dismutase 2 and adipocyte enhancer binding protein 1 are primary GBM-specific diagnostic markers. Whereas GADD45α overexpression confers a favorable prognosis, FSTL1 overexpression is a hallmark of poor prognosis in GBM patients

Whole exome sequencing in an Indian family links Coats plus syndrome and dextrocardia with a homozygous novel CTC1 and a rare HES7 variation

Background: Coats plus syndrome is an autosomal recessive, pleiotropic, multisystem disorder characterized by retinal telangiectasia and exudates, intracranial calcification with leukoencephalopathy and brain cysts, osteopenia with predisposition to fractures, bone marrow suppression, gastrointestinal bleeding and portal hypertension. It is caused by compound heterozygous mutations in the CTC1 gene. Case presentation: We encountered a case of an eight-year old boy from an Indian family with manifestations of Coats plus syndrome along with an unusual occurrence of dextrocardia and situs inversus. Targeted resequencing of the CTC1 gene as well as whole exome sequencing (WES) were conducted in this family to identify the causal variations. The identified candidate variations were screened in ethnicity matched healthy controls. The effect of CTC1 variation on telomere length was assessed using Southern blot. A novel homozygous missense mutation c.1451A > C (p.H484P) in exon 9 of the CTC1 gene and a rare 3'UTR known dbSNP variation (c.*556 T > C) in HES7 were identified as the plausible candidates associated with this complex phenotype of Coats plus and dextrocardia. This CTC1 variation was absent in the controls and we also observed a reduced telomere length in the affected individual's DNA, suggesting its likely pathogenic nature. The reported p.H484P mutation is located in the N-terminal 700 amino acid regionthat is important for the binding of CTC1 to ssDNA through its two OB domains. WES data also showed a rare homozygous missense variation in the TEK gene in the affected individual. Both HES7 and TEK are targets of the Notch signaling pathway. Conclusions: This is the first report of a genetically confirmed case of Coats plus syndrome from India. By means of WES, the genetic variations in this family with unique and rare complex phenotype could be traced effectively. We speculate the important role of Notch signaling in this complex phenotypic presentation of Coats plus syndrome and dextrocardia. The present finding will be useful for genetic diagnosis and carrier detection in the family and for other patients with similar disease manifestations

The Management of Patients With Penetrating Aortic Ulcers: A Systematic Review

Background: Penetrating aortic ulcers (PAUs) are an entity within acute aortic syndrome. They often remain undiagnosed and are found incidentally or when they become symptomatic. Management is currently guided by clinical judgment. This review aims to identify indications for treatment and inform management. Methods: We searched PubMed for studies on the management of PAUs. The outcome measures were mortality, progression and resolution of symptoms. Results: This review incorporates 27 studies involving 1356 patients with PAU. Data was available regarding symptoms for 1213 patients (494 symptomatic, 719 asymptomatic). Overall late mortality for PAUs was found to be higher than 30-day mortality. Early mortality was higher for symptomatic patients as compared to those with asymptomatic PAUs. Early mortality was lowest for PAUs treated with endovascular interventions (5%), followed by PAUs managed medically and highest following open surgical management. Indications for treatment included symptoms, progression/instability, aortic diameter &gt;5 cm, concomitant aortic pathology or pleural effusion. 13% of patients managed conservatively at initial presentation demonstrated progression and were considered for intervention subsequently. 9% of patients required reintervention after initial endovascular surgery. Conclusion: Endovascular treatment, if anatomically suitable, should be considered as first line treatment for symptomatic PAUs. Patients with asymptomatic PAUs, if associated with high-risk features such as PAU diameter &gt;20 mm, PAU depth &gt;10 mm, aortic diameter &gt;42 mm, concomitant pathology, morphological change or an infective etiology, should also be considered for intervention. Small asymptomatic PAUs with no high-risk features may be managed conservatively but must undergo regular surveillance. </jats:sec