High-risk third trimester pregnancy with decompensated cirrhosis safely delivered following emergent preoperative interventional radiology for mitigation of variceal bleeding.

Coagulopathy coupled with severe portal hypertension in the setting of cirrhosis increases the risk of mortality from variceal bleeding in pregnant women. Studies suggest transjugular intrahepatic portosystemic shunt (TIPS) creation to be a safe procedure during pregnancy in preventing variceal bleeding complications; however, it is not typically employed in severely decompensated cirrhosis. This case report of a pregnant woman presenting at 34.7 weeks' gestation demonstrates successful variceal mapping, emergent TIPS creation and variceal embolization to allow safe cesarean delivery despite severe hypofibrinogenemia and decompensated alcoholic cirrhosis. With careful medical optimization, angiographic imaging and vascular interventional radiology may be employed outside of usual indications to achieve safe pregnancy delivery and postpartum recovery.

Length of Stay Predicts Risk of Early Infection for Hospitalized Patients Undergoing Central Venous Port Placement.

PURPOSE: To compare early totally implantable central venous port catheter-related infection rates after inpatient vs outpatient placement and to determine whether the risk associated with inpatient placement is influenced by length of hospital stay. MATERIALS AND METHODS: In this single-institution retrospective study, 5,301 patients (3,618 women; mean age 57 y) underwent port placement by interventional radiologists between October 2004 and January 2018. The 30-day infection rate was compared between inpatients and outpatients using survival analysis. Among inpatients, the effect of time from admission to port placement and from placement to discharge was analyzed using a survival regression tree. RESULTS: The 30-day infection rate was 3.6% (95% confidence interval [CI] = 1.9%-6.1%) among 386 inpatients and 1.0% (95% CI = 0.7%-1.3%) among 4,915 outpatients (hazard ratio [HR] = 3.6, 95% CI = 2.0-6.6, P < .001). Inpatient placement was a significant risk factor after accounting for covariates in multivariate analysis (HR = 2.2, 95% CI = 1.0-4.7, P = .05) and controlling for demographic differences by propensity score matching (HR = 2.8, 95% CI = 1.0-7.8, P = .04). Infection rate was 11% (95% CI = 4.7%-22%) among 65 inpatients in whom time from admission to placement was ≥ 7 days, 5.1% (95% CI = 1.9%-11%) among 129 inpatients in whom admission to placement was < 7 days and time to discharge was > 3 days, and 0% (95% CI = 0%-2.1%) among 192 inpatients in whom admission to placement was < 7 days and time to discharge was ≤ 3 days (P < .001). CONCLUSIONS: Inpatient port placement was associated with a higher risk of early infection. However, a clinical decision tree based on shorter length of stay before and after placement may identify a subset of hospitalized patients not at increased risk for infection.

Diagnosis of rare association of orthotopic multicystic dysplasia with crossed fused renal ectopia.

Orthotopic multicystic dysplastic kidney with crossed fused ectopia is a rare congenital anomaly. This congenital anomaly may give an appearance of a solitary kidney morphology during the initial imaging evaluation. A solitary kidney should be carefully evaluated for the presence of duplication, horseshoe configuration, or crossed renal ectopy. Vesicoureteral reflux is a common finding associated with a multicystic dysplastic kidney. We present an infant with an orthotopic multicystic dysplastic kidney and an inferiorly placed crossed fused ectopic kidney. The presence of a complex congenital anomaly may warrant further evaluation with cross-sectional imaging to depict the anatomy and structure.

tsunami, the Dictyostelium homolog of the Fused kinase, is required for polarization and chemotaxis.

In a forward genetic screen for chemotaxis mutants in Dictyostelium discoideum, we identified a loss-of-function mutation, designated tsunami, encoding a homolog of the Fused kinase. Cells lacking tsuA function could not effectively perform chemotaxis and were unable to become polarized or correctly orient pseudopods in chemotactic gradients. While tsuA(-) cells were able to couple receptor occupancy to phosphatidylinositol (3,4,5) trisphosphate (PIP3) production and actin polymerization, the PIP3 response was prolonged and basal F-actin levels were increased. Interestingly, TsuA localizes to the microtubule network and puncta mainly found at the cell periphery. Analysis of the gene uncovered a novel C-terminal domain that we designated the Tsunami Homology (TH) domain. Both the kinase domain and the TH domain are required to rescue the phenotypic defects of tsuA(-) cells. While kinase activity is not required for localization to microtubules, the TH domain is essential. Thus, localization of kinase activity to microtubules is critical for TsuA function. We propose that functions in association with the microtubule network may underlie the divergent roles of Fused kinase proteins in different organisms.

Visualization of G protein betagamma dimers using bimolecular fluorescence complementation demonstrates roles for both beta and gamma in subcellular targeting.

To investigate the role of subcellular localization in regulating the specificity of G protein betagamma signaling, we have applied the strategy of bimolecular fluorescence complementation (BiFC) to visualize betagamma dimers in vivo. We fused an amino-terminal yellow fluorescent protein fragment to beta and a carboxyl-terminal yellow fluorescent protein fragment to gamma. When expressed together, these two proteins produced a fluorescent signal in human embryonic kidney 293 cells that was not obtained with either subunit alone. Fluorescence was dependent on betagamma assembly in that it was not obtained using beta2 and gamma1, which do not form a functional dimer. In addition to assembly, BiFC betagamma complexes were functional as demonstrated by more specific plasma membrane labeling than was obtained with individually tagged fluorescent beta and gamma subunits and by their abilities to potentiate activation of adenylyl cyclase by alpha(s) in COS-7 cells. To investigate isoform-dependent targeting specificity, the localization patterns of dimers formed by pair-wise combinations of three different beta subunits with three different gamma subunits were compared. BiFC betagamma complexes containing either beta1 or beta2 localized to the plasma membrane, whereas those containing beta5 accumulated in the cytosol or on intracellular membranes. These results indicate that the beta subunit can direct trafficking of the gamma subunit. Taken together with previous observations, these results show that the G protein alpha, beta, and gamma subunits all play roles in targeting each other. This method of specifically visualizing betagamma dimers will have many applications in sorting out roles for particular betagamma complexes in a wide variety of cell types.