Publications by authors named "L Naik"

Article Synopsis
  • Mycobacterium tuberculosis is a leading cause of global mortality, and to combat it effectively, improvements in diagnostics, drug regimens, and vaccinations are essential.
  • The study investigates Furamidine, a compound that may enhance autophagy—a defense mechanism against pathogens—by evaluating its effects on tuberculosis bacteria within human cells.
  • Findings demonstrate that Furamidine reduces mycobacterial growth and induces autophagy by affecting intracellular calcium levels and activating specific proteins, suggesting it could be a promising approach to improve TB treatment.
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Under specific external stimulus, misfolded and natively disordered globular proteins undergo irreversible transformation into pathogenic β-sheet-rich insoluble fibrillar structure, and deposition of theses fibrils in cells and tissues leads to disorders like Alzheimer's, Dementia, Type II diabetes, and many more. Here, we have developed a positively-charged Arg-containing hexapeptide, SqP7, and elucidated its anti-amyloidogenic propensity on in vitro HEWL amyloid formation under acidic and neutral fibrillation conditions using computational tools and several biophysical techniques. SqP7, at a five-fold molar excess, displayed excellent amyloid inhibition capability at both pH conditions (~83 % and 72 % inhibition under acidic and neutral fibrillation conditions, respectively), and was further chosen as a coating agent on gold nanoparticles.

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Introduction: Rheumatoid arthritis (RA) guidelines recommend methotrexate (MTX)-anchored therapy with biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs); however, tolerability issues often lead to non-adherence. Canadian data on MTX tapering and/or withdrawal following b/tsDMARD initiation are minimal. This chart review assessed frequency of MTX tapering or withdrawal following b/tsDMARD initiation and the impact on disease status in Canadian adults with RA.

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Under the influence of various conditions, misfolding of soluble proteins occurs, leading to the formation of toxic insoluble amyloids. The formation and deposition of such amyloids within the body are associated with detrimental biological consequences such as the onset of several amyloid-related diseases. Previously, we established a strategy for the rational design of peptide inhibitors against amyloid formation based on the amyloidogenic-prone region of the protein.

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Background: Nonalcoholic fatty liver disease (NAFLD) occurs in 10% to 40% of patients after pancreatic resection. Pancreatic exocrine insufficiency (PEI) is thought to be closely associated with NAFLD; however, the mechanism of NAFLD is not clearly understood. We perform a systematic review and meta-analysis to better understand the risk factors of NAFLD.

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