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Enfermedad Pulmonar Obstructiva Crónica , Embolia Pulmonar , Trombosis , Humanos , Enfermedad Pulmonar Obstructiva Crónica/complicaciones , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico por imagen , Pulmón/diagnóstico por imagen , Embolia Pulmonar/complicaciones , Embolia Pulmonar/diagnóstico por imagen , Trombosis/complicaciones , Trombosis/diagnóstico por imagen , Progresión de la Enfermedad , Enfermedad AgudaRESUMEN
BACKGROUND: The risk factors for osteoporosis and its prognostic value in patients with bronchiectasis is not well characterized. We explored the risk factors for osteoporosis and its prognostic impact in hospitalized non-cystic fibrosis bronchiectasis (NCFB) patients in Southeast China. METHODS: This observational cohort study consecutively enrolled 179 hospitalized patients with NCFB bronchiectasis between 2017 and 2021. The risk factors and the impact of osteoporosis on all-cause mortality were assessed. RESULTS: 21.2% (38/179) of hospitalized NCFB patients were diagnosed with osteoporosis. Patients with osteoporosis had more severe symptoms (assessed by chronic airway assessment test, CAT, median 22 vs. 17, P = 0.017), poorer quality of life (assessed by St. George Respiratory Questionnaires, SQRC, median 42 vs. 27, P = 0.007), more severe disease stage (assessed by bronchiectasis severity index, BSI, median 14 vs. 11, P = 0.02), more comorbidities (assessed by Bronchiectasis Aetiology Comorbidity Index, BACI, median 5 vs. 4, P = 0.021) than patients without. Age, female sex, anemia, post-infection, and history of regular inhaled corticosteroid treatment were independent risk factors for osteoporosis in those patients. 21 patients (11.7%) died over a median follow-up period of 32 months. The all-cause mortality in NCFB patients with osteoporosis [28.94% (11/38)] was significantly higher than those without osteoporosis [7.09% (10/141)] [hazard ratio (HR) 5.34, 95% confidence interval (CI) 2.26-12.67, P < 0.001]. After adjusting for BSI and other confounding factors, osteoporosis was still independently associated with all-cause mortality in hospitalized NCFB patients (HR 4.29, 95% CI 1.75-10.49, P < 0.001). CONCLUSIONS: Osteoporosis had an independent effect on all-cause mortality in hospitalized NCFB patients. Management of comorbidities, including bone health, is a critical aspect of treating NCFB patients.
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Bronquiectasia , Fibrosis Quística , Osteoporosis , Femenino , Humanos , Pronóstico , Calidad de Vida , Bronquiectasia/complicaciones , Bronquiectasia/epidemiología , Bronquiectasia/diagnóstico , Osteoporosis/complicaciones , Osteoporosis/epidemiología , Factores de RiesgoRESUMEN
BACKGROUND: Psittacosis is a relatively uncommon cause of community-acquired pneumonia, often leading to diagnostic difficulty. METHODS: A retrospective study was conducted on the clinical features of psittacosis patients in China. Forty-six cases of Chlamydophila psittaci infection with atypical pneumonia of varying severity in the last two years were described retrospectively. RESULTS: Fever, relative bradycardia, and other systemic upsets were the main clinical presentation. The most common radiographic abnormality was segmental or lobar shadowing or consolidation. The total white cell counts were usually normal or slightly increased. The concentration of creatine kinase, C reactive protein, and lactic dehydrogenase increased, while albumin decreased remarkably. These cases exhibited good recovery after being treated with tetracycline or quinolone antibiotics. CONCLUSION: These features may help differentiate psittacosis from other traditional bacterial pneumonia. However, they do not provide a definitive diagnosis. Psittacosis diagnosis must perform the whole-genome sequencing for Chlamydophila psittaci in respiratory, blood, or sputum specimens. Increased awareness of psittacosis can shorten diagnostic delays and improve patient outcomes.
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Chlamydophila psittaci , Neumonía Bacteriana , Psitacosis , Humanos , Psitacosis/diagnóstico , Psitacosis/tratamiento farmacológico , Estudios Retrospectivos , Pueblos del Este de Asia , Neumonía Bacteriana/microbiología , Antibacterianos/uso terapéuticoRESUMEN
The occurrence of paclitaxel (PTX) resistance in nonsmall cell lung cancer (NSCLC) is a major challenge for NSCLC treatment. Circular RNAs (circRNAs) have been reported to associate with cancer resistance, but the role of circ_0010235 in PTX resistance of NSCLC is unclear. The expression of circ_0010235 and microRNA-512-5p (miR-512-5p) were determined by quantitative real-time PCR. Cell counting kit-8 assay, transwell assay and flow cytometry were performed to measure the PTX resistance, proliferation, migration, invasion and apoptosis of cells. All proteins were assessed via western blot analysis. The combination between miR-512-5p and circ_0010235 or FAM83F was predicted by the online database and confirmed by a dual-luciferase reporter assay. Angiogenesis assay was used to detect the ability of cells to form blood vessels. Animal experiments were employed to confirm the effect of circ_0010235 on NSCLC tumor growth in vivo. Circ_0010235 and FAM83F were upregulated in PTX-resistant NSCLC tissues and cells. Circ_0010235 knockdown suppressed the resistance to PTX, proliferation, angiogenesis and migration/invasion in A549/PTX and H1299/PTX cells but promoted apoptosis rate. MiR-512-5p could be sponged by circ_0010235, and its overexpression had an inhibition effect on the PTX resistance of NSCLC cells. FAM83F was a target of miR-512-5p and circ_0010235 could modulate FAM83F expression by sponging miR-512-5p. In vivo experiments revealed that silenced circ_0010235 could improve the sensitivity of the tumor to PTX. Therefore, these findings advocated targeting the circ_0010235/miR-512-5p/FAM83F axis as a potential therapeutic option for patients with NSCLC who are resistant to PTX.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , MicroARNs , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Carcinoma de Pulmón de Células no Pequeñas/genética , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Línea Celular Tumoral , Proliferación Celular , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Paclitaxel/farmacología , Paclitaxel/uso terapéutico , ARN Circular/genéticaRESUMEN
BACKGROUND: As reported, long non-coding RNAs are a pivotal player in lung squamous cell carcinoma (LSCC) progression. We noticed the remarkably upregulated transmembrane-4-l-six-family-19 antisense RNA 1 (TM4SF19-AS1) in LSCC and further demonstrated the function it played in LSCC and the possible molecular mechanism. METHODS: Via bioinformatics approach, we evaluated TM4SF19-AS1 and TM4SF19 levels in LSCC tissue, and real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot revealed their mRNA and protein levels in LSCC cells. Cell Counting Kit-8 and colony formation assays analyzed the proliferation ability of LSCC cells, and cell adhesion ability was detected via cell adhesion assay. RNA immunoprecipitation and chromatin immunoprecipitation analyzed the underlying mechanism of TM4SF19-AS1 regulating its target, while methylation-specific PCR indicated the methylation level of TM4SF19-AS1. RESULTS: TM4SF19-AS1 was markedly upregulated in LSCC. Functional assays revealed that TM4SF19-AS1 could facilitate the proliferation and adhesion of LSCC. Besides, we revealed the mechanism of TM4SF19-AS1 regulation that it directly bound to WD repeat-containing protein 5 (WDR5), and was then recruited to TM4SF19 promoter region, which activated DNA demethylation, thereby suppressing malignant LSCC progression. CONCLUSION: Our research demonstrated that TM4SF19-AS1 affected LSCC cell proliferation by recruiting WDR5 to manipulate transmembrane-4-lsix-family-member-19 (TM4SF19), which offers a new observation on LSCC pathogenesis, indicating that TM4SF19-AS1 is able to be a promising target for LSCC treatment.
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Carcinoma de Pulmón de Células no Pequeñas , Carcinoma de Células Escamosas , Neoplasias Pulmonares , MicroARNs , ARN Largo no Codificante , Carcinoma de Pulmón de Células no Pequeñas/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Línea Celular Tumoral , Proliferación Celular/genética , Regulación Neoplásica de la Expresión Génica , Humanos , Péptidos y Proteínas de Señalización Intracelular/genética , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Pulmón/metabolismo , Neoplasias Pulmonares/genética , MicroARNs/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , TetraspaninasRESUMEN
PURPOSE: Lung cancer causes significant mortality across the globe. This study aimed at the exploration of the regulatory role of microRNA (miR)-466 in lung cancer. METHODS: qRT-PCR analysis was used to infer the expression levels of miR-466 and Runt-related transcription factor 2 (RUNX2). CCK8 kit was used for assessment of cell proliferation. Colony forming assay was employed for examining the viability of cancer cells. The wound healing and Matrigel assays were used for investigating the rates of migration and invasion of cancer cells, respectively. Dual luciferase assay was performed to assess the interaction between miR-466 and RUNX2. Western blotting was performed to determine the protein expression. RESULTS: The results indicated that miR-466 is downregulated in lung cancer cells. Its overexpression led to significant decline of proliferation of cancer cells. The migration and invasion of lung cancer cells transfected with mir-466 mimics also got repressed. At molecular level, the regulatory role of miR-466 was exerted through the RUNX2 transcription factor whose silencing mimicked the effects of miR-466 overexpression. CONCLUSION: Taken all together, miR-466 suppression is associated with the growth and progression of lung cancer. The miR-466 overexpression declined the proliferation and metastasis of cancer cells and these effects were modulated through miR-466/RUNX2 molecular axis.