Pre-eclampsia is commonly associated with higher serum uric acid levels, which is known to increase vascular tone. A previous retrospective study established a positive correlation between raised serum uric acid levels and reduced incidence of post-spinal hypotension. However, until date, this correlation has not been prospectively evaluated in exclusively pre-eclamptic women. Pre-eclamptic parturients undergoing emergency cesarean delivery under subarachnoid block were included. Sample for measuring serum uric acid level was obtained prior to shifting patients for cesarean delivery. Following spinal anesthesia, we recorded episodes of hypotension (fall of mean arterial pressure more than 20% from baseline values), use of vasopressors, and intraoperative blood loss. Our primary objective was to study the association between maternal hyperuricemia and incidence of post-spinal hypotension. Our secondary objectives included amount of vasopressors administered to maintain targeted mean arterial pressure before delivery of the baby, intraoperative blood loss, and immediate neonatal outcome. A total of 95% parturients had hyperuricemia, with mean serum uric acid level being 6.94 ± 0.9 mg/dl. Incidence of post-spinal hypotension was significantly lower in women who had hyperuricemia as compared with those with normal serum uric acid levels (21% vs 75%; p = 0.015). Mean serum uric acid levels were significantly high (p = 0.001) in patients not requiring any vasopressors (7.2 ± 1.2 mg/dl) than in those requiring moderate (5.70 ± 0.79 mg/dl) to high dose (5.75 ± 0.77 mg/dl) of vasopressors. There is a high incidence of hyperuricemia in pre-eclamptic parturients. In these patients, elevated serum uric acid levels is associated with lower incidence of post-spinal hypotension and reduced need of vasopressors to maintain maternal blood pressure within a normal range.There is growing interest in infections occurring after transcatheter aortic valve implantation (TAVI). The incidence, and clinical and anatomical features suggest many similarities with prosthetic valve endocarditis. The survival of patients with an infected TAVI prosthesis is generally poor; however, only a minority of them (10%) have undergone treatment with surgical explantation of the infected prosthesis. A literature search was performed using online databases. Papers reporting surgical treatment of TAVI prosthesis infections were retrieved, focusing on pre- and intraoperative characteristics and early outcome. Thirty-seven papers ultimately provided information on 107 patients. Their mean ± standard deviation (SD) age was 76 ± 8 years and 72% were male. The mean ± SD time interval between the TAVI procedure and reoperation was 10 ± 10 months. Annular abscess formation was described in 34% of cases and mitral valve involvement in 31%. All patients underwent TAVI prosthesis explantation and surgical aortic valve replacement; concomitant mitral valve replacement was necessary in 22% of cases. Postoperative in-hospital mortality was 28%. Surgical explantation of infected TAVI prostheses was associated with a high postoperative mortality, although these initial experiences included elderly and high-risk patients. Considering the expansion of TAVI procedures towards younger and lower-risk patients, surgical treatment of TAVI endocarditis may represent the best option for a life-saving procedure.

Approximately 1% of the world’s population is impacted by epilepsy, a chronic neurological disorder characterized by seizures. One-third of epileptic patients are resistant to AEDs, or have medically refractory epilepsy (MRE). One non-invasive treatment that exists for MRE includes the ketogenic diet, a high-fat, low-carbohydrate diet. Despite the KD’s success in seizure attenuation, it has a few risks and its mechanisms remain poorly understood. N-Ethylmaleimide chemical structure The KD has been shown to improve metabolism and mitochondrial function in epileptic phenotypes. Potassium channels have implications in epileptic conditions as they have dual roles as metabolic sensors and control neuronal excitation.

The goal of this study was to explore changes in the lipidome in hippocampal and cortical tissue from Kv1.1-KO model of epilepsy.

FT-ICR/MS analysis was utilized to examine nonpolar metabolome of cortical and hippocampal tissue isolated from a Kv1.1 channel knockout mouse model of epilepsy (n = 5) and wild-type mice (n = 5).

Distinct metabolic profiles were observed, significant (p < 0.05) features in hippocampus often being upregulated (FC ≥ 2) and the cortex being downregulated (FC ≤ 0.5). Pathway enrichment analysis shows lipid biosynthesis was affected. Partition ratio analysis revealed that the ratio of most metabolites tended to be increased in Kv1.1-/-. Metabolites in hippocampal tissue were commonly upregulated, suggesting seizure initiation in the hippocampus. Aberrant mitochondrial function is implicated by the upregulation of cardiolipin, a common component in the mitochondrial membrane.

Generally, our study finds that the lipidome is changed in the hippocampus and cortex in response to Kv1.1-KO indicating changes in membrane structural integrity and synaptic transmission.

Generally, our study finds that the lipidome is changed in the hippocampus and cortex in response to Kv1.1-KO indicating changes in membrane structural integrity and synaptic transmission.The BMP/TGFβ-Smad, Notch and VEGF signaling guides formation of endothelial tip and stalk cells. However, the crosstalk of bone morphogenetic proteins (BMPs) and vascular endothelial growth factor receptor 2 (VEGFR2) signaling has remained largely unknown. We demonstrate that BMP family members regulate VEGFR2 and Notch signaling, and act via TAZ-Hippo signaling pathway. BMPs were found to be regulated after VEGF gene transfer in C57/Bl6 mice and in a porcine myocardial ischemia model. BMPs 2/4/6 were identified as endothelium-specific targets of VEGF. BMP2 modulated VEGF-mediated endothelial sprouting via Delta like Canonical Notch Ligand 4 (DLL4). BMP6 modulated VEGF signaling by regulating VEGFR2 expression and acted via Hippo signaling effector TAZ, known to regulate cell survival/proliferation, and to be dysregulated in cancer. In a matrigel plug assay in nude mice BMP6 was further demonstrated to induce angiogenesis. BMP6 is the first member of BMP family found to directly regulate both Hippo signaling and neovessel formation.