Optimized total thoracoscopic and laparoscopic esophagectomy for esophageal cancer.

BACKGROUND: Total thoracoscopic and laparoscopic esophagectomy (TLE) has attracted attention with the advantage of better operative field and minimal wound for the esophageal cancer. However, various severe complications are also reported during the TLE such as cervical anastomotic leakage, chylothorax, and tracheal injury. The aim of this study was to introduce a new optimized TLE procedure for the esophageal cancer and assess its safety and clinical effects. METHODS: We retrospectively collected the clinical data of 30 patients with esophageal cancer who underwent optimized TLE procedures between January 2014 and December 2014. The optimized TLE procedures mainly include as follows: (1) 50 ml of sesame oil-milk mixture (1:1) is injected via gastric tube after endotracheal intubation; (2) patients are intubated with a single lumen endotracheal tube; (3) patients were positioned at 150° in the left prone position rather than lateral decubitus position; and (4) duodenal feeding tube was not placed intraoperatively and however triple lumen nasojejunal feeding tube was placed on the second postoperative day under imaging guidance. Operation time, amount of blood loss, number of dissected nodes, length of hospital stays, and complications were recorded. RESULTS: The mean operation time of the optimized TLE group was 202.13 ± 13.74 min. The mean visible blood loss of the optimized TLE group was 300.00 ± 120.12 ml. The postoperative hospital stays in the optimized TLE group were 16.27 ± 4.51 days. The number of dissected nodes in the optimized TLE group was 13.57 ± 2.76. The postoperative complications for the optimized TLE procedure were seen in one case (3.3%). CONCLUSIONS: The method of optimized TLE is an effective, reliable, and safe procedure for the treatment of esophageal cancer, which provide favorable outcomes in terms of operation time, blood loss, length of hospital stays, the number the dissected nodes, and reduced incidence of postoperative complications compared to previous literatures. Further studies with a large number of samples are warranted.

3,11-Dibromo-14-(4-chloro-phen-yl)-14H-dibenzo[a,j]xanthene dimethyl-formamide monosolvate.

In the title compound, C(27)H(15)Br(2)ClO·C(3)H(7)NO, the xanthene moiety has a flattened boat conformation with a folding angle between the naphthalene units of 9.46 (3)°. The mean planes of the xanthene system and its 4-chloro-phenyl substituent are nearly perpendicular [dihedral angle = 89.43 (5)°]. The dimethyl-formamide solvent mol-ecule is disordered over two sets of sites with an occupancy ratio of 0.520 (11):0.480 (11).

miR-181b inhibits chemoresistance in cisplatin-resistant H446 small cell lung cancer cells by targeting Bcl-2.

INTRODUCTION: MicroRNAs (miRNAs) are a group of small non-coding RNAs that affect multiple aspects of tumor biology including chemo resistance. miR-181b has been reported to modulate multidrug resistance in non-small cell lung cancer cells. This study was undertaken to determine the role of miR-181b in chemo resistance of small cell lung cancer cells. MATERIAL AND METHODS: This study was undertaken to determine the role of miR-181b in chemoresistance of small cell lung cancer cells with use of qRt-PCR, WB, bioinformatics analysis, and double luciferase reporter system. RESULTS: Our data showed that miR-181b was significantly downregulated in cisplatin-resistant H446 small cell lung cancer cells, compared to parental cells, compared to parental cells. Ectopic expression of miR-181b inhibited cell proliferation and invasion in cisplatin-resistant H446 cells (p = 0.023). Moreover, overexpression of miR-181b increased the susceptibility of cisplatin-resistant H446 cells to cisplatin. Mechanistic investigations demonstrated that miR-181b inhibited B-cell lymphoma-2 (Bcl-2) expression by binding to the 3'-untranslated region. Overexpression of Bcl-2 reversed miR-181b-mediated chemo sensitization, which is accompanied by a reduced apoptotic response. CONCLUSIONS: Taken together, this work demonstrated that miR-181b might have the ability to overcome chemo resistance of small cell lung cancer cells, and restoration of this miRNA may represent a potential therapeutic strategy for improving chemo sensitivity in small cell lung cancer.

Cardiac tamponade caused by tuberculosis pericarditis in renal transplant recipients.

A 50-year-old male, renal transplant recipient, was admitted with fever and chest discomfort. At admission, chest radiologic finding was negative and echocardiography showed minimal pericardial effusion. After 2 days of admission, chest pain worsened and blood pressure fell to 60/40 mmHg. Emergency echocardiography showed a large amount of pericardial effusion compressing the entire heart. Pericardiocentesis was performed immediately. Mycobacterium tuberculosis was isolated from pericardial fluid. Tuberculosis pericarditis should be considered as the cause of cardiac tamponade in renal transplant recipients, even with the absence of pericardial effusion in the initial study or suggestive history.