Design Appropriate Incision Length for Uniportal Video-Assisted Thoracoscopic Lobectomy: Take into Account Safety and Minimal Invasiveness.

BACKGROUND: There is no criterion on the length of the uniportal video-assisted thoracoscopic surgery (UVATS) incision when performing lobectomy. We aimed to develop a nomogram to assist surgeons in designing incision length for different individuals. METHODS: A cohort consisting of 290 patients were enrolled for nomogram development. Univariate and multivariate logistic regression analyses were performed to identify candidate variables among perioperative characteristics. C-index and calibration curves were utilized for evaluating the performance of the nomogram. Short-term outcomes of nomogram-predicted high-risk patients were compared between long incision group and conventional incision group. RESULTS: Of 290 patients, 150 cases (51.7%) were performed incision extension during the surgery. Age, tumor size, and tumor location were identified as candidate variables related with intraoperative incision extension and were incorporated into the nomogram. C-index of the nomogram was 0.75 (95% confidence interval: 0.6961-0.8064), indicating the good predictive performance. Calibration curves presented good consistency between the nomogram prediction and actual observation. Of high-risk patients identified by the nomogram, the long incision group (n = 47) presented shorter duration of operation (p = 0.03), lower incidence of total complications (p = 0.01), and lower incidence of prolonged air leak (p = 0.03) compared with the conventional incision group (n = 55). CONCLUSION: We developed a novel nomogram for predicting the risk of intraoperative incision extension when performing uniportal video-assisted thoracoscopic lobectomy. This model has the potential to assist clinicians in designing the incision length preoperatively to ensure both safety and minimal invasiveness.

Development and validation of a new clinical staging system to predict survival for esophageal squamous cell carcinoma patients: Application of the nomogram.

INTRODUCTION: Survival of patients with the same clinical stage varies widely and effective tools to evaluate the prognosis utilizing clinical staging information is lacking. This study aimed to develop a clinical nomogram for predicting survival of patients with Esophageal Squamous Cell Carcinoma (ESCC). MATERIALS AND METHODS: On the basis of data extracted from the SEER database (training cohort, n = 3375), we identified and integrated significant prognostic factors for nomogram development and internal validation. The model was then subjected to external validation with a separate dataset obtained from Jinling Hospital of Nanjing Medical University (validation cohort, n = 1187). The predictive accuracy and discriminative ability of the nomogram were determined by concordance index (C-index), Akaike information criterion (AIC) and calibration curves. And risk group stratification was performed basing on the nomogram scores. RESULTS: On multivariable analysis of the training cohort, seven independent prognostic factors were identified and included into the nomogram. Calibration curves presented good consistency between the nomogram prediction and actual observation for 1-, 3-, and 5-year OS. The AIC value of the nomogram was lower than that of the 8th edition American Joint Committee on Cancer TNM (AJCC) staging system, whereas the C-index of the nomogram was significantly higher than that of the AJCC staging system. The risk groups stratified by CART allowed significant distinction between survival curves within respective clinical TNM categories. CONCLUSIONS: The risk stratification system presented better discriminative ability for survival prediction than current clinical staging system and might help clinicians in decision making.

Catalytic fast pyrolysis of polyethylene terephthalate plastic for the selective production of terephthalonitrile under ammonia atmosphere.

Terephthalonitrile (TPN) was directly produced from polyethylene terephthalate (PET) plastic via catalytic fast pyrolysis with ammonia. The optimal condition for producing TPN was over 1 g γ-Al2O3-2 wt% catalyst at 500 °C under carrier gas (50% NH3 and 50% N2) with yield of nitriles and TPN of 58.1 and 52.3 C%, respectively. The selectivity of TPN in the nitriles was around 90%. Meanwhile, a bit of aromatics, benzonitrile, acetonitrile were also produced as by-products with the total yields of less than 3 C%. The catalyst deactivated slightly after 5 cycles. Possible reaction routes were proposed and it was found that terephthalic acid, benzoic acid, related esters and amides were the major intermediates from PET to nitriles. Acetonitrile could be produced from acetaldehyde and its corresponding imines. In addition, 32.1 C% TPN with high purity (>95%) was obtained via freezing recrystallization. Catalytic pyrolysis with ammonia process was a promising technology for converting waste PET plastics to TPN. This study provided a new method for producing N-containing chemicals from polyester plastics.

HONH3Cl optimized CH3NH3PbI3 films for improving performance of planar heterojunction perovskite solar cells via a one-step route.

Planar heterojunction perovskite solar cells (PHJ-PSCs) constructed with one-step precursor solution spin-coating deposition (OPSSD) usually give an extremely low performance mainly due to the poor morphology and low crystallinity of the perovskite films. In this work, by incorporating a suitable HONH3Cl additive in the perovskite precursor solution, a high quality perovskite film with improved morphology and crystallinity was obtained. The UV-vis measurement of the CH3NH3I solutions without and with HONH3Cl demonstrates that the improved quality of the perovskite film can be easily attributed to a combined effect of N2, I2, H2O and CH3NH3Cl originating from the oxidation of CH3NH3I triggered by the HONH3Cl additive, which can manipulate the crystallization process of the perovskite. Accordingly, the improved performance for the HONH3Cl-induced PHJ-PSCs can also be demonstrated. At the optimized molar ratio of 1 : 1 : 0.1 for PbI2 : CH3NH3I : HONH3Cl, the PHJ-PSCs exhibit an average power conversion efficiency (PCE) of 10.61 ± 0.51%, which is much higher than that of pristine 1 : 1 : 0 based cells without additive (7.21 ± 0.61%), and the best performing HONH3Cl-induced device can yield a PCE as high as 11.12% with a Jsc of 18.42 mA cm-2, Voc of 0.95 V and FF of 0.63. Introducing suitable HONH3Cl as an additive into the perovskite precursor solution is really an effective route to enhance the performance of the PHJ-PSCs via OPSSD.

Curcumin attenuates cardiopulmonary bypass-induced lung oxidative damage in rats.

OBJECTIVE: Acute lung injury is a common complication after cardiopulmonary bypass (CPB). Oxidative damage greatly impacts CPB-induced lung ischemic pathogenesis and may represent a target for treatment. We aimed to investigate whether curcumin upregulates heme oxygenase 1 (HO-1) expression and ameliorates lung injury in a rat CPB model. METHODS: A total of 80 male Sprague-Dawley rats were divided into 2 sets of 5 groups (n = 8 per group): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 hours prior to CPB. Lung tissue, serum, and bronchoalveolar lavage fluid was harvested 2 or 24 hours postoperatively. In the control group, CPB-induced lung injury was confirmed by histopathologic examination and a significantly increased wet-to-dry lung weight ratio and pulmonary permeability index value was observed (P < .05 vs sham group). Cardiopulmonary bypass was associated with a marked rise in the level of malondialdehyde and myeloperoxidase and a fall in superoxide dismutase 2 and 24 hours after surgery (P < .05 vs sham group). Administration of curcumin ameliorated lung damage and reversed the oxidative stress markers in a partially dose-dependent manner (P < .05 vs vehicle group). Furthermore, HO-1 gene transcription and protein expression were elevated to a greater extent in the lungs after curcumin pretreatment compared with the vehicle pretreatment. CONCLUSIONS: Curcumin has the potential to provide protection from CPB-induced lung damage reflected in the expression of oxidative stress markers. The antioxidant effect of curcumin may be partly related to upregulation of HO-1.

The prominent expression of plasma matrix metalloproteinase-8 in acute thoracic aortic dissection.

BACKGROUND: The relationship between elastolytic matrix metalloproteinases (MMPs) (such as MMP-2, MMP-9) and thoracic aortic dissection (TAD) has been described, but little is known regarding the role of collagenolytic MMPs in thoracic aortic dissection. The aim of this study was to determine the role of MMP-8 in acute thoracic aortic dissection. MATERIALS AND METHODS: Forty-five patients affected by TAD and 40 with acute myocardial infarction (AMI) were recruited into this study. Blood samples within 72 h of the onset of symptoms were available for all the 85 patients. Healthy individuals were selected from the out-patients who complained of chest pain but in whom no cardiovascular diseases were found. Plasma levels of MMP-1, -8, -13 were measured by enzyme-linked immunosorbent assay (ELISA) technique in all subjects. Aortic tissue samples obtained during surgery were evaluated by Western blot for MMP-8 and tissue inhibitor of metalloproteinase-1 (TIMP-1) expression. RESULTS: Plasma MMP-8 levels in patients affected by TAD and AMI were both higher than that in healthy subjects (284.35 ± 96.32 ng/mL and 88.57 ± 26.71 ng/mL versus 75.39 ± 23.36 ng/mL). The difference of the MMP-8 level between TAD patients and healthy subjects was significant (P = 0.000). No significant differences were found in MMP-1 and MMP-13 plasma levels among the three groups. CONCLUSIONS: The acute phase of TAD is characterized by a prominent increase of MMP-8 plasma level, which may play a key role in the occurrence of TAD. MMP-8 could be involved in the acute inflammatory reaction and may be a useful marker for the diagnosis of acute TAD.

Cardiopulmonary bypass induced microcirculatory injury of the small bowel in rats.

AIM: To investigate microvascular injury quantitatively in the small bowel with respect to cardiopulmonary bypass (CPB) and related mechanisms. METHODS: In 10 male SD rats, normothermic CPB was established and continued with a flow rate of 100-150 mL/kg per minute for 60 min, while another 10 sham-operated animals served as controls. An approximate 10-cm loop of the terminal ileum was exteriorized for observation by means of intravital fluorescence microscopy. The small bowel microcirculatory network including arterioles, capillaries, and collecting venules was observed prior to CPB, CPB 30 min, CPB 60 min, post-CPB 60 min and post-CPB 120 min. The intestinal capillary perfusion, microvascular permeability and leukocyte adherence were also measured. RESULTS: The systemic hemodynamics remained stable throughout the experiment in both groups. In CPB animals, significant arteriolar vasoconstriction, blood velocity reduction and functional capillary density diminution were found. As concomitances, exaggerated albumin extravasation and increased leukocyte accumulation were also noted. These changes were more pronounced and there were no signs of restitution at the end of the observation period. CONCLUSION: CPB induces significant microcirculatory injury of the small bowel in rats. The major underlying mechanisms are blood flow redistribution and generalized inflammatory response associated with CPB.

Recombinant human erythropoietin pretreatment attenuates myocardial infarct size: a possible mechanism involves heat shock Protein 70 and attenuation of nuclear factor-kappaB.

Erythropoietin (EPO), known for its role in stimulating erythropoiesis, has recently been shown to have a cardio-protective effect in animal models of myocardial ischemia-reperfusion (I-R) injury. The mechanism of the cardio-protective effect of EPO is unclear. Part of the mechanism for EPO-induced cardio-protection may involve inhibition of myocardial apoptosis and preservation of ATP levels in the ischemic myocardium. We studied the expression of heat shock protein 70 (Hsp70) and its possible links to the cardio-protective effect of EPO. A rat model of myocardial I-R injury was established by ligating the left descending coronary artery for 30 min and then reperfusing for 2 hr. Recombinant human EPO (rhEPO) was injected ip 24 hr before the ligation. The myocardial infarct size and the area at risk of ischemia were measured by staining with triphenyltetrazolium chloride (TTC) and Evans blue dye. Expression of Hsp70 in the left ventricle was analyzed by ELISA and that of nuclear factor-kappaB (NF-kappaB) was analyzed by electrophoretic mobility shift assay (EMSA). The results showed that a single ip injection of 3,000 units/kg of rhEPO at 24 hr pre-ligation enhanced the expression of Hsp70 and diminished the expression of NF-kappaB in rat myocardium, and that the myocardial infarct induced by I-R injury was remarkably reduced in size, compared to control rats that received an ip saline injection at 24 hr pre-ligation.

A rat model of cardiopulmonary bypass with excellent survival.

BACKGROUND: Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of cardiopulmonary bypass (CPB) have been hampered due to the absence of a satisfactory long-term recovery animal model. The objective of this study was to establish a survival experimental model of CPB in rats to meet the requirement of these studies. MATERIALS AND METHODS: Male SD rats (450-550 g) were randomly divided into CPB (n = 10) group and Sham group (n = 10). All rats were anaesthetized and mechanically ventilated. The femoral artery and vein were cannulated for continuous blood pressure recordings and fluid replacement, respectively. The CPB circuit comprised a venous reservoir, a membrane oxygenator, and a roller pump. Blood was drained from the right atrium via a jugular vein catheter and returned to the right carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. CPB was conducted for 60 min at a flow rate of 100-150 ml/kg/min in the CPB group. Haemodynamic investigations, blood gas analysis, and survival studies were performed subsequently. RESULTS: Our data show that the rat model principally simulated the clinical setting of CPB in terms of its construction, configuration, performance, material surface area, and priming volume to blood volume ratio. All CPB rats survived and the 2-week follow-up period remained uneventful. CONCLUSIONS: The rat model of CPB was easy to establish and was associated with excellent survival. This model should facilitate the investigation of the pathophysiological processes concerning CPB-related multiple organ dysfunction and possible protective interventions.