Purpose: We aimed to document the time of onset of ultrasonographic and histologic changes in the testes of a rat model following testicular torsion. Methods: Twenty-five Sprague-Dawley rats were divided into four groups. All animals underwent preoperative Doppler ultrasonography. Groups 1, 2, and 3 underwent unilateral surgical torsion of the testis lasting for 72, 24, and 6 hours, respectively. Group 4 underwent a sham operation. The animals were followed with Doppler ultrasonography at 6, 24, 48, and 72 hours postoperatively. Histologic examinations were performed at the designated final time point for each group. Results: After torsion, enlargement of the epididymal head and thickening of the spermatic cord over time were noted. Based on the ultrasonographic dimensions, the ratio of the epididymal volume increased with time following torsion (p=0.002). The torsed testes had an average weight gain of 0.27 g at 6 hours compared to the control testes, but an average weight loss of 0.22 g at 72 hours (P=0.006). Changes in testicular echotexture were noted as soon as 6 hours after torsion, but there was no consistent pattern of echotexture change thereafter. Histologically, viable tubules were seen 6 hours after torsion, while extensive hemorrhagic necrosis was found at 72 hours. Conclusion In evaluating testicular torsion, the enlargement ratio of the epididymis and thickening of the spermatic cord on Doppler ultrasonography may be useful for determining the urgency of immediate surgery. Changes in testicular echotexture may not be a reliable indicator of the time of onset.

Although genome-wide association studies have identified more than eighty genetic variants associated with non-small cell lung cancer (NSCLC) risk, biological mechanisms of these variants remain largely unknown. By integrating a large-scale genotype data of 15 581 lung adenocarcinoma (AD) cases, 8350 squamous cell carcinoma (SqCC) cases, and 27 355 controls, as well as multiple transcriptome and epigenomic databases, we conducted histology-specific meta-analyses and functional annotations of both reported and novel susceptibility variants. We identified 3064 credible risk variants for NSCLC, which were overrepresented in enhancer-like and promoter-like histone modification peaks as well as DNase I hypersensitive sites. Transcription factor enrichment analysis revealed that USF1 was AD-specific while CREB1 was SqCC-specific. Functional annotation and gene-based analysis implicated 894 target genes, including 274 specifics for AD and 123 for SqCC, which were overrepresented in somatic driver genes (ER = 1.95, P = 0.005). Pathway enrichment analysis and Gene-Set Enrichment Analysis revealed that AD genes were primarily involved in immune-related pathways, while SqCC genes were homologous recombination deficiency related. Our results illustrate the molecular basis of both well-studied and new susceptibility loci of NSCLC, providing not only novel insights into the genetic heterogeneity between AD and SqCC but also a set of plausible gene targets for post-GWAS functional experiments.
Adenocarcinoma of Lung/genetics* ; Carcinoma, Non-Small-Cell Lung/genetics* ; Carcinoma, Squamous Cell/genetics* ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Lung Neoplasms/genetics* ; Polymorphism, Single Nucleotide