Retinoids, such as all-trans-retinoic acid, play an essential role in the regulation of airway epithelial cell growth, differentiation, and gene expression. Using cDNA microarray, we identified a clone, DD4, that contains the cDNA of a novel gene, spurt (secretory protein in upper respiratory tracts) that was significantly induced by all-trans-retinoic acid in primary cultured human tracheobroncheal epithelia. Two alternatively spliced spurt transcripts of 1090 and 1035 base pairs exist that contain the same open reading frame expressing a 256-amino acid peptide. The full-length spurt cDNA sequence spans a genomic DNA fragment of 7,313 bp, and the gene is located on chromosome 20q11.21. spurt mRNA is notably expressed at high levels in human nasal, tracheal, and lung tissues. In situ hybridization demonstrated that spurt message is often present in secretory cell types. The human spurt gene product is a secretory protein that contains a distinct signal peptide sequence in its first 19 amino acids. Mono-specific antibodies were generated to characterize spurt expression. Our data demonstrate that spurt is secreted onto the apical side of primary human airway epithelial cultures and is present in clinical sputum samples. spurt gene expression is higher in sputum and tissue samples obtained from patients with chronic obstructive lung disease. Our results provide the cloning and characterization of this tissue-specific novel gene and its possible relationship with airway diseases.

The etiology and severity of FSF has changed from 1974 to 2002. This is reflected in a reduced number of fractures resulting from MVAs as well as a reduced severity of injury. The most likely explanation is the use of safety belts and airbags.

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Objectives Granulosa cell tumors (GCTs) comprise 2–5% of ovarian tumors. Serum Müllerian Inhibiting Substance (MIS, also known as anti-Müllerian Hormone, or AMH) levels have been validated as a marker of GCT recurrence and progression. There has been little correlation between serum MIS/AMH levels several clinical parameters in GCTs, including tumor burden. We have performed a retrospective review correlating aggregate tumor mass as reported by pathologic examination or by radiology with serum MIS/AMH levels drawn on the date of examination. Methods We retrospectively identified 32 GCT patients at our institution over the last 15 years who had serum MIS/AMH measurements. Patients who had serum MIS/AMH measurements within three days of surgery or on the same day as abdominal computerized tomography scan (CT) or magnetic resonance imaging (MRI) were further evaluated. Results We found a significant direct correlation between patient serum MIS/AMH levels and gross aggregate tumor mass determined by pathology (slope=15.4±6.06, r=0.65, p<0.04) or by radiographic aggregate tumor mass for all data points identified (slope=0.07±0.03, r=0.33, p<0.04) and after correcting for selection bias (slope=1.45±0.17, r=0.93, p<0.01). We also identified a significant difference between serum MIS/AMH levels between samples drawn the same day as negative and positive abdominal CT or MRI scans (8.16±1.54 vs. 158.7±32.2 ng/ml, p<0.0001). Conclusions These data indicate a significant direct correlation between serum MIS/AMH levels and both gross and radiographic aggregate tumor mass in GCT patients. Together with the current literature, the present data argues for a more prominent role for serum MIS/AMH in the management of GCTs.