Allergic rhinitis is a prevalent disease in developed nations, and its prevalence has been increasing throughout the world. Nasal congestion is the most common and bothersome symptoms of rhinitis. Congestion is associated with sleep-disordered breathing and is thought to be a key cause of sleep impairment in individuals with rhinitis. The end result is a decrease in quality of life and productivity and an increase in daytime sleepiness. Treatment with intranasal corticosteroids has been shown to reduce nasal congestion. Data on sleep-related end points from clinical trials of intranasal corticosteroids indicate that this reduction is associated with improved sleep, reduced daytime fatigue, and improved quality of life. Other therapies, such as montelukast, also have a positive influence on congestion and sleep. This review examines nasal congestion and the associated sleep impairment of allergic rhinitis patients. It explores the adverse effects of disturbed sleep on quality of life and how these conditions can be reduced by therapies that decrease congestion.

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Background: Breast cancer (BC) is one of the most common cancers worldwide and is associated with a high rate of cancer mortality in women. Resistance to chemotherapy is considered a significant problem and a major challenge for the treatment of patients with BC. miR-200c belongs to a family of miRNAs that act as tumor inhibitors. The expression level of miR-200c has been reported to be decreased in cancers, especially in BC. The increased miR-200c expression can be considered as a potent inhibitor of drug resistance and tumor progression. Methods and Results: The current study examined the effect of miR-200c on enhancing the BC cells' sensitivity to Carboplatin through targeting MDR1 expression. To perform functional analyses, mimic miR-200c transfected to MCF7 cells. Then, the viability of the cells was investigated via MTT assay. Finally, the expression of associated genes assessed using qRT-PCR. The results indicated that downregulation of miR-200c was occurred in MCF7 cells in comparison to control. Besides, restoring miR-200c expression by regulating the expression level of the apoptotic gene reduces the viability of cancer cells. Moreover, miR-200c increased the sensitivity of MCF7 cells to Carboplatin via reducing the MDR1 gene expression. Conclusions: This study provided valuable data showing that miR-200c enhances the effect of carboplatin as a clinically approved chemotherapeutic agent, and restoring its expression could be considered as a promising targeted adjuvant therapy for BC management.