Correlation Analysis of the Change Law of Index Gas and Active Functional Groups in the Process of High-Temperature Spontaneous Combustion of Minerals in the Fushun West Mine.

The spontaneous combustion of underground minerals causes huge property losses and ecological damage. Coal and oil shale are co-associated minerals in the Fushun West Mine, and both have the ability to undergo oxidative spontaneous combustion. To study the effect of microstructure changes on the macroscopic gas product concentration during the mineral oxidation spontaneous combustion process in the Fushun West Mine, this study used a high-temperature temperature-programmed test to obtain the change trend of gas product concentration in different oxidation stages of minerals. Using Fourier transform infrared spectroscopy technology, the changes in active functional groups of surface molecules during the process of mineral oxidation and spontaneous combustion were identified. Finally, using the gray correlation degree, correlation analysis between the concentration of gas products and the concentration of active functional groups in different oxidation stages was carried out. The key reactive functional groups affecting mineral spontaneous combustion were identified. The essential reason for the change in the gas product was revealed.

Targeting cancer stemness mediated by BMI1 and MCL1 for non-small cell lung cancer treatment.

Lung cancer is the leading cause of cancer-associated death, with a global 5-year survival rate <20%. Early metastasis and recurrence remain major challenges for lung cancer treatment. The stemness property of cancer cells has been suggested to play a key role in cancer plasticity, metastasis and drug-resistance, and is a potential target for drug development. In this study, we found that in non-small cell lung cancer (NSCLC), BMI1 and MCL1 play crucial roles of cancer stemness including invasion, chemo-resistance and tumour initiation. JNK signalling serves as a link between oncogenic pathway or genotoxicity to cancer stemness. The activation of JNK, either by mutant EGFR or chemotherapy agent, stabilized BMI1 and MCL1 proteins through suppressing the expression of E3-ubiquitin ligase HUWE1. In lung cancer patient samples, high level of BMI1 is correlated with poor survival, and the expression of BMI1 is positively correlated with MCL1. A novel small-molecule, BI-44, was developed, which effectively suppressed BMI1/MCL1 expressions and inhibited tumour formation and progression in preclinical models. Targeting cancer stemness mediated by BMI1/MCL1 with BI-44 provides the basis for a new therapeutic approach in NSCLC treatment.

Pendulone induces apoptosis via the ROS-mediated ER-stress pathway in human non-small cell lung cancer cells.

PURPOSE: Pendulone, an isoflavone compound, is known to act against human cancer cells. However, its role in human non-small cell lung cancer (NSCLC) and the exact molecular mechanisms of action have never been reported. METHODS: We investigated the effects of pendulone on cell proliferation and apoptosis in human NSCLC H1299 cells. Cell viability was examined using the methyl-thiazol-diphenyl-tetrazolium (MTT) assay. Flow cytometry was employed to evaluate apoptotic indices such as the cell cycle, mitochondrial membrane potential, cytochrome c release, caspase activity, and death receptor expression. The expression of proteins related to the cell cycle and apoptosis were analyzed by Western blot analysis. RESULTS: Pendulone significantly decreased H1299 cell viability by inducing endoplasmic reticulum (ER) stress through the accumulation of reactive oxygen species (ROS). Pendulone induced the expression of ER stress-associated proteins, such as ATF4 and CHOP, which promoted the expression of death receptors. Activation of caspase 8 induced extrinsic pathway apoptosis. Pendulone also caused the loss of mitochondrial membrane potential, inhibited the anti-apoptotic proteins BCL-2 and activated the pro-apoptotic protein BAX, which promoted the release of cytochrome c to activate caspase 9. Antioxidant N-acetylcysteine (NAC), with its ROS-suppressive property, reversed pendulone-induced ER stress and cell apoptosis. CONCLUSION: Our findings provide evidence that pendulone induces apoptosis by inducing ER stress through ROS accumulation and mitochondrial dysfunction in NSCLC cell lines.

Autophagy drives plasticity and functional polarization of tumor-associated macrophages.

Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment (TME) and are key cells in regulating tumor development, metastasis, immune responses, inflammation, and chemoresistance. In response to TME stimulation, circulating monocytes are recruited and differentiated as TAMs. Most TAMs are defined as alternatively activated (M2) phenotype to create immunosuppressive TME and support tumor progression. In contrast, classically activated (M1) TAMs can produce pro-inflammatory cytokines and enhance immune responses against tumor development. Autophagy is a conserved catabolic process to control cellular homeostasis and biological function. Emerging evidence reveals crucial contribution of autophagy in modulating TAM plasticity and functional polarization in TME. In this review, we introduce the current understanding of autophagy-regulated TAM function in development of cancer. We focus on how autophagy modulates antigen presentation, LC3-associated phagocytosis, cytokine secretion, inflammasome regulation, recruitment, differentiation, and polarization of TAMs and suggest strategies for potential therapeutics by targeting autophagy in TAMs. We expect this review can provide a new notion of future cancer immunotherapy.

Circulating Exosomal miRNAs as Biomarkers in Epithelial Ovarian Cancer.

Failure to detect early-stage epithelial ovarian cancer (EOC) is a major contributing factor to its low survival rate. Increasing evidence suggests that different subtypes of EOC may behave as distinct diseases due to their different cells of origins, histology and treatment responses. Therefore, the identification of EOC subtype-specific biomarkers that can early detect the disease should be clinically beneficial. Exosomes are extracellular vesicles secreted by different types of cells and carry biological molecules, which play important roles in cell-cell communication and regulation of various biological processes. Multiple studies have proposed that exosomal miRNAs present in the circulation are good biomarkers for non-invasive early detection of cancer. In this review, the potential use of exosomal miRNAs as early detection biomarkers for EOCs and their accuracy are discussed. We also review the differential expression of circulating exosomal miRNAs and cell-free miRNAs between different biofluid sources, i.e., plasma and serum, and touch on the issue of endogenous reference miRNA selection. Additionally, the current clinical trials using miRNAs for detecting EOCs are summarized. In conclusion, circulating exosomal miRNAs as the non-invasive biomarkers have a high potential for early detection of EOC and its subtypes, and are likely to be clinically important in the future.

9-O-Terpenyl-Substituted Berberrubine Derivatives Suppress Tumor Migration and Increase Anti-Human Non-Small-Cell Lung Cancer Activity.

Lung cancer is one of the most common cancers and the leading cause of death in humans worldwide. Non-small-cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer cases and is often diagnosed at a late stage. Among patients with NSCLC, 50% die within 1 year after diagnosis. Even with clinical intervention, the 5-year survival rate is only approximately 20%. Therefore, the development of an advanced therapeutic strategy or novel agent is urgently required for treating NSCLC. Berberine exerts therapeutic activity toward NSCLC; therefore, its activity as an antitumor agent needs to be explored further. In this study, three terpenylated-bromide derivatives of berberrubine were synthesized and their anti-NSCLC activities were evaluated. Each derivative had higher anti-NSCLCs activity than berberrubine and berberine. Among them, 9-O-gernylberberrubine bromide (B4) and 9-O-farnesylberberrubine bromide (B5) showed greater growth inhibition, cell-cycle regulation, in vitro tumorigenesis suppression, and tumor migration reduction. In addition, some degree of apoptosis and autophagic flux blocking was noted in the cells under B4 and B5 treatments. Our study demonstrates that the berberrubine derivatives, B4 and B5, exhibit impressive anti-NSCLC activities and have potential for use as chemotherapeutic agents against NSCLC.

Prognostic Factor of Completely Resected and Pathologic T3 N0 M0 Thymic Epithelial Tumor.

BACKGROUND: A multiinstitutional study was conducted to analyze prognosticators of completely resected and pathologic T3 N0 M0 (pT3 N0 M0) stage thymic epithelial tumors. METHODS: A total of 607 patients with surgically treated thymic epithelial tumors between June 1988 and December 2017 were enrolled. A Cox proportional hazards model and an inverse probability of treatment weighting-adjusted analysis using the propensity score were performed. RESULTS: A total of 394 patients with thymoma and 130 patients with thymic carcinoma underwent complete tumor resections. Forty-one thymomas and 49 thymic carcinomas were confirmed as pT3 N0 M0 stage tumors. Postoperative adjuvant radiotherapy was associated with improved disease-free and overall survival in patients with thymoma (hazard ratio [HR], 0.40; 95% confidence interval [CI], 0.23 to 0.69; and HR, 0.24; 95% CI, 0.11 to 0.52, respectively) and in patients with thymic carcinoma (HR, 0.15; 95% CI, 0.07 to 0.33; and HR, 0.12; 95% CI, 0.05 to 0.31, respectively). Although lung invasion was associated with poor disease-free survival (HR, 3.28; 95% CI, 1.90 to 5.89) and overall survival (HR, 2.60; 95% CI, 1.21 to 6.07), male sex (HR, 1.88; 95% CI, 1.10 to 3.18), older age (HR, 2.77; 95% CI, 1.29 to 5.70), and advanced histologic features (HR, 3.84; 95% CI, 1.42 to 14.51) were associated with poor overall survival in patients with pT3 N0 M0 thymoma. Adjuvant chemotherapy was associated with improved disease-free survival (HR, 0.11; 95% CI, 0.03 to 0.41) and overall survival (HR, 0.11; 95% CI, 0.06 to 0.20) in patients with pT3 N0 M0 thymic carcinoma with superior vena cava or innominate vein invasion. CONCLUSIONS: Postoperative radiotherapy was associated with improved survival in patients with pT3 N0 M0 thymic epithelial tumors. Lung invasion was associated with poor survival in patients with pT3 N0 M0 thymoma. Adjuvant chemotherapy was associated with improved survival in patients with pT3 N0 M0 thymic carcinoma with superior vena cava or innominate vein invasion.

Berberine Derivatives Suppress Cellular Proliferation and Tumorigenesis In Vitro in Human Non-Small-Cell Lung Cancer Cells.

Lung cancer is the leading cause of death in the world, and the most common type of lung cancer is non-small-cell lung cancer (NSCLC), accounting for 85% of lung cancer. Patients with NSCLC, when detected, are mostly in a metastatic stage, and over half of patients diagnosed with NSCLC die within one year after diagnosis; the 5-year survival rate is 24%. However, in patients with metastatic NSCLC, the 5-year survival rate is 6%. Therefore, development of a new therapeutic agent or strategy is urgent for NSCLCs. Berberine has been illustrated to be a therapeutic agent of NSCLC. In the present study, we synthesized six derivatives of berberine, and the anti-NSCLC activity of these agents was examined. Some of them exert increasing proliferation inhibition comparing with berberine. Further studies demonstrated that two of the most effective agents, 9-O-decylberberrubine bromide (B6) and 9-O-dodecylberberrubine bromide (B7), performed cell cycle regulation, in-vitro tumorigenesis inhibition and autophagic flux blocking, but not induction of cellular apoptosis in NSCLC cells. Moreover, B6 and B7 were determined to be green fluorescent and could be penetrated and localized in cellular mitochondria. Herein, B6 and B7, the berberine derivatives we synthesized, revealed better anti-NSCLC activity with berberine and may be used as therapeutic candidates for the treatment of NSCLCs.

Discovery of T-1101 tosylate as a first-in-class clinical candidate for Hec1/Nek2 inhibition in cancer therapy.

Highly expressed in cancer 1 (Hec1) plays an essential role in mitosis and is correlated with cancer formation, progression, and survival. Phosphorylation of Hec1 by Nek2 kinase is essential for its mitotic function, thus any disruption of Hec1/Nek2 protein-protein interaction has potential for cancer therapy. We have developed T-1101 tosylate (9j tosylate, 9j formerly known as TAI-95), optimized from 4-aryl-N-pyridinylcarbonyl-2-aminothiazole of scaffold 9 by introducing various C-4' substituents to enhance potency and water solubility, as a first-in-class oral clinical candidate for Hec1 inhibition with potential for cancer therapy. T-1101 has good oral absorption, along with potent in vitro antiproliferative activity (IC50: 14.8-21.5 nM). It can achieve high concentrations in Huh-7 and MDA-MB-231 tumor tissues, and showed promise in antitumor activity in mice bearing human tumor xenografts of liver cancer (Huh-7), as well as of breast cancer (BT474, MDA-MB-231, and MCF7) with oral administration. Oral co-administration of T-1101 halved the dose of sorafenib (25 mg/kg to 12.5 mg/kg) required to exhibit comparable in vivo activity towards Huh-7 xenografts. Cellular events resulting from Hec1/Nek2 inhibition with T-1101 treatment include Nek2 degradation, chromosomal misalignment, and apoptotic cell death. A combination of T-1101 with either of doxorubicin, paclitaxel, and topotecan in select cancer cells also resulted in synergistic effects. Inactivity of T-1101 on non-cancerous cells, a panel of kinases, and hERG demonstrates cancer specificity, target specificity, and cardiac safety, respectively. Subsequent salt screening showed that T-1101 tosylate has good oral AUC (62.5 µM·h), bioavailability (F = 77.4%), and thermal stability. T-1101 tosylate is currently in phase I clinical trials as an orally administered drug for cancer therapy.

MS2CNN: predicting MS/MS spectrum based on protein sequence using deep convolutional neural networks.

BACKGROUND: Tandem mass spectrometry allows biologists to identify and quantify protein samples in the form of digested peptide sequences. When performing peptide identification, spectral library search is more sensitive than traditional database search but is limited to peptides that have been previously identified. An accurate tandem mass spectrum prediction tool is thus crucial in expanding the peptide space and increasing the coverage of spectral library search. RESULTS: We propose MS2CNN, a non-linear regression model based on deep convolutional neural networks, a deep learning algorithm. The features for our model are amino acid composition, predicted secondary structure, and physical-chemical features such as isoelectric point, aromaticity, helicity, hydrophobicity, and basicity. MS2CNN was trained with five-fold cross validation on a three-way data split on the large-scale human HCD MS2 dataset of Orbitrap LC-MS/MS downloaded from the National Institute of Standards and Technology. It was then evaluated on a publicly available independent test dataset of human HeLa cell lysate from LC-MS experiments. On average, our model shows better cosine similarity and Pearson correlation coefficient (0.690 and 0.632) than MS2PIP (0.647 and 0.601) and is comparable with pDeep (0.692 and 0.642). Notably, for the more complex MS2 spectra of 3+ peptides, MS2PIP is significantly better than both MS2PIP and pDeep. CONCLUSIONS: We showed that MS2CNN outperforms MS2PIP for 2+ and 3+ peptides and pDeep for 3+ peptides. This implies that MS2CNN, the proposed convolutional neural network model, generates highly accurate MS2 spectra for LC-MS/MS experiments using Orbitrap machines, which can be of great help in protein and peptide identifications. The results suggest that incorporating more data for deep learning model may improve performance.

The Alteration of CTNNBIP1 in Lung Cancer.

ß-catenin is a major component of the Wnt/ß-catenin signaling pathway, and is known to play a role in lung tumorigenesis. ß-catenin-interacting protein 1 (CTNNBIP1) is a known repressor of ß-catenin transactivation. However, little is known about the role of CTNNBIP1 in lung cancer. The aim of this study was to carry out a molecular analysis of CTNNBIP1 and its effect on ß-catenin signaling, using samples from lung cancer patients and various lung cancer cell lines. Our results indicate a significant inverse correlation between the CTNNBIP1 mRNA expression levels and the CTNNBIP1 promoter hypermethylation, which suggests that the promoter hypermethylation is responsible for the low levels of CTNNBIP1 present in many lung cancer patient samples. The ectopic expression of CTNNBIP1 is able to reduce the ß-catenin transactivation; this then brings about a decrease in the expression of ß-catenin-targeted genes, such as matrix metalloproteinase 7 (MMP7). Conversely, CTNNBIP1 knockdown is able to increase ß-catenin transactivation and the expression of MMP7. In agreement with these findings, a low level of CTNNBIP1 was found to be correlated with a high level of MMP7 when a publicly available microarray dataset for lung cancer was analyzed. Also, in agreement with the above, the ectopic expression of CTNNBIP1 inhibits the migration of lung cancer cells, whereas the CTNNBIP1 knockdown increases cancer cell migration. Our findings suggest that CTNNBIP1 is a suppressor of cancer migration, thus making it a potential prognostic predictor for lung cancer.

Recurrent tertiary hyperparathyroidism due to supernumerary parathyroid glands in a patient receiving long-term hemodialysis: a case report.

BACKGROUND: Renal hyperparathyroidism is a common complication of chronic kidney disease (CKD) or end-stage renal disease (ESRD) characterized by elevated parathyroid hormone levels secondary to derangements in the homeostasis of calcium, phosphate, and vitamin D. Rapid correction of severe and prolonged hyperparathyroidism by surgical parathyroidectomy in long-term hemodialysis patients occasionally causes hungry bone syndrome. These patients then exhibit severe and long-lasting secondary or tertiary hyperparathyroidism with high bone turnover. CASE PRESENTATION: We report a case of recurrent tertiary hyperparathyroidism after total parathyroidectomy due to supernumerary parathyroid gland in a patient with long-term hemodialysis. Supplementation with intravenous calcium, oral calcium, and vitamin D immediately after patient surgery helps to prevent and treat hungry bone syndrome. CONCLUSIONS: We should prompt a search for the supernumerary parathyroid glands in ESRD patients, who have recurrent or persistent hyperparathyroidism after total parathyroidectomy. ESRD patients are more likely to develop hungry bone syndrome after parathyroidectomy. Prevention and treatment of hungry bone syndrome may be required after ectopic parathyroidectomy in clinical practice.

Pharmacological inhibition of bacterial ß-glucuronidase prevents irinotecan-induced diarrhea without impairing its antitumor efficacy in vivo.

Irinotecan (CPT-11), a first-line chemotherapy for advanced colorectal cancer, causes serious diarrhea in patients receiving treatment. The underlying mechanism has been shown that the active metabolite of CPT-11, SN-38, is metabolized to the inactive metabolite SN-38 glucuronide (SN-38 G) during hepatic glucuronidation, and subsequently is exported into the intestine, where SN-38 G is hydrolyzed by bacterial ß-glucuronidase (ßG) to be SN-38, thus leading to intestinal toxicity. Thus, inhibition of the intestinal bacterial ßG activity is expected to prevent CPT-11-induced diarrhea. However, the effects of such inhibition on serum pharmacokinetics of SN-38, the key determinant of CPT-11 treatment, are uncertain. Here, we determined the effects of a potent E. coli ßG (eßG)-specific inhibitor pyrazolo[4,3-c]quinoline derivative (TCH-3562) for the potential use in preventing CPT-11-induced diarrhea. TCH-3562 exhibited efficacious inhibitory potency of endogenous ßG activity in two anaerobes, Eubacteriumsp. and Peptostreptococcus anaerobius. Oral administration of TCH-3562 also effectively reduced the bacterial ßG activity in mice intestine. Moreover, pharmacokinetic analysis of TCH-3562 revealed a relatively low amount of TCH-3562 was detected in the plasma whereas the majority of TCH-3562 was found in the feces. Importantly, co-treatment of CPT-11 and TCH-3562 did not decrease active SN-38 level in mice plasma. Finally, we established that TCH-3562 as an adjuvant treatment showed protective effects on CPT-11-induced diarrhea and had no negative effects on the therapeutic efficacy of CPT-11 in tumor-bearing mice. Therefore, inhibition of the intestinal bacterial ßG activity by the specific inhibitor, TCH-3562, is promising to prevent CPT-11-induced diarrhea while maintaining its anti-tumor efficacy that may have clinical potentials for the treatment with CPT-11.

From one incision to one port: The surgical technique and the evolution of segmentectomy in patients with pulmonary tuberculosis.

OBJECTIVES: We retrospectively reviewed the evolution of segmentectomy for pulmonary tuberculosis (TB) and the feasibility of multi- and single-incision video-assisted thoracoscopic segmentectomy. METHODS: Of 348 patients undergoing surgery for TB, the medical records of 121 patients undergoing segmentectomy between January 1996 and November 2015 were reviewed. Clinical information and computed tomography (CT) image characteristics were investigated and analyzed. RESULTS: Eighteen patients underwent direct or intended thoracotomy. Sixty-four underwent video-assisted thoracoscopic segmentectomy (VATS), including 53 multi-incision thoracoscopic segmentectomy (MITS), and 11 single-incision thoracoscopic segmentectomy (SITS). Thirty-nine were converted to thoracotomy. The intended thoracotomy group had more operative blood loss (p = 0.005) and hospital stay (p = 0.001) than the VATS group although the VATS group had higher grade of cavity (p = 0.007). The intended thoracotomy group did not differ from converted thoracotomy in operative time, blood loss, or hospital stay, and the grade of pleural thickening was higher in the converted thoracotomy group (p = 0.001). The converted thoracotomy group had more operative blood loss, hospital stay, and complication rate than the MITS group (p = 0.001, p<0.001, and p = 0.009, respectively). The MITS group had lower pleural thickening, peribronchial lymph node calcification, cavity, and tuberculoma grading than the converted thoracotomy group (p<0.001, p = 0.001, 0.001, and 0.017, respectively). The SITS group had lower grading in pleural thickening, peribronchial lymph node calcification, and aspergilloma grading than the converted thoracotomy group (p = 0.002, 0.010, and 0.031, respectively). Four patients in the intended thoracotomy group and seven in the converted thoracotomy group had complications compared with three patients in the MITS and two in the SITS group. Risk factors of conversion were pleural thickening and peribronchial lymph node calcification. CONCLUSION: Although segmentectomy is technically challenging in patients with pulmonary TB, it could be safely performed using MITS or SITS and should be attempted in selected patients. Its efficacy for medical treatment failure needs investigation.

MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1.

MicroRNAs (miRs) play critical roles in cancer development, proliferation, epithelial-mesenchymal transition (EMT), invasion, and migration through regulating the expression of oncogenes and tumour suppressor genes. Previous studies have indicated that miR-200c acts as a tumour suppressor in various cancers by downregulating high-mobility group box 1 (HMGB1) and thereby suppressing EMT and metastasis. In addition, miR-200c was reported to be downregulated and correlated with poor outcomes in non-small cell lung cancer (NSCLC). However, its functional role in HMGB1 regulation in NSCLC is still unclear. This study aimed to clarify whether miR-200c acts as a tumour suppressor in NSCLC by downregulating HMGB1, which is associated with EMT, invasion, cytoskeleton rearrangement, and migration in vitro and in vivo. In order to demonstrate HMGB1 downregulation by miR-200c, the NSCLC cell line A549 was transfected with miR-200c mimic or inhibitor. The mimic significantly reduced HMGB1 expression and suppressed EMT, invasion, and migration, while the inhibitor generated the opposite effects. Additionally, using xenograft mouse models, we confirmed that HMGB1 overexpression increased tumour EMT. In summary, our results demonstrated that miR-200c could suppress EMT, invasion, and migration of NSCLC cells by downregulating HMGB1.

Curcumin Inhibits LIN-28A through the Activation of miRNA-98 in the Lung Cancer Cell Line A549.

Metastasis is common in lung cancer and is associated with poor clinical outcomes and increased mortality. Curcumin is a natural anti-cancer agent that inhibits the metastasis of various cancers by modulating the expression of micro (mi) RNAs such as miR-98, which acts as a tumor suppressor. This study investigated the effect of curcumin on miR-98 expression and in vitro cell line growth and invasiveness in lung cancer. Curcumin treatment enhanced the expression of miR-98 and reduced that of the miR-98 target gene LIN28A as well as matrix metalloproteinase (MMP) 2 and MMP9 in vitro and in vivo. MiR-98 overexpression suppressed lung cancer cell migration and invasion by inhibiting LIN28A-induced MMP2 and MMP9 expression. Meanwhile, LIN28A level was downregulated by overexpression of miR-98 mimic. Induction of miR-98 by curcumin treatment suppressed MMP2 and MMP9 by targeting LIN28A. These findings provide insight into the mechanisms by which curcumin suppresses lung cancer cell line growth in vitro and in vivo and invasiveness in vitro.

From biportal to uniportal video-assisted thoracoscopic anatomical lung resection: A single-institute experience.

Our study sought to review our experience from biportal to uniportal video-assisted thoracoscopic surgery (VATS) major lung resection. Lessons we learned from the evolution regarding technical aspects were also discussed.We retrospectively reviewed patients who underwent VATS lobectomy or segmentectomies in Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan, during January 2012 and December 2014. Patient clinical profiles, surgical indications and procedures, postoperative course, and oncological parameters were analyzed and compared between the biportal and uniportal groups.A total of 121 patients were enrolled in this study with median follow-up of 19.5 ±â€Š11.6 months for all patients and 22.5 ±â€Š11.5 months for primary lung cancer patients. Operation time (146.1 ±â€Š31.9-158.7 ±â€Š40.5 minutes; P = 0.077), chest drainage time (3.8 ±â€Š3.3-4.4 ±â€Š2.4 days; P = 0.309), conversion to thoracotomy rate (2.2%-2.6%; P = 0.889), and complication rate (15.6%-19.7%; P = 0.564) were equal between the groups, whereas blood loss (96.7 ±â€Š193.2-263.6 ±â€Š367; P = 0.006) was lower in the uniportal group. For lung cancer cases, there were no statistical differences in the histology, cancer staging, mediastinal lymph node dissection stations, numbers of dissected N1, N2, and overall lymph nodes between uniportal and biportal groups.Our preliminary data showed that uniportal VATS anatomical lung resection is as feasible, equally safe, and of comparative oncological clearance efficacy to biportal VATS.

The Role of Video-Assisted Thoracoscopic Therapeutic Resection for Medically Failed Pulmonary Tuberculosis.

There are few reports regarding video-assisted thoracoscopic therapeutic resection for medically failed pulmonary tuberculosis (TB). We reviewed our surgical results of video-assisted thoracoscopic surgery (VATS) therapeutic resection for pulmonary TB with medical failure, and its correlation with image characteristics on chest computed tomography (CT) scan.Between January 2007 and December 2012, among the 203 patients who had surgery for TB, the medical records of 89 patients undergoing therapeutic resection for medically failed pulmonary TB were reviewed. Clinical information and the image characteristics of CT scan were investigated and analyzed.Forty-six of the 89 patients undergoing successful VATS therapeutic resection had significantly lower grading in pleural thickening (P < 0.001), peribronchial lymph node calcification (P < 0.001), tuberculoma (P = 0.015), cavity (P = 0.006), and aspergilloma (P = 0.038); they had less operative blood loss (171.0 ±â€Š218.7 vs 542.8 ±â€Š622.8 mL; P < 0.001) and shorter hospital stay (5.2 ±â€Š2.2 vs 15.6 ±â€Š15.6 days; P < 0.001). They also had a lower percentage of anatomic resection (73.9% vs 93.0%; P = 0.016), a higher percentage of sublobar resection (56.5% vs 32.6%; P = 0.023), and a lower disease relapse rate (4.3% vs 23.3%; P = 0.009). Eighteen of the 38 patients with multi-drug resistant pulmonary tuberculosis (MDRTB) who successfully underwent VATS had significantly lower grading in pleural thickening (P = 0.001), peribronchial lymph node calcification (P = 0.019), and cavity (P = 0.017). They were preoperatively medicated for a shorter period of time (221.6 ±â€Š90.8 vs 596.1 ±â€Š432.5 days; P = 0.001), and had more sublobar resection (44.4% vs 10%), less blood loss (165.3 ±â€Š148.3 vs 468.0 ±â€Š439.9 mL; P = 0.009), and shorter hospital stay (5.4 ±â€Š2.6 vs 11.8 ±â€Š6.9 days; P = 0.001).Without multiple cavities, peribronchial lymph node calcification, and extensive pleural thickening, VATS therapeutic resection could be safely performed in selected patients with medically failed pulmonary TB as an effective adjunct with satisfactory results.