Interobserver variability in target volume delineation in definitive radiotherapy for thoracic esophageal cancer: a multi-center study from China.

PURPOSE: To investigate the interobserver variability (IOV) in target volume delineation of definitive radiotherapy for thoracic esophageal cancer (TEC) among cancer centers in China, and ultimately improve contouring consistency as much as possible to lay the foundation for multi-center prospective studies. METHODS: Sixteen cancer centers throughout China participated in this study. In Phase 1, three suitable cases with upper, middle, and lower TEC were chosen, and participants were asked to contour a group of gross tumor volume (GTV-T), nodal gross tumor volume (GTV-N) and clinical target volume (CTV) for each case based on their routine experience. In Phase 2, the same clinicians were instructed to follow a contouring protocol to re-contour another group of target volume. The variation of the target volume was analyzed and quantified using dice similarity coefficient (DSC). RESULTS: Sixteen clinicians provided routine volumes, whereas ten provided both routine and protocol volumes for each case. The IOV of routine GTV-N was the most striking in all cases, with the smallest DSC of 0.37 (95% CI 0.32-0.42), followed by CTV, whereas GTV-T showed high consistency. After following the protocol, the smallest DSC of GTV-N was improved to 0.64 (95% CI 0.45-0.83, P = 0.005) but the DSC of GTV-T and CTV remained constant in most cases. CONCLUSION: Variability in target volume delineation was observed, but it could be significantly reduced and controlled using mandatory interventions.

Synthesis of Ag@chitosan/copolymer with dual-active centers for high antibacterial activity.

The prevention and treatment of microorganism contamination on substrate surfaces have recently generated significant concern of scientists. In this paper, a novel diblock copolymer containing antibacterial quaternary ammonium groups as pendant groups, poly(3-(methacryloylamino) propyltrimethyl ammonium chloride)-b-poly(styrene) (PMS), was synthesized by interfacial polymerization. Also, PMS anisotropic particles (APs) could be successfully obtained based on different assembly behaviors by adjusting the ratios of monomers and the toluene/styrene (Tol/St). Moreover, silver loaded chitosan (Ag@CS) and PMS APs were combined to prepare natural/synthetic polymer antibacterial materials with dual-active centers (Ag@CS/PMS-4 APs), aiming to expand the application of carbohydrate polymers and improve the antibacterial activity of composite materials. Remarkably, the resulting series of PMS particles, especially worm-like PMS-4 APs, and Ag@CS/PMS-4 APs composite film ((Ag@CS/PMS-4 APs)-F) exhibited excellent antibacterial properties, which can be employed as interface materials to prevent the transmission of infectious diseases caused by microorganism contamination.

Inhibiting microRNA-301b suppresses cell growth and targets RNF38 in cervical carcinoma.

It has been reported microRNA-301b (miR-301b) was involved in the tumorigenesis of some cancers, but it has not been investigated in cervical carcinoma yet. In this study, miR-301b was found significantly upregulated in cervical carcinoma, and patients with high miR-301b expression had a shorter overall survival. When miR-301b was knocked down in cervical carcinoma cells, the cell growth could be significantly abolished. Our further studies showed miR-301b targeted RNF38, and inhibited its expression in cervical carcinoma cells. Moreover, RNF38 was found downregulated in cervical carcinoma, and miR-301b expression in cervical tissues was found negatively correlated with RNF38 expression. In addition, overexpression of RNF38 significantly inhibited cervical carcinoma cell growth, but overexpression of miR-301b suppressed RNF38-induced cell growth inhibition in cervical carcinoma. Collectively, this study suggested miR-301b could be a novel target for cervical carcinoma treatment.

MiR-155-5p accelerates the metastasis of cervical cancer cell via targeting TP53INP1.

Background: The dysregulation of microRNAs has been implicated in the progression of different malignancies. Herein, we sought to identify the precise roles of miR-155-5p in the progression of cervical cancer. Materials and methods: The expressions of miR-155-5p in cervical carcinoma cells and clinical tissues were assessed using qRT-PCR analysis. The functions of miR-155-5p on the growth of cervical cancer cell were investigated using MTT and colony formation. The Transwell and wound closure assays were selected to explore the influence of miR-155-5p on the invasion and migration of cervical cancer cell. The effect of miR-155-5p on cervical carcinoma cell growth and metastasis in vivo was investigated using xenograft model and experimental lung metastasis model. Bioinformatics analysis and luciferase reporter assay were applied to identify that tumor protein p53-inducible nuclear protein 1 (TP53INP1) was the target of miR-155-5p. Results: MiR-155-5p was significantly upregulated in cervical cancer tissue than that in control normal tissue. Downexpression of miR-155-5p decreased the growth, migration as well as invasiveness abilities of cervical cancer cell in vitro whereas overregulation of miR-155-5p caused the opposite outcomes. In addition, the in vivo mice xenograft model suggested that downexpression of miR-155-5p restrained the progression of cervical cancer cell whereas overexpression of miR-155-5p caused opposite outcomes. Furthermore, we revealed that TP53INP1 was the target of miR-155-5p and the level of TP53INP1 was inversely associated with miR-155-5p level in cervical carcinoma. Furthermore, TP53INP1 knockdown mimicked the influence of miR-155-5p on cervical cancer proliferation, migration and invasion phenotypes. Finally, overexpression of TP53INP1 impaired the promote effect of miR-155-5p on cervical cancer cell and downregulation of TP53INP1 counteracted the suppressive impact of miR-155-5p on the aggressiveness of cervical cancer cell. Conclusion: Our study indicated that miR-155-5p regulated the development of cervical cancer cell by regulating the expression of TP53INP1.

Diagnostic Value of Urinary Microalbumin Level in Postpartum Acute Kidney Injury.

BACKGROUND: We aimed to explore the diagnostic value of urinary microalbumin (mALB) level in postpartum acute kidney injury. METHODS: A total of 127 maternity patients were selected from December 2013 to January in 2016 in Binzhou Central Hospital, Binzhou, Shandong, China and divided into two groups: the kidney injury and normal kidney group. The dynamic changes and diagnostic value of urine microprotein in postpartum acute kidney injury were analyzed. RESULTS: The postpartum mean arterial pressure of maternity patients in the kidney injury group was 104.3 ± 11.6 mmHg, which was significantly higher than that of the normal kidney group (P<0.05). The mean age of the kidney injury group was 32.3 ± 11.6 years, which was significantly higher than that of the normal kidney group (P=0.006). In the kidney injury group, the postpartum glomerular filtration rate (GFR) was 78.4 ± 11.5 mL/min, which was significantly lower than the normal group (P=0.001), and urinary microalbumin was 2.87 ± 1.24 mg/mmol·Cr. The difference was statistically significant (P=0.002). mALB/GFR, Cr, urinary mALB, and GFR were the independent risk factors of postpartum acute kidney injury. The area under the ROC curve for mALB/GFR was 0.759, whereas the area under the ROC curve for Cr was 0.681, which was smaller (P = 0.042). The area under the ROC curve of mALB was 0.785 (P=0.027), which was close to the area under the ROC curve of mALB/GFR. CONCLUSION: Urinary mALB test is noninvasive and has high diagnostic value for postpartum kidney injury.

Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94.

MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR­150 in hypoxia­injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR­150 and the underlying molecular mechanisms of miR­150 in hypoxia­induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR­150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR­150 significantly decreased hypoxia­induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR­150. Additionally, GRP94 was demonstrated to be involved in hypoxia­induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR­150 is involved in hypoxia­mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia­impaired HCMs with miR­150 mimic or miR­150 inhibitor transfection. In conclusion, miR­150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury.

Association of an IL-4 gene haplotype with Graves disease in children: experimental study and meta-analysis.

Investigations of an association between Graves disease (GD) and the IL-4 gene have yielded conflicting results. We performed a case-control study of IL-4 gene polymorphisms possibly associated with GD, as well as a meta-analysis of other such studies. We genotyped IL-4 single nucleotide polymorphisms (SNPs) rs2243250 and rs2243289 in 220 unrelated children with GD and 904 healthy controls. No significant differences between patients and controls were observed in the genotype, allele, or carrier frequencies of the 2 SNPs. The levels of autoantibodies did not differ significantly between the genotypes of each SNP. Linkage disequilibrium between the 2 SNPs was strong in the controls (D', 0.916; r(2), 0.824). Haplotype TA conferred a significant risk of GD (odds ratio = 2.47, 95% confidence interval 1.24-4.95, corrected p value = 0.033). The T allele frequency of rs2243250 was 80.0% in Asians, significantly higher than the 12.6% in Caucasians (p = 1.4 × 10(-269)). Meta-analysis of data from 8 published reports and our own study did not reveal any significant association between these SNPs and GD. Our study showed an association between the IL-4 gene and GD in children, but only using a haplotype-based method, suggesting that this might be a better approach than evaluating individual SNPs.

Improved diabetic control during oral sulfonylurea treatment in two children with permanent neonatal diabetes mellitus.

Permanent neonatal diabetes mellitus (PND), defined as diabetes diagnosed in the first 6 months of age and requiring life-long insulin therapy, is a rare disorder of unknown etiology. Activating mutations of the KCNJ11 gene, which encodes the Kir6.2 subunit of the ATP-dependent potassium channel in beta-cells, have been found to cause 30-58% of cases of PND. Sulfonylurea treatment in theses patients reduces or eliminates the need for exogenous insulin. We report two Taiwanese boys who were diagnosed with PND at 1 and 4.5 months of age. They had been treated with exogenous insulin for 6 and 15 years, respectively. In September 2006, they were both found to have a KCNJ11 mutation (valine-to-methionine at codon 59; V59M). Glibenclamide successfully increased the basal C-peptide level, lowered HbA(1c), and reduced blood sugar excursions. In one patient, the insulin dose was reduced to 0.2 U/kg/day, and the other was able to discontinue insulin altogether. These two cases from Taiwan add to the experience with similar mutations reported in Caucasians.

[Effects of amiodarone versus sotalol in treatment of atrial fibrillation: a random controlled clinical study].

OBJECTIVE: To evaluate the effects and adverse reactions of amiodarone and sotalol in treatment of atrial fibrillation. METHODS: One hundred and two patients with atrial fibrillation, 56 males and 46 females, aged 56 +/- 11, were randomized into 2 equal groups: amiodarone group, taking amiodarone 600 mg/d for 7 days, 400 mg/d for 7 days, 200 mg/d for 7 days, and then 200 mg/d as maintenance dosage if conversion to sinus rhythm occurred; and sotalol group, taking sotalol 40-80 mg/d for one week, 160 mg/d for 2 weeks and then 40-80 mg/d as maintenance dosage if conversion to sinus rhythm occurred. If the cardiac rhythm failed to be converted to sinus rhythm after three week the medication was stopped. All the patients were followed up for 12-24 months and therapeutic effects were evaluated by echocardiography, electrocardiogram and Holter monitor. RESULTS: (1) Conversion to sinus rhythm occurred in 40 patients in the amiodarone group with an effective rate of 78.4%, and in 36 patients in the sotalol group with an effective rate of 70.6%. (2) Conversion to sinus rhythm occurred in the first week in 34 patients of the amiodarone group and in 10 patients of the sotalol group. (3) 67.5% of the patients with conversion to sinus rhythm in the amiodarone group and 41.7% of the patients with conversion to sinus rhythm in the sotalol group maintained sinus rhythm in the following 12 months; and 44.4% patients with conversion to sinus rhythm in the amiodarone group and 26.7% of the patients with conversion to sinus rhythm in the following 24 months. (4) 10 patients in the sotalol group taking a maintenance dosage of 80 mg/d showed atrial ventricular block and severe bradycardia during the follow-up of 6-2 months, then the medication was stopped, but there was no severe arrhythmia in amiodarone group. (5) It was difficult to maintain sinus rhythm when atrial fibrillation lasting longer than 12 months was a predictive factor of failure to maintain sinus rhythm. CONCLUSION: There is no significant difference between amiodarone and sotalol in converting atrial fibrillation to sinus rhythm. However, amiodarone is more effective in maintenance of sinus rhythm than sotalol. The adverse reaction of amiodarone on heart is less severe than that of sotalol.