Management of ingested magnets in children

ABSTRACT: We describe a comprehensive algorithm for the management of ingested rare-earth magnets in children. These newer and smaller neodymium magnets sold as adult toys are much stronger than the traditional magnets, and can attract each other with formidable forces. If >1 magnet is swallowed at the same time, or a magnet is co-ingested with another metallic object, the loops of intestine can be squeezed between them resulting in bowel damage including perforations. An algorithm that uses the number of magnets ingested, location of magnets, and the timing of ingestion before intervention helps to delineate the roles of the pediatric gastroenterologists and surgeons in the management of these cases.     

Differentiated thyroid carcinoma in a juvenile patient

Juvenile differentiated carcinoma thyroid is a rare entity. It differs from adult differentiated thyroid carcinoma in a variety of ways, including large tumor volume at presentation with early involvement of the capsule, more frequent nodal and distant metastases, greater expression of sodium-iodide symporter and early recurrence. The overall survival seems to be better than for adult patients; however, due to high and early recurrence rates, prompt and adequate treatment is advocated. The mainstay of treatment includes total thyroidectomy, central lymphadenectomy with modified radical lateral lymphadenectomy, followed by ablation with radioactive iodine (RAI). Both modalities improve the final outcome, but RAI ablation decreases cause-specific death risk independent of the extent of surgery. We present the case of a 5-year-old girl, the youngest ever treated in our country with surgery and RAI therapy successfully after being diagnosed as papillary carcinoma of the thyroid, follicular variant.     

Extending slice coverage for breathhold fat-suppressed T2-weighted fast spin-echo of the liver at 3.0T: application of variable-rate selective-excitation (VERSE) RF pulses

PURPOSE: To determine the benefits of variable-rate selective-excitation (VERSE) radio frequency (RF) pulses for increased slice coverage in breathhold (BH) fat-suppressed T2-weighted fast spin-echo (FS-T2W-FSE) liver imaging at 3.0T. MATERIALS AND METHODS: A total of 12 healthy volunteers were imaged on 3.0T, using FS-T2W-FSE. Slice coverage and specific absorption rate (SAR) levels were monitored for VERSE-RF and standard-RF (sRF), respectively. BH time was 25 seconds; slice thickness 3.5 mm. Maximum coverage was recorded for interactive variation of repetition time (TR), bandwidth (BW), and echo-train length (ETL). Image quality was assessed qualitatively and quantitatively. RESULTS: Total slice coverage was always higher using VERSE-RF, but varied depending on the selected parameters. For BW > or = 62.5 kHz, slice coverage using VERSE increased between 38% (TR = 8200 msec) and 58% (TR = 2500 msec). Maximum coverage was obtained for TR = 5000 msec, ETL = 12, and BW > or = 62.5 kHz; with a mean of 31.8 slices for VERSE-RF and 22.5 slices for sRF, respectively (P < 0.005, 41% increased coverage). SAR was lower for VERSE-RF using BW < 41.67 kHz (P < 0.05), and equal to sRF for higher BW. Image quality was best for TR < or = 5000 msec (P < 0.05). FS was more homogeneous for lower ETL (P < 0.05). Blood suppression was best for TR < or = 5000 msec (P < 0.05). CONCLUSION: VERSE-RF pulses can be applied for thin-slice BH FS-T2W liver imaging at 3.0T, with significantly improved slice coverage.     

The histone deacetylase inhibitor, vorinostat, reduces tumor growth at the metastatic bone site and associated osteolysis, but promotes normal bone loss

Vorinostat, an oral histone deacetylase inhibitor with antitumor activity, is in clinical trials for hematologic and solid tumors that metastasize and compromise bone structure. Consequently, there is a requirement to establish the effects of vorinostat on tumor growth within bone. Breast (MDA-231) and prostate (PC3) cancer cells were injected into tibias of SCID/NCr mice and the effects of vorinostat on tumor growth and osteolytic disease were assessed by radiography, micro-computed tomography, and histologic and molecular analyses. Vorinostat-treated and control mice without tumors were also examined. Tumor growth in bone was reduced ～33% by vorinostat with inhibited osteolysis in the first few weeks of the experiment. However, osteolysis became more severe in both the vehicle and vorinostat-treated groups. Vorinostat increased the expression of tumor-derived factors promoting bone resorption, including PTHrP, IL-8, and osteopontin. After 4 weeks of vorinostat therapy, the non-tumor-bearing contralateral femurs and limbs from vorinostat-treated tumor-free SCID mice showed significant bone loss (50% volume density of controls). Thus, our studies indicate that vorinostat effectively inhibits tumor growth in bone, but has a negative systemic effect reducing normal trabecular bone mass. Vorinostat treatment reduces tumor growth in bone and accompanying osteolytic disease as a result of decreased tumor burden in bone. However, vorinostat can promote osteopenia throughout the skeleton independent of tumor cell activity.     

p57(KIP2) expression in normal islet cells and in hyperinsulinism of infancy.

Most cases of hyperinsulinism of infancy (HI) are caused by mutations in either the sulfonylurea receptor-1 (SUR1) or the inward rectifying K(+) channel Kir6.2, two subunits of the beta-cell ATP-sensitive K(+) channel (K(ATP) channel). Histologically, HI can be divided into two major subtypes. The diffuse form is recessively inherited and involves all beta-cells within the pancreas. Focal HI consists of adenomatous hyperplasia within a limited region of the pancreas, and it is caused by somatic loss of heterozygosity (LOH), including maternal Ch11p15-ter in a beta-cell precursor carrying a germ-line mutation in the paternal allele of SUR1 or Kir6.2. Several imprinted genes are located within this chromosomal region, some of which, including p57(KIP2) and IGF-II, have been associated with the regulation of cell proliferation. Using double immunostaining, we examined p57(KIP2) expression in different islet cell types, in control pancreases from different developmental stages (n = 15), and in pancreases from patients with both diffuse (n = 4) and focal HI (n = 9). Using immunofluorescence and computerized image analysis, we quantified IGF-II expression in beta-cells from patients with focal HI (n = 8). Within the pancreas, p57(KIP2) was specifically localized to the endocrine portion. beta-Cells demonstrated the highest frequency of expression (34.9 +/- 2.7%) compared with approximately 1-3% in other cell types. The fraction of beta-cells expressing p57(KIP2) did not vary significantly during development. beta-Cells within the focal lesions did not express p57(KIP2), whereas IGF-II staining inside focal lesions was mildly increased compared with unaffected surrounding tissue. In conclusion, we demonstrate that p57(KIP2) is expressed and is paternally imprinted in human pancreatic beta-cells. Loss of expression in focal HI is caused by LOH and is associated with increased proliferation and increased IGF-II expression. Manipulation of p57(KIP2) expression in beta-cells may provide a mechanism by which proliferation can be modulated, and thus this gene is a potential therapeutic target for reversing the beta-cell failure observed in diabetes.