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A 49-year-old female patient developed chest tightness and shortness of breath without apparent cause and presented to a local hospital. Chest radiography indicated increased thickening of the lung texture, increased multiple patchy densities in the lower lobes of the bilateral lungs and a slightly enlarged thyroid. The patient was treated for pulmonary infection with antibiotics but the symptoms persisted. A repeated CT scan revealed ground-glass attenuation of the bilateral lungs with multiple flaky exudates and visible bronchogenic signs. The symptoms did not improve after broadening anti-microbial coverage. Bronchoscopy and biopsy confirmed cryptogenic organizing pneumonia (COP). Thyroid ultrasound and thyroid function tests jointly confirmed the diagnosis of Hashimoto's thyroiditis (HT). After receiving corticosteroid treatment, the patient's condition improved and she was discharged. This case demonstrates that COP may present in combination with Hashimoto's thyroiditis (HT) and may possibly even be caused by HT. Early confirmation of diagnosis and treatment will help to improve the prognosis of such patients. [ABSTRACT FROM AUTHOR]

Background: MicroRNAs play crucial roles in tumorigenesis and tumor progression. miR-770 has been reported to be downregulated in several cancers and affects cancer cell proliferation, apoptosis, metastasis and drug resistance. However, the role and underlying molecular mechanism of miR-770 in human glioma remain unknown and need to be further elucidated. Methods: The expression of miR-770 in glioma tissues and cell lines was measured by quantitative real-time PCR (qRT-PCR) to explore the association of miR-770 expression with clinicopathological characteristics. The expression of CDK8 was detected by qRT-PCR and Western blotting in glioma tissues. A target prediction program and a dual-luciferase reporter assay were used to confirm that CDK8 is a target gene of miR-770. MTT and cell counting assays were used to assess the effect of miR-770 on glioma cell proliferation. The cell cycle distribution and apoptosis were examined by flow cytometry. CDK8 siRNA and overexpression were used to further confirm the function of the target gene. Results: We demonstrated that miR-770 expression was downregulated in human glioma tissues and cell lines. The overexpression of miR-770 inhibited glioma cell proliferation and cell cycle G1-S transition and induced apoptosis. The inhibition of miR-770 facilitated cell proliferation and G1-S transition and suppressed apoptosis. miR-770 expression was inversely correlated with CDK8 expression in glioma tissues. CDK8 was confirmed to be a direct target of miR-770 by using a luciferase reporter assay. The overexpression of miR-770 decreased CDK8 expression at both the mRNA and protein levels, and the suppression of miR-770 increased CDK8 expression. Importantly, CDK8 silencing recapitulated the cellular and molecular effects observed upon miR-770 overexpression, and CDK8 overexpression eliminated the effects of miR-770 overexpression on glioma cells. Moreover, both exogenous expression of miR-770 and silencing of CDK8 resulted in suppression of the Wnt/β-catenin signaling pathway. Conclusions: Our study demonstrates that miR-770 inhibits glioma cell proliferation and G1-S transition and induces apoptosis through suppression of the Wnt/β-catenin signaling pathway by targeting CDK8. These findings suggest that miR-770 plays a significant role in glioma progression and serves as a potential therapeutic target for glioma. [ABSTRACT FROM AUTHOR]

Background: MicroRNAs play crucial roles in tumorigenesis and tumor progression. miR-770 has been reported to be downregulated in several cancers and affects cancer cell proliferation, apoptosis, metastasis and drug resistance. However, the role and underlying molecular mechanism of miR-770 in human glioma remain unknown and need to be further elucidated., Methods: The expression of miR-770 in glioma tissues and cell lines was measured by quantitative real-time PCR (qRT-PCR) to explore the association of miR-770 expression with clinicopathological characteristics. The expression of CDK8 was detected by qRT-PCR and Western blotting in glioma tissues. A target prediction program and a dual-luciferase reporter assay were used to confirm that CDK8 is a target gene of miR-770. MTT and cell counting assays were used to assess the effect of miR-770 on glioma cell proliferation. The cell cycle distribution and apoptosis were examined by flow cytometry. CDK8 siRNA and overexpression were used to further confirm the function of the target gene., Results: We demonstrated that miR-770 expression was downregulated in human glioma tissues and cell lines. The overexpression of miR-770 inhibited glioma cell proliferation and cell cycle G1-S transition and induced apoptosis. The inhibition of miR-770 facilitated cell proliferation and G1-S transition and suppressed apoptosis. miR-770 expression was inversely correlated with CDK8 expression in glioma tissues. CDK8 was confirmed to be a direct target of miR-770 by using a luciferase reporter assay. The overexpression of miR-770 decreased CDK8 expression at both the mRNA and protein levels, and the suppression of miR-770 increased CDK8 expression. Importantly, CDK8 silencing recapitulated the cellular and molecular effects observed upon miR-770 overexpression, and CDK8 overexpression eliminated the effects of miR-770 overexpression on glioma cells. Moreover, both exogenous expression of miR-770 and silencing of CDK8 resulted in suppression of the Wnt/β-catenin signaling pathway., Conclusions: Our study demonstrates that miR-770 inhibits glioma cell proliferation and G1-S transition and induces apoptosis through suppression of the Wnt/β-catenin signaling pathway by targeting CDK8. These findings suggest that miR-770 plays a significant role in glioma progression and serves as a potential therapeutic target for glioma.

Objective: To investigate the migration and differentiation of ependymal/subventricular zone cells after focal cerebral ischemia in rats, and reveal the origin of the newly generated neural cells in the peri-infarct region., Methods: Normal adult male Sprague Dawley rats weighing 250-350 g were used in this study. Before middle cerebral artery occlusion (MCAO), 10 microl of 0.2% DiI was injected into the lateral ventricle for prelabeling the ependymal/subventricular zone cells. After ischemia, cumulative BrdU labeling was employed to detect the newly generated cells and double immunofluorescent staining to identify cell differentiation. The labeled cells were observed with laser confocal microscopy., Results: In the non-ischemic control rats, DiI-labeled cells resided in the ependyma/subventricular zone. After focal cerebral ischemia, DiI-labeled cells were found in the corpus callosum, adjacent striatum and cortex, and some DiI/BrdU/glial fibrillary acidic protein (GFAP)-positive cells or DiI/BrdU/ neuronal nuclear antigen (NeuN)-positive cells were observed in the peri-infarct region in the striatum or cortex since day 14 after MCAO., Conclusion: After focal cerebral ischemia, ependymal/subventricular zone cells migrate into the peri-infarct region where they differentiate into neurons and astrocytes. This finding may be important for understanding the source of adult neural stem cells and for developing new therapeutic intervention strategy through enhancing endogenous neurogenesis after brain injury.