A variety of medical devices have evolved throughout the years. Commonly used devices have typical radiological appearances which are familiar to radiologists. However, some new devices, as well as devices that are not commonly used, may be missed or misinterpreted by radiologists. It is even more difficult to identify a certain medical device with limited clinical history. Therefore, accurate identification of medical devices is crucial to diagnose malposition and potential complications. In this article, we provide a pictorial review of medical devices of the abdomen and pelvis according to classifications that include gastrointestinal devices, hepatobiliary devices, genitourinary devices, and miscellaneous. We also comprehensively review the clinical and radiologic features of complications related to these medical devices.

We have been testing familial relationships based on short tandem repeats (STRs) in families who requested it either voluntarily or by order of the court. Here, we present a summary of our 5-year experience of autosomal STR-based paternity tests. A total of 1,431 individuals from 588 cases were tested, including 878 pairs of either of the parent, and a child. Among these 588 cases, genetic information about the other parent was available only for 135 cases. Five hundred eighteen pairs were concluded to be parent-child relations, for which the median paternity index (PI) was 72,826, and the median decimal logarithm was 4.860. Autosomal mutation was observed in nine pairs (1.74%), and the pairs harbored only one mismatched locus among the 15 standard loci (D8S1179, D21S11, D7S820, CSF1PO, D3S1358, TH01, D13S317, D16S539, D2S1338, D19S433, vWA, TPOX, D18S51, D5S818, and FGA). The number of mismatched loci did not increase even after additional loci were included in the study. The observed mutation rates were D13S317 (0.193%), D18S51 (0.193%), D19S433 (0.193%), FGA (0.193%), vWA (0.386%), Penta D (0.387%), and Penta E (0.193%). There were 14 pairs with two mismatched loci, which we excluded through additional tests on either autosomal or X chromosomal STRs, and mitochondrial sequencing. Although PI is useful for determining parent-child relation, it provides indirect information; it is an interpretation of the test results that is based on probability. Additional genotyping on sex chromosome and mitochondrial DNA, or participation of other family members might be beneficial for a reliable conclusion.
Child ; DNA, Mitochondrial ; Humans ; Microsatellite Repeats ; Mutation Rate ; Parent-Child Relations ; Parents ; Paternity* ; Sex Chromosomes

PURPOSE: Malignant pleural effusions (MPEs) are often observed in lung cancer, particularly adenocarcinoma. The aim of this study was to investigate epidermal growth factor receptor (EGFR) mutation status in lung adenocarcinoma-associated MPEs (LA-MPEs) and its correlation with efficacy of EGFR tyrosine kinase inhibitor (TKI) therapy. MATERIALS AND METHODS: Samples comprised 40 cell blocks of pathologically-confirmed LA-MPEs collected before the start of EGFR TKI therapy. EGFR mutation status was re-evaluated by peptide nucleic acid clamping and the clinical outcomes of EGFR TKI-treated patients were analyzed retrospectively. RESULTS: EGFR mutations were detected in 72.5% of LA-MPE cell blocks (29/40). The median progression-free survival for patients with EGFR mutations in LA-MPEs was better than that for patients with wild-type EGFR (7.33 months vs. 2.07 months; hazard ratio, 0.486; 95% confidence interval, 0.206 to 1.144; p=0.032). The objective response rate (ORR) of 26 patients with EGFR mutations in LA-MPEs among the 36 patients with measurable lesions was 80.8%, while the ORR of the 10 patients with wild-type EGFR in LA-MPEs was 10% (p < 0.001). Among the 26 patients with EGFR mutations in LA-MPEs, the ORR of target lesions and LA-MPEs were 88.5% and 61.5%, respectively (p=0.026). CONCLUSION: EGFR mutation status in cell blocks of LA-MPEs confirmed by pathologic diagnosis is highly predictive of EGFR TKI efficacy. For patients with EGFR mutations in LA-MPEs, the response to EGFR TKIs seems to be worse for pleural effusions than for solid tumors.
Adenocarcinoma ; Constriction ; Diagnosis ; Disease-Free Survival ; Humans ; Lung Neoplasms ; Lung* ; Pleural Effusion ; Pleural Effusion, Malignant* ; Protein-Tyrosine Kinases* ; Receptor, Epidermal Growth Factor ; Retrospective Studies ; Tyrosine*