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ObjectiveTo evaluate the value of early identification and endovascular treatment of iliac vein compression syndrome (IVCS), with or without deep vein thrombosis (DVT).Materials and MethodsThree groups of patients, IVCS without DVT (group 1, n = 39), IVCS with fresh thrombosis (group 2, n = 52) and IVCS with non-fresh thrombosis (group 3, n = 34) were detected by Doppler ultrasonography, magnetic resonance venography, computed tomography or venography. The fresh venous thrombosis were treated by aspiration and thrombectomy, whereas the iliac vein compression per se were treated with a self-expandable stent. In cases with fresh thrombus, the inferior vena cava filter was inserted before the thrombosis suction, mechanical thrombus ablation, percutaneous transluminal angioplasty, stenting or transcatheter thrombolysis.ResultsStenting was performed in 111 patients (38 of 39 group 1 patients and 73 of 86 group 2 or 3 patients). The stenting was tried in one of group 1 and in three of group 2 or 3 patients only to fail. The initial patency rates were 95% (group 1), 89% (group 2) and 65% (group 3), respectively and were significantly different (p = 0.001). Further, the six month patency rates were 93% (group 1), 83% (group 2) and 50% (group 3), respectively, and were similarly significantly different (p = 0.001). Both the initial and six month patency rates in the IVCS patients (without thrombosis or with fresh thrombosis), were significantly greater than the patency rates of IVCS patients with non-fresh thrombosis.ConclusionFrom the cases examined, the study suggests that endovascular treatment of IVCS, with or without thrombosis, is effective.

To evaluate the impact of thyroid nodule sizes on the diagnostic performance of thyroid imaging reporting and data system (TIRADS) and ultrasound patterns of 2015 American Thyroid Association (ATA) guidelines. Total 734 patients with 962 thyroid nodules were recruited in this retrospective study. All nodules were divided into three groups according to the maximal diameter (d < 10 mm, d = 10–20 mm and d > 20 mm). The ultrasound images were categorized based on TIRADS and ATA ultrasound patterns, respectively. A total of 931 (96.8%) and 906 (94.2%) patterns met the criteria for TIRADS and ATA ultrasound patterns. The AUC (0.849) and sensitivity (85.3%) of TIRADS were highest in d = 10–20 mm group. However, ATA had highest AUC (0.839) and specificity (89.8%) in d > 20 mm group. ATA ultrasound patterns had higher specificity (P = 0.04), while TI-RADS had higher sensitivity (P = 0.02). In nodules d > 20 mm, the specificity of ATA patterns was higher than TIRADS (P = 0.003). Our results indicated that nodule sizes may influence the diagnostic performance of TIRADS and ATA ultrasound patterns. The ATA patterns may yield higher specificity than TIRADS, especially in nodules larger than 20 mm.

Nuclear factor-κB is associated with the pathogenesis of numerous malignancies, and the functional polymorphism −94ins/del ATTG (rs28362491) in the human NFKB1 gene is associated with cancer risk. Previous studies on the association between the −94ins/del ATTG polymorphism and cancer risk reported conflicting results. To clarify this relationship, we performed a meta-analysis of 21 case-control studies involving 6127 cases and 9238 controls. We used pooled odds ratios (ORs) with their 95% confidence intervals (95% CIs) to assess the association. We found that the NFKB1 promoter −94ins/del ATTG polymorphism was significantly associated with cancer risk in four genetic models (ins/ins versus del/del, OR = 1.47, 95% CI = 1.11–1.93; dominant model, OR = 1.26, 95% CI = 1.03–1.53; recessive model, OR = 1.26, 95% CI = 1.05–1.51; ins allele versus del allele, OR = 1.19, 95% CI = 1.05–1.35). Stratified analyses revealed a significant association between the polymorphism and ovarian, oral, and prostate cancers. Similar results were determined in an Asian population and not in a Caucasian population. Thus, our results suggested that the polymorphism can contribute to cancer risk. Moreover, the polymorphism can exert race- and cancer-specific effects on cancer risk. Further large-scale and functional studies are necessary to elucidate this possible effect.

BackgroundA functional -94 insertion/deletion polymorphism (rs28362491) in the promoter of the NFKB1 gene was reported to influence NFKB1 expression and confer susceptibility to different types of cancer. This study aims to determine whether the polymorphism is associated with risk of bladder cancer.Materials and methodsTaqMan assay was used to determine genotype among 609 cases and 640 controls in a Chinese population. Logistic regression was used to assess the association between the polymorphism and bladder cancer risk, and quantitative real-time polymerase chain reaction was used to determine NFKB1 mRNA expression.ResultsCompared with the ins/ins/ins/del genotypes, the del/del genotype was associated with a significantly increased risk of bladder cancer [adjusted odd ratio (OR)  = 1.92, 95% confidence interval (CI)  = 1.42–2.59]. The increased risk was more prominent among subjects over 65 years old (OR  = 2.37, 95% CI  = 1.52–3.70), male subjects (OR  = 1.97, 95% CI = 1.40–2.79) and subjects with self-reported family history of cancer (OR  = 3.59, 95% CI  = 1.19–10.9). Furthermore, the polymorphism was associated with a higher risk of developing non-muscle invasive bladder cancer (OR  = 2.07, 95% CI  = 1.51–2.85), grade 1 bladder cancer (OR  = 2.40, 95% CI  = 1.68–3.43), single tumor bladder cancer (OR  = 2.04, 95% CI  = 1.48–2.82) and smaller tumor size bladder cancer (OR  = 2.10, 95% CI  = 1.51–2.92). The expression of NFKB1 mRNA in bladder cancer tissues with homozygous insertion genotype was higher than that with deletion allele.ConclusionsIn conclusion, the -94 ins/del ATTG polymorphism in NFKB1 promoter may contribute to the etiology of bladder cancer in the Chinese population.

Purpose To explore the role of indocyanine green (ICG) fluorescence navigation in laparoscopic hepatectomy and investigate if the timing of its administration influences the intraoperative observation. Methods The subjects of this retrospective study were 120 patients who underwent laparoscopic hepatectomy; divided into an ICG-FN group (n = 57) and a non-ICG-FN group (n = 63). We analyzed the baseline data and operative data. Results There were no remarkable differences in baseline data such as demographic characteristics, lesion-related characteristics, and liver function parameters between the groups. Operative time and intraoperative blood loss were significantly lower in the ICG-FN group. The rate of R0 resection of malignant tumors was comparable in the ICG-FN and non-ICG-FN groups, but the wide surgical margin rate was significantly higher in the ICG-FN group. The administration of ICG 0–3 or 4–7 days preoperatively did not affect the intraoperative fluorescence imaging. Operative time, intraoperative blood loss, and a wide surgical margin correlated with ICG fluorescence navigation. ICG fluorescence navigation helped to minimize intraoperative blood loss and achieve a wide surgical margin. Conclusion ICG fluorescence navigation is safe and efficient in laparoscopic hepatectomy. It helps to achieve a wide surgical margin, which could result in a better prognosis. The administration of ICG 0–3 days preoperatively is acceptable.

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BackgroundGlutathione S-transferases (GSTs) are a family of multifunctional enzymes that are involved in the metabolism of many xenobiotics, including a wide range of environmental carcinogens. While the null genotypes in GSTM1 and GSTT1 have been implicated in tumorigenesis, it remains inconsistent and inconclusive. Herein, we aimed to assess the possible associations of the GSTM1 and GSTT1 null genotype in cancer risks.MethodsA meta-analysis based on 506 case-control studies was performed. Odds ratios (OR) with corresponding 95% confidence intervals (CIs) were used to assess the association.ResultsThe null genotypes of GSTM1 and GSTT1 polymorphisms were associated with a significantly increased risk in cancer (for GSTM1: OR = 1.17; 95%CI = 1.14–1.21; for GSTT1: OR = 1.16; 95%CI = 1.11–1.21, respectively). When the analysis was performed based on their smoking history, the risk associated of GSTM1 null and GSTT1 null genotypes with cancer is further increased (for GSTM1: OR = 2.66; 95%CI = 2.19–3.24; for GSTT1: OR = 2.46; 95%CI = 1.83–3.32, respectively).ConclusionsThese findings indicate that GSTM1 and GSTT1 polymorphisms may play critical roles in the development of cancer, especially in smokers.