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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 construct a plasmid vector with EGFP reporter gene for functional analysis of enhancers., Methods: EGFP DNA was amplified by PCR from plasmid pEGFP-N1 DNA and subcloned into plasmid PGL3-promoter backbone without luc(+) gene to construct the enhancer-identifying vector pEGFP-enhancer. Different copies of hypoxia response element (HRE) sequence were synthetized and subcloned into the multiple cloning site of the plasmid pEGFP-enhancer. Using Lipofectamine 2000, the recombined pEGFP-HRE and pEGFP-5HRE plasmids were transfected into the Hela cells respectively. After hypoxic or normoxic cell culture, EGFP expression in the cells was detected by flow cytometry and fluorescence microscopy., Results: After hypoxic exposure, the fluorescence intensity of EGFP in the Hela cells transfected with the plasmid increased with the enhancer HRE copies, while the fluorescence intensity underwent no significant changes after normoxic cell culture., Conclusion: we have successfully constructed the enhancer expression vector plasmid pEGFP-enhancer, which can identify the activity of the enhancers through EGFP expression.

Objective: To identify the labeled cells in the ependyma/subventricular zone (SVZ) of normal adult rats by DiI injected into the lateral ventricle., Methods: Fifty male Sprague-Dawley rats were divided randomly into five groups (10 per group). All of the rats were injected with 10 microL of 2 g/L fluorescence dye DiI into the right lateral ventricle. The five groups of rats were sacrificed at 6 h, 12 h, 24 h, 36 h or 48 h after injection respectively. Hoechst 33258 staining was used to identify nuclei and laser confocal microscopy was used to detect the DiI-labeled cells and to measure the thickness of the tissue with DiI fluorescence in the wall of the left lateral ventricle., Results: After injection of the DiI into the right lateral ventricle, DiI- Hoechst 33258 double positive cells were found in the ependymal layer of the left lateral ventricular wall at 24 h and in the SVZ at 48 h as well. The thickness of the tissue with DiI fluorescence in the left ependyma/septal subventricular zone (SVZspt) and ependyma/postnatal equivalent of the ganglionic eminences (SVZge) remained unchanged at 12 h and 24 h after DiI injection. The thickness of the tissue with DiI fluorescence in the left ependyma/SVZge was significantly greater than that in the ependyma/SVZspt at all of the time points (P<0.05)., Conclusion: The ependyma/SVZ cells can be labeled by Dil 24-48 h after injection (10 microL of 2 g/L) into the lateral ventricle.

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.