Publications by authors named "N B Lawand"

Article Synopsis
  • Modern patient care relies on improving pharmacy services, and AI could significantly enhance this evolution, yet there's limited knowledge about the views and practices of pharmacy students and faculty towards AI.
  • This study aimed to explore the knowledge, attitudes, and practices (KAP) of pharmacy students and faculty concerning AI across six Middle Eastern countries and identify factors influencing their understanding of AI in healthcare.
  • Results showed that while most participants had heard of AI, only about 39.5% understood its concepts well, highlighting a moderate overall knowledge level, and although attitudes were positive regarding AI's potential benefits for patient care, there were concerns about job security and safety.
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Patients with long COVID suffer from many neurological manifestations that persist for 3 months following infection by SARS-CoV-2. Autonomic dysfunction (AD) or dysautonomia is one complication of long COVID that causes patients to experience fatigue, dizziness, syncope, dyspnea, orthostatic intolerance, nausea, vomiting, and heart palpitations. The pathophysiology behind AD onset post-COVID is largely unknown.

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Objective: To investigate the potential for noninvasive low frequency, low intensity ultrasound to suppress evoked potentials in the reflex arc neural pathway in anesthetized animal.

Material And Methods: Single unit Electromyographic recordings of gastrocnemius muscle activity were obtained in response to electrical activation of the sciatic nerve, in anesthetized animal, with and without US stimulation. Reflex related potentials were evoked via electrical stimulation and low-intensity, low-frequency ultrasound was applied to the sciatic nerve.

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Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis.

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Rheumatoid arthritis (RA) is a chronic inflammatory and autoimmune disease characterized by the attack of the immune system on the body's healthy joint lining and degeneration of articular structures. This disease involves an increased release of inflammatory mediators in the affected joint that sensitize sensory neurons and create a positive feedback loop to further enhance their release. Among these mediators, the cytokines and neuropeptides are responsible for the crippling pain and the persistent neurogenic inflammation associated with RA.

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