ABSTRACT
BACKGROUND: Correction of significant tricuspid regurgitation (TR) at the time of continuous-flow (CF) left ventricular assist device (LVAD) implantation has been shown to be beneficial in several recently published studies. The most common technique is ring annuloplasty followed by valve replacement. Our center has primarily used the De Vega annuloplasty, and the durability of this repair is the focus of this study. METHODS: This was a retrospective review of 35 consecutive patients who underwent CF LVAD implantation and De Vega tricuspid valve annuloplasty (TVA) for severe TR and were alive at 1 year. Echocardiograms were obtained preoperatively, intraoperatively, at discharge, and at 1 year after operation. RESULTS: The TR in 32 of 35 patients (91.4%, group A) improved from severe preoperatively to insignificant at the time of discharge after De Vega TVA, and 3 patients (8.6%, group B) had moderate residual TR. At 1-year follow-up, 29 of 32 (90.6%) patients in group A had insignificant TR, 2 (6.3%) had moderate TR, and 1 (3.1%) had severe TR. In group B, 2 of 3 patients had no progression of their moderate TR at 1 year and 1 had severe TR. Overall, 2 of 35 (5.7%) patients had severe TR at 1 year after De Vega TVA and LVAD implantation. CONCLUSIONS: We conclude from this consecutive cohort of patients undergoing CF LVAD implantation and De Vega TVA that this technique is very durable at 1 year and has the advantages of a shorter operative time relative to ring annuloplasty and decreased cost because a prosthetic implant is not used.
Subject(s)
Cardiac Valve Annuloplasty/methods , Heart-Assist Devices , Tricuspid Valve Insufficiency/surgery , Tricuspid Valve/surgery , Echocardiography , Female , Follow-Up Studies , Humans , Intraoperative Period , Male , Middle Aged , Retrospective Studies , Severity of Illness Index , Time Factors , Treatment Outcome , Tricuspid Valve Insufficiency/diagnostic imagingABSTRACT
Patients with pancreatic cancer have little hope for cure because no effective therapies are available. Sansalvamide A is a cyclic depsipeptide produced by a marine fungus. We investigated the effect of a novel sansalvamide A analogue on growth, cell-cycle phases, and induction of apoptosis in human pancreatic cancer cells in vitro. The sansalvamide analogue caused marked time- and concentration-dependent inhibition of DNA synthesis and cell proliferation of two human pancreatic cancer cell lines (AsPC-1 and S2-013). The analogue induced G0/G1 phase cell-cycle arrest and morphological changes suggesting induction of apoptosis. Apoptosis was confirmed by annexin V binding. This novel sansalvamide analogue inhibits growth of pancreatic cancer cells through G0/G1 arrest and induces apoptosis. Sansalvamide analogues may be valuable for the treatment of pancreatic cancer.
Subject(s)
Cell Cycle/drug effects , Cell Proliferation/drug effects , Depsipeptides/administration & dosage , Pancreatic Neoplasms/pathology , Antineoplastic Agents/administration & dosage , Cell Line , Cell Survival/drug effects , Dose-Response Relationship, Drug , HumansABSTRACT
BACKGROUND: Many chemotherapeutic agents have been used to treat pancreatic cancer without success. Apigenin, a naturally occurring flavonoid, has been shown to inhibit growth in some cancer cell lines but has not been studied in pancreatic cancer. We hypothesized that apigenin would inhibit pancreatic cancer cell growth in vitro. RESULTS: Apigenin caused both time- and concentration-dependent inhibition of DNA synthesis and cell proliferation in four pancreatic cancer cell lines. Apigenin induced G2/M phase cell cycle arrest. Apigenin reduced levels of cyclin A, cyclin B, phosphorylated forms of cdc2 and cdc25, which are all proteins required for G2/M transition. CONCLUSION: Apigenin inhibits growth of pancreatic cancer cells through suppression of cyclin B-associated cdc2 activity and G2/M arrest, and may be a valuable drug for the treatment or prevention of pancreatic cancer.
Subject(s)
Apigenin/pharmacology , Cell Cycle/drug effects , Cell Proliferation/drug effects , G2 Phase/drug effects , Mitosis/drug effects , Blotting, Western , CDC2 Protein Kinase/metabolism , Cell Cycle Proteins/metabolism , Cell Line, Tumor , Cyclin A/metabolism , Cyclin B/metabolism , DNA, Neoplasm/antagonists & inhibitors , DNA, Neoplasm/biosynthesis , Dose-Response Relationship, Drug , Flow Cytometry , Humans , Nucleic Acid Synthesis Inhibitors/pharmacology , Phosphorylation/drug effects , cdc25 Phosphatases/metabolismABSTRACT
Diabetic nephropathy in type I diabetic patients, as it is currently understood, progresses in a stepwise fashion from normoalbuminuria to microalbuminuria, then to overt proteinuria and progression to chronic renal failure, and ultimately to end-stage renal disease. The role of early blood pressure changes in relation to diabetic nephropathy is now better understood in light of recent data using ambulatory blood pressure monitoring as a means to monitor blood pressure changes noninvasively throughout the day. Cross-sectional studies with type I diabetic patients with microalbuminuria have shown that the normal nocturnal blood pressure often fails to fall normally during sleep. The question of which comes first, microalbuminuria or a rise in blood pressure in patients with type I diabetes, was recently addressed in a prospective study. An increase in systolic blood pressure during sleep precedes the development of microalbuminuria and may play a causative role in its development.
