• The median age of the patients was 14 (0-92) years. 51% ( n = 89) had testicular torsion, 24% ( n = 42) had torsion of testicular appendages, 9% ( n = 16) had epididymo-orchitis, and other pathology made up 5%.• No obvious pathology was seen in 10% ( n = 17).• Patients with Torsion of Appendages were significantly younger than other patients with scrotal pain ( P < 0.0001).• Age was not useful in discriminating between patients with Testicular Torsion from other patients with scrotal pain. 9% ( n = 16) of all patients required an orchidectomy.• Frequency of Testicular Torsion was higher during the colder half of the year ( n = 0.02). CONCLUSIONS• Testicular torsion was the most common finding at surgical exploration, followed by torsion of testicular appendages.• Age had limited value in diagnosing the cause of acute scrotal pain.• Testicular torsion was associated with cold weather.• Our findings support the practice of surgical exploration for acute scrotal pain suspicious of testicular torsion in patients of any age.

Prostate cancer is a major cause of mortality, largely as a consequence of metastases and transformation to androgen-independent growth. Metalloproteinases are implicated in cancer progression. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) are expressed in prostate cancer cells, with ADAMTS-1 and ADAMTS-15 being the most abundant. ADAMTS-15 but not ADAMTS-1 expression was downregulated by androgen in LNCaP prostate cancer cells, possibly through androgen response elements associated with the gene. ADAMTS-15 expression is predictive for survival in breast cancer, and the situation may be similar in prostate cancer, as androgen independence is usually due to aberrant signaling through its receptor.

No abstract

Treatment‐induced adaptive pathways converge to support androgen receptor (AR) reactivation and emergence of castration‐resistant prostate cancer (PCa) after AR pathway inhibition (ARPI). We set out to explore poorly defined acute adaptive responses that orchestrate shifts in energy metabolism after ARPI and identified rapid changes in succinate dehydrogenase (SDH), a TCA cycle enzyme with well‐known tumor suppressor activity. We show that AR directly regulates transcription of its catalytic subunits (SDHA, SDHB) via androgen response elements (AREs). ARPI acutely suppresses SDH activity, leading to accumulation of the oncometabolite, succinate. Succinate triggers calcium ions release from intracellular stores, which in turn phospho‐activates the AR‐cochaperone, Hsp27 via p‐CaMKK2/p‐AMPK/p‐p38 axis to enhance AR protein stabilization and activity. Activation of this pathway was seen in tissue microarray analysis on prostatectomy tissues and patient‐derived xenografts. This adaptive response is blocked by co‐targeting AR with Hsp27 under both in vitro and in vivo studies, sensitizing PCa cells to ARPI treatments.

No abstract