Developing a Stable and Selective Non-Enzymatic Electrochemical Glucose Biosensor

The goal of this Major Qualifying Project was to develop a stable and sensitive interface architecture for an easy and reusable non-enzymatic electrochemical glucose biosensor. This was achieved by changing the copper oxide nanoparticle morphology that was deposited onto a titanium oxide nanotube array. The interface architecture was manipulated by varying the concentration of the equimolar CuSO4/H2SO4 solution from 7.8 mM to 250 mM during electrodeposition. Through SEM imaging, cyclic voltammetry scans, and chronoamperometric readings, it was determined that the biosensor interface architecture affected its overall glucose sensing capabilities. The most ideal interface architecture was produced in an electrolyte solution of 50 mM CuSO4/H2SO4

Analysis of paralytic shellfish toxins using high field asymmetric waveform Ion mobility spectrometry with liquid chromatography-mass spectrometry

We investigate the potential utility of high-field asymmetric waveform ion mobility spectrometry (FAIMS) as a gas-phase ion separation tool for analysis of PSTs by mass spectrometry.We investigate the separation of PSTs using FAIMS with two divergent goals: using FAIMS as a primary separation tool for rapid screening by electrospray ionization (ESI)-FAIMSMS or combined with LC in a multidimensional LC-ESIFAIMS-MS separation.Peer reviewed: YesNRC publication: Ye

Improving Water Quality in the Villages of Himachal Pradesh: Revising Monitoring and Treatment Techniques

The goal of our project was to assess the quality, monitoring, and treatment methods of drinking water in rural villages of Himachal Pradesh. To realize this goal we assessed local perceptions of water, investigated the relationship between water quality and public health, and measured the level of contamination. We found high bacteriological contamination in untreated natural water sources. The project resulted in recommendations to improve the current water quality testing program and to promote public awareness regarding drinking water quality

The SARS-CoV-2 RNA-protein interactome in infected human cells.

Characterizing the interactions that SARS-CoV-2 viral RNAs make with host cell proteins during infection can improve our understanding of viral RNA functions and the host innate immune response. Using RNA antisense purification and mass spectrometry, we identified up to 104 human proteins that directly and specifically bind to SARS-CoV-2 RNAs in infected human cells. We integrated the SARS-CoV-2 RNA interactome with changes in proteome abundance induced by viral infection and linked interactome proteins to cellular pathways relevant to SARS-CoV-2 infections. We demonstrated by genetic perturbation that cellular nucleic acid-binding protein (CNBP) and La-related protein 1 (LARP1), two of the most strongly enriched viral RNA binders, restrict SARS-CoV-2 replication in infected cells and provide a global map of their direct RNA contact sites. Pharmacological inhibition of three other RNA interactome members, PPIA, ATP1A1, and the ARP2/3 complex, reduced viral replication in two human cell lines. The identification of host dependency factors and defence strategies as presented in this work will improve the design of targeted therapeutics against SARS-CoV-2

PPM1D mutations are oncogenic drivers of de novo diffuse midline glioma formation

Abstract The role of PPM1D mutations in de novo gliomagenesis has not been systematically explored. Here we analyze whole genome sequences of 170 pediatric high-grade gliomas and find that truncating mutations in PPM1D that increase the stability of its phosphatase are clonal driver events in 11% of Diffuse Midline Gliomas (DMGs) and are enriched in primary pontine tumors. Through the development of DMG mouse models, we show that PPM1D mutations potentiate gliomagenesis and that PPM1D phosphatase activity is required for in vivo oncogenesis. Finally, we apply integrative phosphoproteomic and functional genomics assays and find that oncogenic effects of PPM1D truncation converge on regulators of cell cycle, DNA damage response, and p53 pathways, revealing therapeutic vulnerabilities including MDM2 inhibition