BackgroundCigarette smoking (CS) triggers an intense and harmful inflammatory response in lungs mediated by alveolar and blood macrophages, monocytes, and neutrophils and is closely associated with prevalence of tuberculosis (TB). The risk of death in patients with long-term cigarette smoking-related pulmonary tuberculosis (LCS-PTB) is approximately 4.5 times higher than those with nonsmoking pulmonary tuberculosis (N-PTB). However, the mechanisms underlying the harmful inflammatory responses in the setting of LCS-PTB have not been well documented.Methods28 cases LCS-PTB patients, 22 cases N-PTB patients and 20 cases healthy volunteers were enrolled in this study. Monocytes were isolated from peripheral blood mononuclear cells. Differentiated human MDM and U937 cell were prepared with M-CSF and PMA stimulation, respectively. The miR-196b-5p, STAT1, STAT3, STAT4, STAT5A, STAT5B, STAT6, SOCS1 and SOCS3 mRNA expression were detected by qRT-PCR. Western blot was performed according to SOCS1, SOCS3, and pSTAT3 expression. The mycobacterial uptake by MDMs from different groups of patients after Bacillus Calmette–Guérin (BCG) infection and agomir-196b-5p or antagomir-196b-5p transfection were used by flow cytometry analysis. Human IL-6, IL-10 and TNF-α levels on the plasma and cell culture supernatant samples were measured using ELISA. For dual-luciferase reporter assay, the SOCS3 3′-UTR segments, containing the binding elements of miR-196b-5p or its mutant versions were synthesized as sense and antisense linkers.ResultsIn this study, we found that IL-6, TNF-α production, SOCS3 mRNA expression were downregulated, while miR-196b-5p and STAT3 mRNA expression were upregulated in monocytes from LCS-PTB patients as compared to N-PTB patients. Meanwhile, we demonstrated that miR-196b-5p could target SOCS3 and activate STAT3 signaling pathway, which may possibly contribute to attenuation of BCG uptake and decrease in IL-6 and TNF-α production in macrophages.ConclusionsOur findings revealed that CS exposure regulates inflammatory responses in monocyte/macrophages from LCS-PTB patients via upregulating miR-196b-5p, and further understanding of the specific role of miR-196b-5p in inflammatory responses mightfacilitate elucidating the pathogenesis of LCS-PTB, thus leading to the development of new therapeutic strategies for PTB patients with long-term cigarette smoking.Electronic supplementary materialThe online version of this article (10.1186/s12967-018-1654-9) contains supplementary material, which is available to authorized users.

No abstract

Polygalacturonase-inhibiting proteins (PGIPs) are plant defense proteins. To date, no spatial distribution of PGIPs and interaction between PGIPs and nitric oxide (NO) in plant were described. Here, we first reported the full-length cDNA sequence of PGIP of Chorispora bungeana (CbPGIP1). Notably, immunofluorescence localization showed that the CbPGIP was evenly distributed in leaves but it was mainly localized in epidermis and vascular bundle in stems and roots. Further studies indicated that CbPGIP had higher abundance in roots than in stems and leaves. Conversely, the bulk PGIP of C. bungeana showed a higher activity in leaves than in stems and roots. In addition, quantitative real-time polymerase chain reaction demonstrated that CbPGIP1 expression was induced by Stemphylium solani, salicylic acid (SA), 4, -4 degrees C and NO. This is a first report attempting to predict if NO can induce the PGIP expression. Taken together, these findings showed that the gene was spatially regulated and NO and SA might take part in CbPGIP1 expression induced by biotic and abiotic stresses. This study highlighted the potential importance of CbPGIP1 and NO in plant resistance.

Our study is aim to explore predictors for failure of anterolateral thigh (ALT) flap in the reconstruction of upper extremity. We performed a retrospective study for 509 patients who underwent ALT flap in the reconstruction of upper extremity. Among them, 27 patients suffered from necrosis of ALT flap (necrosis group, NG) and 482 gained survival of this flap (survival group, SG). We collected possible factors including 3 aspects: demographic variables – age, sex, body mass index (BMI), history of hypertension, diabetes, heart disease, smoking and alcohol, trauma mechanism, and postmenopausal; surgical-related variables – surgical duration, blood loss, number of reconstructed veins, flap size, perforator type, diameter of perforator, and vein graft; blooding variables – hemoglobin, D-dimer, white blood cell, red blood cell, and platelet count (PLT). We compared the above data between NG and SG by univariate, multivariate, and Kaplan–Meier method coupled with a log-rank test linear regression analysis. The survival incidence of ALT flap repairing upper extremity was 94.7% (482 of 509). The outcome of univariate analysis showed that age (53.5 ± 9.2), BMI (26.7 ± 4.5), larger flap size (24.3∗9.2), D-dimer (0.58 ± 0.10), and PLT (278.1 ± 34.4) in NG were significantly higher than these (44.2 ± 7.9, 22.3 ± 4.2, 19.1∗7.9, 0.48 ± 0.08, 236.6 ± 30.5) in SG. However, diameter of perforator (1.07 ± 0.02) in NG was markedly smaller than that (1.12 ± 0.02) in SG. Additionally, female patients, postmenopausal, patients with using venous stapler or 1 reconstructed vein had a higher failure rate. Multivariate and Kaplan–Meier method implied the same results. In summary, many factors were related with failure of ALT in the reconstruction of upper extremity. Postmenopausal, D-dimer, and PLT were the first considered as risk factors for ALT flap repairing upper extremity.

Background In patients of chronic thromboembolic pulmonary hypertension undergoing pulmonary endarterectomy, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides full haemodynamic support. However, during a rescue treatment of VA-ECMO for patients with difficulty weaning from cardiopulmonary bypass, a significantly increase left ventricular afterload through retrograde infusion of arterialized blood into the descending aorta may occur. Case presentation We report a 70-year-old man who suffered severe residual pulmonary hypertension following pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension. Preoperative echocardiogram showed a dilated and poorly functioning right ventricle, as well as a small left heart with normal function (TAPES9.6 mm, LVEF64%, average E/E′11.94, lateral E′12.1 cm/s, tricuspid regurgitation velocity 2.5 m/s), while postoperative echocardiography revealed a significant decrease of whole ventricular function on postoperative day 1(TAPES4mm, LVEF28%, average E/E′15, lateral E′6.7 cm/s, tricuspid regurgitation velocity 4.1 m/s), indicating the patient developed severe secondary left ventricular dysfunction on the basis of right ventricular dysfunction, during VA-ECMO support. Then comprehensive measures were adopted, such as down-regulating VA-ECMO flow rate, adjusting respiratory parameters, using vasoactive drugs, as well as prostacyclin. Eventually, the pulmonary hypertension decreased to moderate degree, and the heart function improved gradually. Conclusions In the face of severe residual pulmonary hypertension and sencondary left ventricular dysfunction associated with VA-ECMO, comprehensive measures described above may facilitate recovery. ECMO flow titration to maintain relatively low flow rate is very important to not only maintain systemic perfusion, but also reduce left ventricular afterload and ensure pulsatile perfusion of pulmonary artery.