RESUMO
Hydrocele of the canal of Nuck is a rare condition in females. It results from the failure of obliteration of the distal portion of evaginated parietal peritoneum within the inguinal canal which forms a sac containing fluid. Patients generally present with inguinal swelling. We present a case of left sided cyst of canal of Nuck with left inguinal hernia in a 28-year-old female, which was diagnosed on ultrasonography. Patient underwent laparoscopic excision of cyst of canal of nuck with hernioplasty. Histopathology confirmed the diagnosis. To our knowledge, this is the first reported case of laparoscopic excision of a cyst (encysted hydrocele) of the canal of Nuck.
RESUMO
Post-transcriptional switches are flexible effectors of dynamic changes in gene expression. Here we report a new post-transcriptional switch that dictates the spatiotemporal and mutually exclusive expression of two alternative gene products from a single transcript. Expression of primate-specific exonic microRNA-198 (miR-198), located in the 3'-untranslated region of follistatin-like 1 (FSTL1) messenger RNA, switches to expression of the linked open reading frame of FSTL1 upon wounding in a human ex vivo organ culture system. We show that binding of a KH-type splicing regulatory protein (KSRP, also known as KHSRP) to the primary transcript determines the fate of the transcript and is essential for the processing of miR-198: transforming growth factor-ß signalling switches off miR-198 expression by downregulating KSRP, and promotes FSTL1 protein expression. We also show that FSTL1 expression promotes keratinocyte migration, whereas miR-198 expression has the opposite effect by targeting and inhibiting DIAPH1, PLAU and LAMC2. A clear inverse correlation between the expression pattern of FSTL1 (pro-migratory) and miR-198 (anti-migratory) highlights the importance of this regulatory switch in controlling context-specific gene expression to orchestrate wound re-epithelialization. The deleterious effect of failure of this switch is apparent in non-healing chronic diabetic ulcers, in which expression of miR-198 persists, FSTL1 is absent, and keratinocyte migration, re-epithelialization and wound healing all fail to occur.