Hydronephrosis Secondary to an Ectopic Decidual Reaction in the Urinary Bladder.

A 28-year-old pregnant woman at 19 weeks gestation presented with dysuria as well as lower abdominal and left flank pain. Imaging revealed left-sided hydronephrosis and a mass invading the posterior bladder wall. Management included placement of a left nephrostomy tube and transurethral resection of ~25% of the mass. Microscopy showed an ectopic decidual reaction within the muscularis propria. The patient improved symptomatically and continued prenatal care. Complete resolution of her ureteral obstruction was demonstrated during the postpartum period. Ectopic decidual reactions involving the urinary bladder are extremely rare, and ureteral obstruction secondary to this phenomenon has not yet been reported.

"Atypical" salivary gland fine needle aspiration: Risk of malignancy and interinstitutional variability.

BACKGROUND: Fine needle aspiration (FNA) is widely used in the diagnosis of salivary gland lesions. Salivary gland FNAs are often difficult to diagnose because of morphologic heterogeneity, a small but significant number of the FNAs yield "atypical" diagnosis. However, systematic evaluation of the risk of malignancy (ROM) of the atypical diagnoses across institutions and the variability of ROM among institutions are still lacking. METHODS: Salivary gland FNAs from five tertiary medical centers of United States, Europe and China were reviewed. Cases with "atypical" diagnosis and histological follow-up were included in this study. The diagnostic category of "atypical" was adopted from Milan System for Reporting Salivary Gland Cytopathology (MSRSGC, personal communication). RESULTS: Among the 12,606 salivary gland FNAs, 504 (4.0%) cases were reported as "atypical", with 154 cases (30.6%) having histological follow-ups. Histological follow-ups revealed 94 malignant tumors (61.0%, 57 lymphomas, 33 carcinomas, 2 sarcomas, 1 metastatic melanoma, 1 metastatic neuroblastoma), 33 benign tumors (21.4%), and 25 benign lesions (16.2%). ROM in the subset of "atypical" cases with histological follow-up from different institutions vary from 73.08% to 0.00%, the Pearson chi2 = 24.38 and P < .001. CONCLUSIONS: More than half of the subset of "atypical" salivary gland FNAs with histological resection turned out to be malignant tumors; another one-fourth were benign neoplasms. Further, the highly variable ROMs of the "atypical" category amongst different institutions likely reflect the variable practices at each individual institution.

Multiple Drug Treatments That Increase cAMP Signaling Restore Long-Term Memory and Aberrant Signaling in Fragile X Syndrome Models.

Fragile X is the most common monogenic disorder associated with intellectual disability (ID) and autism spectrum disorders (ASD). Additionally, many patients are afflicted with executive dysfunction, ADHD, seizure disorder and sleep disturbances. Fragile X is caused by loss of FMRP expression, which is encoded by the FMR1 gene. Both the fly and mouse models of fragile X are also based on having no functional protein expression of their respective FMR1 homologs. The fly model displays well defined cognitive impairments and structural brain defects and the mouse model, although having subtle behavioral defects, has robust electrophysiological phenotypes and provides a tool to do extensive biochemical analysis of select brain regions. Decreased cAMP signaling has been observed in samples from the fly and mouse models of fragile X as well as in samples derived from human patients. Indeed, we have previously demonstrated that strategies that increase cAMP signaling can rescue short term memory in the fly model and restore DHPG induced mGluR mediated long term depression (LTD) in the hippocampus to proper levels in the mouse model (McBride et al., 2005; Choi et al., 2011, 2015). Here, we demonstrate that the same three strategies used previously with the potential to be used clinically, lithium treatment, PDE-4 inhibitor treatment or mGluR antagonist treatment can rescue long term memory in the fly model and alter the cAMP signaling pathway in the hippocampus of the mouse model.