Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the first four cases of LASS for endometrial cancer in Mexico. Four patients diagnosed with endometrial adenocarcinoma were selected. These patients underwent peritoneal washing, vaginally assisted laparoscopic hysterectomy, bilateral salpingo-oophorectomy and pelvic biopsies. These biopsies included dissection of common iliac vessel, hypogastric and external vessels, and obturator nerve. An average of 10 nodes were obtained (8-11). In all patients both the nodes and the peritoneal washings were negative. The pathologic surgical staging was: three patients with IBG2 and one patient with IAG2. The patients were discharged on the sixth postoperative day, without complications. The follow-up is of 1 to 7 months and all are alive and without tumor activity. Patients with endometrial cancer often have associated obesity, diabetes and hypertension. For this reason the practice of minimally invasive surgery reduces morbidity. However, a full knowledge of anatomy, oncologic gynecology, and operative laparoscopy is imperative.
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PMID:Laparoscopic Assisted Surgical Staging (LASS) for Endometrial Cancer 907 70

Epidemiological, clinical and experimental evidence indicates an inverse association between Mg(2+) levels (serum and tissue) and blood pressure. Magnesium may influence blood pressure by modulating vascular tone and structure through its effects on numerous biochemical reactions that control vascular contraction/dilation, growth/apoptosis, differentiation and inflammation. Magnesium acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoactive agonists. Mammalian cells regulate Mg(2+) concentration through specialized influx and efflux transport systems that have only recently been characterized. Magnesium efflux occurs via Na(2+)-dependent and Na(2+)-independent pathways. Mg(2+) influx is controlled by recently cloned transporters including Mrs2p, SLC41A1, SLC41A1, ACDP2, MagT1, TRPM6 and TRPM7. Alterations in some of these systems may contribute to hypomagnesemia and intracellular Mg(2+) deficiency in hypertension. In particular increased Mg(2+) efflux through altered regulation of the vascular Na(+)/Mg(2+) exchanger and decreased Mg(2+) influx due to defective vascular and renal TRPM6/7 expression/activity may be important. This review discusses the role of Mg(2+) in vascular biology and implications in hypertension and focuses on the putative transport systems that control vascular magnesium homeostasis. Much research is still needed to clarify the exact mechanisms of Mg(2+) regulation in the cardiovascular system and the implications of aberrant transcellular Mg(2+) transport in the pathogenesis of cardiovascular disease.
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PMID:Magnesium transport in hypertension. 1802 56

Magnesium may influence blood pressure by modulating vascular tone and structure through its effects on myriad biochemical reactions that control vascular contraction/dilation, growth/apoptosis, differentiation and inflammation. Magnesium acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoconstrictor agents. Mammalian cells regulate Mg2+ concentration through special transport systems that have only recently been characterized. Magnesium efflux occurs via Na2+-dependent and Na2+-independent pathways. Mg2+ influx is controlled by recently cloned transporters including Mrs2p, SLC41A1, SLC41A2, ACDP2, MagT1, TRPM6 and TRPM7. Alterations in some of these systems may contribute to hypomagnesemia and intracellular Mg2+ deficiency in hypertension and other cardiovascular pathologies. In particular, increased Mg2+ efflux through dysregulation of the vascular Na+/Mg2+ exchanger and decreased Mg2+ influx due to defective vascular and renal TRPM6/7 expression/activity may be important in altered vasomotor tone and consequently in blood pressure regulation. The present review discusses the role of Mg2+ in vascular biology and implications in hypertension and focuses on the putative transport systems that control magnesium homeostasis in the vascular system. Much research is still needed to clarify the exact mechanisms of cardiovascular Mg2+ regulation and the implications of aberrant cellular Mg2+ transport and altered cation status in the pathogenesis of hypertension and other cardiovascular diseases.
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PMID:Vascular biology of magnesium and its transporters in hypertension. 2119 86

Mg2+-deficiency is linked to hypertension, Alzheimer's disease, stroke, migraine headaches, cardiovascular diseases, and diabetes, etc., but its exact role in these pathophysiological conditions remains elusive. Mg2+ can regulate vascular functions, yet the mechanistic insight remains ill-defined. Data show that extracellular Mg2+ enters endothelium mainly through the TRPM7 channel and MagT1 transporter. Mg2+ can act as an antagonist to reduce Ca2+ signaling in endothelium. Mg2+ also reduces the intracellular reactive oxygen species (ROS) level and inflammation. In addition, Mg2+-signaling increases endothelial survival and growth, adhesion, and migration. Endothelial barrier integrity is significantly enhanced with Mg2+-treatment through S1P1-Rac1 pathways and barrier-stabilizing mediators including cAMP, FGF1/2, and eNOS. Mg2+ also promotes cytoskeletal reorganization and junction proteins to tighten up the barrier. Moreover, Mg2+-deficiency enhances endothelial barrier permeability in mice, and Mg2+-treatment rescues histamine-induced transient vessel hyper-permeability in vivo. In summary, Mg2+-deficiency can cause deleterious effects in endothelium integrity, and Mg2+-treatment may be effective in the prevention or treatment of vascular dysfunction.
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PMID:Magnesium Regulates Endothelial Barrier Functions through TRPM7, MagT1, and S1P1. 3155 37