Publications by authors named "H A Murad"

Ovarian cancer is a common and lethal malignancy among women, whereas chemoresistance is one of the major challenges to its treatment and prognosis. Chemoresistance is a multifactorial phenomenon, involving various mechanisms that collectively modify the cell's response to treatment. Among the changes that arise in cells after acquiring chemoresistance is miRNA dysregulation.

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Background/objectives: Millions of individuals worldwide continue to experience symptoms following SARS-CoV-2 infection. This study aimed to assess the prevalence and phenotype of multi-system symptoms attributed to Long COVID-including fatigue, pain, cognitive-emotional disturbances, headache, cardiopulmonary issues, and alterations in taste and smell-that have persisted for at least two years after acute infection, which we define as "persistent Long COVID". Additionally, the study aimed to identify clinical features and blood biomarkers associated with persistent Long COVID symptoms.

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Acute flaccid paralysis (AFP) case surveillance is pivotal for the early detection of potential poliovirus, particularly in endemic countries such as Ethiopia. The community-based surveillance system implemented in Ethiopia has significantly improved AFP surveillance. However, challenges like delayed detection and disorganized communication persist.

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Chemotherapy for hepatoblastoma is limited by organ toxicity and poor outcomes, prompting the search for new, more effective treatments with minimal side effects. Vincristine sulfate, a potent chemotherapeutic, faces challenges due to P-glycoprotein-mediated resistance and its systemic toxicity. Nanoparticles offer a promising solution by improving pharmacokinetics, targeting tumor cells, thus reducing side effects.

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Objective: Tamoxifen is the most used agent to treat estrogen receptor-positive (ER+) breast cancer (BC). While it decreases the risk of cancer recurrence by 50%, many patients develop resistance to this treatment, culminating in highly aggressive disease. Tamoxifen resistance comes from the repression of ER transcriptional activity that switches the cancer cells to proliferation via nonhormonal signaling pathways.

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