Lower Urinary Tract Symptoms Including Bladder Outlet Obstruction: What's New in Diagnostics?

It is well known that lower urinary tract symptoms (LUTS) have a multifactorial etiology. Therefore, there is an increased need for improved diagnostics for the optimal assessment of patients with LUTS in order to identify the various causes of symptoms and improve disease phenotyping. Research has focused on the development of improved urodynamic technologies and the development of noninvasive tests that could replace urodynamic studies. This mini-review will present the most recently published studies on the topic including new technologies in the diagnosis of bladder outlet obstruction, novel metrics for bladder sensation, analysis of filling phase rhythm, measurement of detrusor wall tension, and brain imaging during urodynamic studies. Patient summary: Lower urinary tract symptoms (LUTS) have a multifactorial etiology; therefore there is a need for the development of new tests that can help LUTS diagnosis. The present mini-review highlights the new tests and novel concepts in the field. New tests/technologies for the improvement of lower urinary tract symptom diagnosis are under development and evaluation. The most recent findings are highlighted, although these new diagnostics are at a different degree of maturation. © 201

Proximal Splenic Artery Embolization In Blunt Splenic Trauma

Proximal embolization of the splenic artery (PSAE) has recently been reported for traumatic splenic injury. The suggested mechanism of action entails a decrease in the splenic blood pressure without ischemia due to collateral blood supply. The main complications of selective embolization are continuous bleeding, splenic infarcts and splenic abscesses. The main complications of observation alone are continuous bleeding and formation of splenic pseudoaneurysms. Our aim was to assess the efficacy of PSAE in the cessation of bleeding without formation of pseudoaneurysms, and the outcome of the spleen after such intervention. A prospective observational study of all patients undergoing PSAE for traumatic splenic injury in our institution over a 33-month period. Clinical and Doppler sonographic examinations were performed to assess cessation of bleeding, splenic blood flow, and formation of splenic pseudoaneurysms, infarcts or abscesses. During 33 months, 11 patients with blunt abdominal trauma and tomographic evidence of either high grade or actively bleeding splenic injuries were treated by PSAE. During follow-up, no patient underwent surgery or repeated embolization. Preserved blood flow was found on Doppler sonography in 82% of the patients and no pseudoaneurysms were demonstrated. A perisplenic collection was found in one patient and responded well to percutaneous drainage. Proximal embolization of the splenic artery for severe splenic injury is highly successful in cessation of bleeding while preserving splenic architecture. There were minimal complications in this series demonstrated by clinical and Doppler examinations

GS15 Forms a SNARE Complex with Syntaxin 5, GS28, and Ykt6 and Is Implicated in Traffic in the Early Cisternae of the Golgi Apparatus

The subcellular localization, interacting partners, and function of GS15, a Golgi SNARE, remain to be established. In our present study, it is revealed that unlike proteins (Bet1 and the KDEL receptor) cycling between the Golgi and the intermediate compartment (IC, inclusive of the ER exit sites), GS15 is not redistributed into the IC upon incubation at 15°C or when cells are treated with brefeldin A. Immuno-electron microscopy (immuno-EM) reveals that GS15 is mainly found in the medial-cisternae of the Golgi apparatus and adjacent tubulo-vesicular elements. Coimmunoprecipitation experiments suggest that GS15 exists in a distinct SNARE complex that contains SNAREs (syntaxin5, GS28, and Ykt6) that are implicated in both ER-to-Golgi and intra-Golgi transport but not with SNAREs involved exclusively in ER-to-Golgi traffic. Furthermore, components of COPI coat can be selectively coimmunoprecipitated with GS15 from Golgi extracts. Overexpression of mutant forms of GS15 affects the normal distribution of cis- and medial-Golgi proteins (GS28, syntaxin 5, and Golgi mannosidase II), whereas proteins of the trans-Golgi and TGN (Vti1-rp2/Vti1a and syntaxin 6) and Golgi matrix/scaffold (GM130 and p115) are less affected. When the level of GS15 is reduced by duplex 21-nt small interfering RNA (siRNA)-mediated knockdown approach, diverse markers of the Golgi apparatus are redistributed into small dotty and diffuse labeling, suggesting an essential role of GS15 in the Golgi apparatus