17 research outputs found
Three-Dimensional Radiofrequency Tissue Tightening: A Proposed Mechanism and Applications for Body Contouring
The use of radiofrequency energy to produce collagen matrix contraction is presented. Controlling the depth of energy delivery, the power applied, the target skin temperature, and the duration of application of energy at various soft tissue levels produces soft tissue contraction, which is measurable. This technology allows precise soft tissue modeling at multiple levels to enhance the result achieved over traditional suction-assisted lipectomy as well as other forms of energy such as ultrasonic and laser-generated lipolysis
Should complete stripping operation to the ankle be avoided in the treatment of primary varicose veins due to greater saphenous vein insufficiency?
Treatment of varicose veins of lower limb: A prospective randomized comparison of radiofrequency ablation and conventional surgery
Impact of Renal Function on Survival in Patients with Implantable Cardioverter-Defibrillators
Impact of transvenous cardiac implantable electronic devices in chronic hemodialysis patients: a single-center, observational comparative study
Evasion of the p53 tumour surveillance network by tumour-derived MYC mutants
The c-Myc oncoprotein promotes proliferation and apoptosis, such that mutations that disable apoptotic programmes often cooperate with MYC during tumorigenesis. Here we report that two common mutant MYC alleles derived from human Burkitt's lymphoma uncouple proliferation from apoptosis and, as a result, are more effective than wild-type MYC at promoting B cell lymphomagenesis in mice. Mutant MYC proteins retain their ability to stimulate proliferation and activate p53, but are defective at promoting apoptosis due to a failure to induce the BH3-only protein Bim (a member of the B cell lymphoma 2 (Bcl2) family) and effectively inhibit Bcl2. Disruption of apoptosis through enforced expression of Bcl2, or loss of either Bim or p53 function, enables wild-type MYC to produce lymphomas as efficiently as mutant MYC. These data show how parallel apoptotic pathways act together to suppress MYC-induced transformation, and how mutant MYC proteins, by selectively disabling a p53-independent pathway, enable tumour cells to evade p53 action during lymphomagenesis
