Long-Term Ultrasonography Follow-Up of Thyroid Colloid Cysts at the Health Center: A Single-Center Study

Objective. No previous study has employed long-term follow-up ultrasonography (US) examinations for evaluating thyroid colloid cysts (TCCs) in the general population. This study aimed to assess the interval changes of TCCs at the health center by evaluating long-term US follow-up examinations.Methods. For evaluation of the thyroid gland at our health center from 2006 to 2010, 3692 individuals underwent 4 or more thyroid US examinations at an interval of 1 year or 2 years. We assessed the interval changes of TCCs ≥ 5 mm on US follow-up examinations.Results. Of the 3692 subjects, only 115 (3.1%) showed TCCs ≥ 5 mm on one or more thyroid US examinations. The interval changes in TCCs, as shown by the thyroid US examinations performed during the study period, were classified as follows: no interval change (n=60), gradual increase (n=37), gradual decrease (n=6), positive fluctuation (n=10), negative fluctuation (n=0), and disappearance (n=2). No subject reported any relevant symptom pertaining to TCCs.Conclusions. Overall, follow-up US examinations showed various interval changes in TCCs, but a majority of TCCs showed no interval change or a gradual increase in size.

Long-Term Ultrasound Follow-Up of Thyroid Colloid Cysts

Objective. This study aimed to assess the interval changes of thyroid colloid cysts (TCCs) by performing long-term ultrasound (US) follow-up examinations.Methods. From 2007 to 2008, 437 patients underwent a lobectomy for the treatment of papillary thyroid microcarcinoma. Among them, 268 patients underwent 4 or more postoperative US follow-ups after surgery. This study investigated the prevalence and interval changes of TCCs≥3 mm by using US follow-ups.Results. Among 268 patients, 35 (13.1%) had TCCs≥3 mm by a preoperative thyroid US, and 6 (2.2%) had newly detected TCCs at a US follow-up. Through long-term US follow-up, the interval changes for TCCs were classified as follows: no interval change (n=8), gradual increase (n=8), gradual decrease (n=5), positive fluctuation (n=3), negative fluctuation (n=6), disappearance (n=5), and new detection (n=6). None of the TCC cases had a TCC that was ≥10 mm at its largest diameter, and no patient complained of any relevant symptoms pertaining to the TCCs.Conclusions. In this study, TCCs demonstrated various interval changes, but no abrupt increase was found or acute onset of symptoms occurred.

Megalin binds and internalizes angiotensin II

Megalin is an abundant membrane protein heavily involved in receptor-mediated endocytosis. The major functions of megalin in vivo remain incompletely defined as megalin typically faces specialized milieus such as glomerular filtrate, airways, epididymal fluid, thyroid colloid, and yolk sac fluid, which lack many of its known ligands. In the course of studies on ANG II internalization, we were surprised when only part of the uptake of labeled ANG II into immortalized yolk sac cells (BN-16 cells) was blocked by specific peptide inhibitors and direct competitors of the angiotensin type 1 receptor. This led us to test if megalin was a receptor for ANG II. Four lines of direct evidence demonstrate that megalin and, to a lesser extent, its chaperone protein cubilin are receptors for ANG II. First, in BN-16 cells anti-megalin and anti-cubilin antisera interfere with ANG II uptake. Second, also in BN-16 cells, pure ANG II competes for uptake of a known megalin ligand. Third, in proximal tubule cell brush-border membrane vesicles extracted from mice, anti-megalin antisera interfere with ANG II binding. Fourth, purified megalin binds ANG II directly in surface plasmon resonance experiments. The finding that megalin is a receptor for ANG II suggests a major new function for the megalin pathway in vivo. These results also indicate that ANG II internalization in some tissues is megalin dependent and that megalin may play a role in regulating proximal tubule ANG II levels.

Prevention of diabetes in BioBreeding/Worcester rats with monoclonal antibodies that recognize T lymphocytes or natural killer cells.

Diabetes-prone BioBreeding/Worcester (BB/Wor) rats received thrice weekly injections of mAb against antigens expressed on the surface of all T cells (OX19), cytotoxic/suppressor, and NK cells (OX8), helper/inducer cells (W3/25, OX35, OX38), and Ia+ cells (OX6, 3JP, OX17). Treatment with OX8 or OX19 achieved stable reductions of splenic and peripheral blood NK cells and helper/inducer T lymphocytes, respectively, and protected against diabetes. OX19 injections also prevented lymphocytic insulitis, thyroiditis, and the synthesis of autoantibodies to thyroid colloid and smooth muscle antigens. OX8 injections reduced splenic NK-mediated YAC-1 cell lysis, but did not prevent insulitis, thyroiditis, or autoantibody synthesis. Injections of mAb specific for antigens on the surface of helper/inducer cells, and for cells expressing IaE antigens provided marginal protection against diabetes without reductions of phenotypic subsets. These findings suggest that pancreatic beta cell destruction in the spontaneously diabetic BB/Wor rat is mediated by the combined action of NK and helper/inducer cells.