Publications by authors named "Alima Khamidulla"

Over the past decade, there has been a notable surge in research dedicated to unraveling the intricate role of tight junction proteins in blood-brain barrier (BBB) damage associated with ischemic stroke. This bibliometric analysis explores the expansive landscape of occludin research, a key tight junction protein, during the years 2000-2023, shedding light on the global scientific contributions, collaborations, and emerging trends in this critical area of stroke pathogenesis. China and the United States emerge as significant contributors, underscoring their prominence in advancing our understanding of tight junction proteins.

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Objectives: This research aims to study the prognostic role of serum S100 as a predictor of mortality in vascular and traumatic brain injuries.

Methods: This prospective cohort study involved 219 patients. In the blood serum, neuron-specific markers (S100, NSE) and glucose, acid-base state and gas composition of arterial blood were obtained at admission, on the 3rd, 5th and 7th days of patients' stay in the intensive care unit.

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Background: While interferon beta-1b (IFN-β-1b) is still a commonly used disease-modifying drug in the treatment of multiple sclerosis (MS), therapeutic possibilities are expanding, and treatment failure should be identified early. Markers to predict response to IFN-β-1b, either clinical or biochemical, are therefore urgently needed. Interferon-induced proteins, including viperin, suppressor of cytokine signaling 3 (SOCS3), ubiquitin specific peptidase-18 (USP18), and myxovirus resistance protein A (MxA), are possible markers of IFN-β-1b bioavailability and treatment response.

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Aim Of The Study: To determine the prevalence of anti-interferon-β binding (BAb) and neutralising antibodies (NAb), and to investigate whether NAb measured by luciferase-based cell assay can predict treatment response in multiple sclerosis (MS) patients treated with interferon-β-1b (IFNβ-1b).

Clinical Rationale For The Study: A subgroup of IFNβ-treated MS patients develop NAb directed against the drug. The clinical significance remains controversial, which could be explained to some extent by technical difficulties in NAb detection and quantification.

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