Shiv Nadar University

About: Shiv Nadar University is a education organization based out in Dadri, Uttar Pradesh, India. It is known for research contribution in the topics: Population & Graphene. The organization has 1015 authors who have published 1924 publications receiving 18420 citations.

How Many Eigenvalues of a Product of Truncated Orthogonal Matrices are Real

Abstract: A truncation of a Haar distributed orthogonal random matrix gives rise to a matrix whose eigenvalues are either real or complex conjugate pairs, and are supported within the closed unit disk. This ...

Adaptation to chronic exposure to sepantronium bromide (YM155), a prototypical survivin suppressant is due to persistent DNA damage-response in breast cancer cells

Abstract: Sepantronium bromide (YM155), originally developed against the anti-apoptotic protein survivin, performed exceptionally well in pre-clinical and phase I clinical trials However, in phase II trials of several cancer types including breast cancer it performed poorly Additionally, no definitive correlation between survivin level and response to therapy was found In an attempt to understand the true reason of the late-stage failure of this promising drug, we developed YM155-resistant MCF-7 breast cancer cell line and characterized side-by-side with the drug-naive parental cell line Chronic YM155 treatment resulted in downregulation of survivin expression yet triggered cellular responses typical of adaptation to persistent DNA damage Lowering endogenous antioxidant glutathione level and activity of cell cycle check-point kinase restored YM155 activity Thus, contrary to its development as a survivin suppressant, YM155 primarily acts as a chemotherapeutic drug causing oxidative stress-mediated DNA damage Adaptation to long-term exposure to YM155 can be prevented and/or overcome by interfering with detoxification and DNA damage-response pathways Finally, proteins associated with DNA damage-response pathway will be more appropriate as predictive biomarkers of YM155 in breast tumor cells

3D Hierarchical Boron-Doped Diamond-Multilayered Graphene Nanowalls as an Efficient Supercapacitor Electrode

Abstract: Synthesis of stable hybrid carbon nanostructure for high-performance supercapacitor electrode with long life-cycle for electronic and energy storage devices is a real challenge. Here, we present a one-step synthesis method to produce conductive boron-doped hybrid carbon nanowalls (HCNWs), where sp²-bonded graphene has been integrated with and over a three-dimensional curved wall-like network of sp³-bonded diamond. The spectroscopic studies such as X-ray absorption, Raman, and X-ray photoelectrons clearly reveal the coexistence of diamond and graphene in these nanowalls, while the detailed transmission electron microscopy studies confirm the unique microstructure where a diamond nanowall is encased by a multilayered graphene. Interestingly, these HCNWs yield a high double layer capacitance value of 0.43 mF cm–² and electrode retention of 98% over 10 000 cycles of charging/discharging in 1 M Na₂SO₄ electrolyte. The remarkable supercapacitive performance can be attributed to the 3D interconnected network of diamond nanowalls surrounded by highly conducting graphene.

Erythrocyte sphingosine kinase regulates intraerythrocytic development of Plasmodium falciparum

Abstract: The sphingolipid pool is key regulator of vital cellular functions in Plasmodium falciparum a causative agent for deadly malaria. Erythrocytes, the host for asexual stage of Plasmodium, are major reservoir for Sphingosine-1-phosphate (S1P). Erythrocyte possesses Sphingosine kinase (SphK) that catalyzed its biosynthesis from sphingosine (Sph). Since, Plasmodium lacks SphK homologous protein it can be envisaged that it co-opts sphingolipids from both intraerythrocytic as well as extracellular pools for its growth and development. Herein, by sphingosine-NBD probing, we report that infected erythrocytes imports Sph from extracellular pool, which is converted to S1P and thereby taken by P. falciparum. Next, by targeting of the SphK through specific inhibitor N,N-Dimethylsphingosine DMS, we show a reduction in erythrocyte endogenous S1P pool and SphK-phosphorylation that led to inhibition in growth and development of ring stage P. falciparum. Owing to the role of S1P in erythrocyte glycolysis we analyzed uptake of NBD-Glucose and production of lactate in DMS treated and untreated plasmodium. DMS treatment led to decreased glycolysis in Plasmodium. Interestingly the host free Plasmodium did not show any effect on glycolysis with DMS treatment indicating its host-mediated effect. Further to understand the in-vivo anti-plasmodial effects of exogenous and endogenous erythrocyte S1P level, Sphingosine-1-phosphate lyase (S1PL) inhibitor (THI), S1P and SphK-1 inhibitor (DMS), were used in Plasmodium berghei ANKA (PbA) mice model. DMS treatment led to reduction of endogenous S1P conferred significant decrease in parasite load, whereas the plasma level S1P modulated by (THI) and exogenous S1P have no effect on growth of Plasmodium. This suggested erythrocyte endogenous S1P pool is important for Plasmodium growth whereas the plasma level S1P has no effect. Altogether, this study provides insight on cellular processes regulated by S1P in P. falciparum and highlights the novel mechanistically distinct molecular target i.e. SphK-1.