Manipal University

About: Manipal University is a education organization based out in Manipal, Karnataka, India. It is known for research contribution in the topics: Population & Medicine. The organization has 9525 authors who have published 11207 publications receiving 110687 citations.

Raman spectroscopy of breast tissues.

Abstract: Breast cancer is one of the leading female cancers. The major drawback of the gold standard of screening, mammography, is the high rate of false reports, aside from the risk from repeated exposure to harmful ionizing radiations. Histopathology, the gold standard of diagnosis, is time consuming and often prone to subjective interpretations. Molecular level diagnosis 'omics' is becoming increasingly popular; among these is metabolomics, diagnosis based on 'metabolic fingerprinting'. In the present article we review a Raman spectroscopic approach to metabolic fingerprinting in breast cancer detection. This review opens with a brief background on anatomical and etiological aspects of breast cancers. We present an overview of conventional detection approaches in breast cancer screening and diagnosis methods, followed by a concise note on the basics of optical spectroscopy and its applications in the screening/diagnosis of breast malignancy. We present the recent developments in Raman spectroscopic diagnosis of breast cancers and also share our experience in Raman spectroscopic classification of normal, benign and malignant breast tissues. Perspectives and current status of Raman spectroscopic screening/diagnosis of breast cancers are also discussed.

α-decay half-lives of the observed superheavy nuclei (Z = 108-118)

Abstract: A systematic and comprehensive study of the decay half-lives of nuclei appearing in the observed α-decay chains of superheavy elements (Z = 108−118) is presented. The calculation proceeds in three steps. First, the relativistic mean-field equations are solved in the axially symmetric deformed oscillator basis to obtain ground-state properties such as binding energies, radii, deformations, and densities. The results are in good agreement with the available experimental systematics, as expected. Next, the calculated densities are used in the double-folding prescription to determine the interaction potentials for the α-daughter systems. Finally, these potentials, along with calculated and experimental Q values, are used in the WKB approximation to estimate the decay half-lives. The calculated half-lives, which sensitively depend on Q values, qualitatively reproduce the experiment.

SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stress.

Abstract: Corneal endothelial dystrophy is a progressive disease with gradual loss of vision and characterized by degeneration and dysfunction of corneal endothelial cells. Mutations in SLC4A11, a Na+ dependent OH− transporter, cause congenital hereditary endothelial dystrophy (CHED) and Fuchs’ endothelial corneal dystrophy (FECD), the two most common forms of endothelial degeneration. Along with genetic factors, oxidative stress plays a role in pathogenesis of several corneal diseases. In this study we looked into the role of SLC4A11 in antioxidant stress response in human corneal endothelial cells (HCEnC). We found increased expression of SLC4A11 in presence of oxidative stress. Depletion of SLC4A11 using targeted siRNA, caused an increase in reactive oxygen species, cytochrome c, lowered mitochondrial membrane potential, and reduced cell viability during oxidative stress. Moreover, SLC4A11 was found to be necessary for NRF2 mediated antioxidant gene expression in HCEnC. On the other hand, over expression of SLC4A11 reduces reactive oxygen species levels and increases cell viability. Lastly, CHED tissue specimens show evidence of oxidative stress and reduced expression of NRF2. In conclusion, our data suggests a possible role of SLC4A11 in regulating oxidative stress, and might be responsible for both the etiology and treatment of corneal endothelial dystrophy.