Search

Objective: We aimed to evaluate whether types of vascular anastomoses affect fetal demise (FD) in twin-twin transfusion syndrome (TTTS) after fetoscopic laser photocoagulation (FLP).Methods: All TTTS patients who underwent FLP in our institution from 2005 to 2017 were included. We described vascular anastomoses during FLP as either arterio-arterial (AA), veno-venous (VV), or arterial-venous (AV), and abnormal fetal Doppler waveforms before FLP. We also analyzed risk factors for FD following FLP.Results: In total, 184 TTTS placentas following FLP were analyzed (36 cases of donor-only FD, 12 cases of recipient-only FD, 3 cases of double FD, and 133 cases of both alive). AA anastomoses prevalence, absent or reverse end-diastolic velocity of umbilical artery (UAAREDV) of donor before FLP, gestational age at the time of FLP and operation time of FLP were independent risk factors for donor FD. VV anastomoses prevalence and UAAREDV of recipient before FLP were independent risk factors for recipient FD. VV anastomoses prevalence was higher in double FD cases than in FD of one twin or both alive (p = 0.002). AV anastomoses number and number of cases with more AV anastomoses from donor to recipient were not significantly different between FD and non-FD cases.Discussion: AA anastomoses are associated FD of the donor following FLP and may protect the donor from hypovolemia before FLP. VV anastomoses are detected more frequently in FD of the recipient and double FD placentas following FLP and may rescue hypervolemia of the recipient or circulations of both fetuses before FLP. [ABSTRACT FROM AUTHOR]

The distribution and morphology of the endoplasmic reticulum (ER) in mammalian cells depend on both dynamic and static interactions of ER membrane proteins with microtubules (MTs). Cytoskeleton-linking membrane protein (CLIMP)- 63 is exclusively localized in sheet-like ER membranes, typical structures of the rough ER, and plays a pivotal role in the static interaction with MTs. Our previous study showed that the 42-kDa ER-residing form of syntaxin 5 (Syn5L) regulates ER structure through the interactions with both CLIMP-63 and MTs. Here, we extend our previous study and show that the valosin-containing protein/p97-interacting membrane protein (VIMP)/SelS is also a member of the family of proteins that shape the ER by interacting with MTs. Depletion of VIMP causes the spreading of the ER to the cell periphery and affects an MT-dependent process on the ER. Although VIMP can interact with CLIMP-63 and Syn5L, it does not interact with MT-binding ER proteins (such as Reep1) that shape the tubular smooth ER, suggesting that different sets of MT-binding ER proteins are used to organize different ER subdomains. [ABSTRACT FROM AUTHOR]