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Twenty-three patients with primary spontaneous pneumothorax and 30 patients with secondary spontaneous pneumothorax treated by intercostal catheter drainage with underwater seal were divided randomly into two groups, one receiving suction drainage (up to 20 cm H20 pressure) and the other no suction. The success rate was 570% for the former and 50 / for the latter. The suction group spent an average of five days in hospital, whereas the non-suction group averaged four days. Suction drainage therefore did not have any advantage. To determine how soon the catheter could be removed without complication, patients were also divided randomly into two subgroupsone had the catheter removed, without previous clamping, as soon as the lung was expanded; the other had the catheters left in situ for a further three days. The success rate was 52 % for the former, and 53 % for the latter. But most of the failure in the early removal group was caused by re-collapse of the lung rather than persistent air leakage; hence removal of the catheter too early was not recommended.Spontaneous pneumothorax is usually treated by insertion of an intercostal catheter connected to underwater seal drainage. However there is no agreement on the routine use of suction drainage. Several textbooks on respiratory medicine in fact gave conflicting views. Croften and Douglas' were against suction; Holman2 seemed to recommend it whereas Hinshaw and Murray3 and Fishman4 did not specify it clearly. Moreover we know of no study to determine the best time to remove the intercostal catheter. When the lung has expanded and there is no more air leak, most would clamp the catheter for 24-48 hours. If there is no re-collapse of the lung, the catheter can be taken out. If we assume that the air leak has sealed off once the lung has fully expanded, the catheter could in theory be taken out at once without complication; hospital stay can then be shortened. We therefore undertook a prospective study to assess the efficacy of suction drainage and the optimal timing of catheter removal. MethodsBetween mid-1979 and mid-1980, 53 consecutive patients with spontaneous pneumothorax treated by intercostal catheter drainage at

The origin of rhabdomyosarcoma (RMS) remains controversial. However, specific microRNAs (miRNAs) are downregulated in RMS and it is possible that re-expression of these miRNAs may lead to differentiation. Transforming growth factor-β1 (TGF-β1) is known to block differentiation of RMS. We therefore analyzed miRNA microarrays of RMS cell lines with or without TGF-β1 knockdown and identified a novel anti-oncogene miR-411-5p. Re-expression of miR-411-5p inhibited RMS cell proliferation in vitro and tumorigenicity in vivo. Using a luciferase reporting system and sequence analysis, the potential target of miR-411-5p was identified as sprouty homolog 4 (SPRY4), which inhibits protein kinase Cα-mediated activation of mitogen-activated protein kinases (MAPKs), especially p38MAPK phosphorylation. These results revealed an inverse correlation between TGF-β1/SPRY4 and miR-411-5p levels. SPRY4 small interfering RNA and miR-411-5p both activated p38MAPK phosphorylation and also promoted apoptosis and myogenic differentiation, indicated by increased caspase-3, myosin heavy chain, and myosin expression. SPRY4 and miR-411 mRNA levels correlated with TGF-β1 expression levels in RMS tissues, which was confirmed by immunohistochemical staining for TGF-β1, SPRY4, and phosphorylated p38MAPK proteins. Overall, these results indicate that miR-411-5p acts as an RMS differentiation-inducing miRNA prompting p38MAPK activation via directly downregulating SPRY4. These results establish an autoregulatory loop between TGF-β1/miR-411-5p/SPRY4 and MAPK in RMS, which governs the switch between proliferation and differentiation.

Controversial findings are reported about the relationship between floppy eyelid syndrome (FES) and obstructive sleep apnea syndrome (OSAS). The main goal of this study was to evaluate whether FES is more prevalent in OSAS patients by performing a meta-analysis. A comprehensive literature search of Pubmed, Embase, and Cochrane databases was performed. Only studies related to the prevalence of FES in OSAS were included in the meta-analysis. We estimated a pooled odds ratio (OR) for the prevalence of FES in OSAS. In total, 6 studies with 767 participants met the inclusion criteria. Using a fixed-effects model, the pooled OR was 4.12. The test for the overall effect revealed that FES was statistically prevalent in OSAS patients when compared with that in non-OSAS subjects (Z = 4.98, p < 0.00001). In the subgroup analysis by OSAS severity, the incidence of FES in OSAS increased with severity of OSAS as indicated with increased OR values (OR = 2.56, 4.62, and 7.64 for mild, moderate, and severe OSAS). In conclusion, the results indicate that FES is more prevalent in OSAS patients. However, this result was based only on unadjusted estimates. Prospective cohort studies are needed to determine whether OSAS is an independent risk factor for FES.

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Radiation-induced skin fibrosis is a detrimental and chronic disorder that occurs after radiation exposure. The molecular changes underlying the pathogenesis of radiation-induced fibrosis of human skin have not been extensively reported. Technical advances in proteomics have enabled exploration of the biomarkers and molecular pathogenesis of radiation-induced skin fibrosis, with the potential to broaden our understanding of this disease. In this study, we compared protein expression in radiation-induced fibrotic human skin and adjacent normal tissues using iTRAQ-based proteomics technology. We identified 186 preferentially expressed proteins (53 upregulated and 133 downregulated) between radiogenic fibrotic and normal skin tissues. The differentially expressed proteins included keratins (KRT5, KRT6A, KRT16 and KRT17), caspase-14, fatty acid-binding protein 5 (FABP5), SLC2A14 and resistin. Through bioinformatic analysis of the proximal promoters, common motifs and corresponding transcriptional factors were identified that associate with the dysregulated proteins, including PAX5, TBX1, CLOCK and AP2D. In particular, FABP5 (2.15-fold increase in fibrotic skin tissues), a transporter of hydrophobic fatty acids, was investigated in greater detail. Immunohistochemistry confirmed that the protein level of FABP5 was increased in fibrotic human skin tissues, especially in the epidermis. Overexpression of FABP5 resulted in nuclear translocation of SMAD2 and significant activation of the profibrotic TGF-β signaling pathway in human fibroblast WS1 cells. Moreover, exogenous FABP5 (FABP5-EGFP) could be incorporated by skin cells and intensify TGF-β signaling, indicating a communication between the microenvironment and skin fibrosis. Taken together, our findings illustrate the molecular changes during radiation-induced human skin fibrosis and the critical role of FABP5 in activating the TGF-β signaling pathway.

The dome-shaped cornea is a transparent, non-vascularized, and epithelialized highly organized tissue. Physical and chemical injuries may trigger corneal wound healing (CWH) response and result in neovascularization that impairs the visual function. CWH involves not only migration, proliferation, and differentiation of the cells in different layers of cornea, but also the mobilization of immune cells. We demonstrated here that human adipose-derived mesenchymal stromal cells (ADSCs) could effectively inhibit neovascularization during ethanol-induced injury in mouse cornea. Importantly, we found that while neutrophils are essential for CWH, excessive and prolonged neutrophil retention during the granulation stage contributes to neovascularization. ADSCs were found to promote the clearance of neutrophils in the cornea during the granulation stage, likely via increasing the reverse transendothelial cell migration of CXCR4 high neutrophils from cornea to the lung. Our results demonstrate that ADSCs are effective in treating CWHinduced neovascularization and modulation of neutrophil clearance could be novel strategies for better vision recovery after injury.

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