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Biomedical subjects

Peter C Weber

Publications and source records attributed to Peter C Weber.

27 records · Page 2Linked to original sources
PubMed2003

HMG-CoA reductase inhibitors induce apoptosis in neointima-derived vascular smooth muscle cells.

In the context of atherogenesis and restenosis, vascular smooth muscle cell (SMC) proliferation and apoptosis play a crucial role. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) have been shown to inhibit the migration and proliferation of SMC, and to induce apoptosis in different cell types including SMC. However, it is not known whether these agents induce apoptosis in neointimal SMC. We investigated the effects of statin treatment on neointimal SMC as compared to medial cells by using trypan blue counting, MTT test, Annexin V staining, cell cycle analysis and a co-culture model. The incubation of neointimal or medial SMC with lovastatin reduced the MTT activity as well as the total cell number, and increased the amount of trypan blue positive cells, indicative of cell death. We tested by staining with Annexin V/propidium iodide, specific antibodies to active caspase-3, TUNEL reaction, and by the appearance of a sub-G1 peak, whether the observed increase in cell death was due to apoptosis. After treatment with lovastatin, programmed cell death was slightly increased in medial SMC, while neointimal cells showed a pronounced rate of apoptosis. In an attempt to mimic early phases of restenosis in vitro by seeding low density neointimal cells onto high density medial cells, we found that statin treatment induced cell death preferentially in the neointimal SMC. Our results suggest that statins enhance the rate of apoptosis in neointimal SMC, which may be an interesting feature to reduce restenosis after successful angioplasty.

Animals↗
PubMed2003

Endothelial progenitor cells: isolation and characterization.

Bone marrow of adults contains a subtype of progenitor cells that have the capacity to differentiate into mature endothelial cells and have therefore been termed endothelial progenitor cells (EPCs). Of the three cell markers (CD133, CD34, and the vascular endothelial growth factor receptor 2) that characterize the early functional EPCs, located predominantly in the bone marrow, EPCs obviously lose CD133/CD34 and start to express CD31, vascular endothelial cadherin, and von Willebrand factor when migrating to the circulation. Various isolation procedures of EPCs from different sources by using adherence culture or magnetic microbeads have been described, but published findings with regard to the number of EPCs in the peripheral circulation of healthy adults are scanty and no data regarding the lifetime of EPCs in vivo exist. Clinical studies employing EPCs for neovascularization of ischemic organs have just been started; however, the mechanisms stimulating or inhibiting the differentiation of bone marrow-derived EPCs in vivo and the signals causing their adhesion, migration, and homing to sites of injured tissue are largely unknown at present.

Cell Separation↗
PubMed2002

Sphingosine 1-phosphate dynamically regulates myosin light chain phosphatase activity in human endothelial cells.

Sphingosine 1-phosphate (S1P) is known to induce reorganization of the actin cytoskeleton through activation of the GTPase Rho. We have investigated the dynamic behavior of Rho/Rho kinase-regulated myosin light chain (MLC) phosphatase activity and MLC phosphorylation in Human Umbilical Vein Endothelial Cells (HUVEC) stimulated with S1P. Immediately (30-60 s) after S1P stimulation, MLC phosphatase activity dropped and MLC phosphorylation increased in a Rho/Rho kinase-dependent manner. Shortly thereafter (2 min), MLC phosphatase increased above baseline and MLC phosphorylation correspondingly decreased to near control values. At this time point, formation of actin ruffles and Rac activity assays indicated activation of Rac. Finally, between 5 and 15 min, MLC phosphatase dropped to a plateau below baseline. In parallel, MLC phosphorylation became constantly elevated above control values. These findings indicate that S1P is able to induce dynamic cycles of MLC phosphatase deactivation and activation. This novel feature of S1P could contribute to its chemotactic and angiogenic activity.

Actin Cytoskeleton↗
PubMed2002

Medical and surgical considerations for implantable hearing prosthetic devices.

Today, technology allows us the opportunity to make a substantial difference in the quality of life for individuals who have been unsuccessful with traditional amplification. This article examines the medical and surgical aspects of four types of implantable hearing devices: bone-anchored hearing aid (BAHA), middle ear implants, cochlear implants, and auditory brainstem implants.

Acoustic Stimulation↗
PubMedDate not supplied

Outcome of hearing and vertigo after surgery for congenital perilymphatic fistula in children.

PURPOSE: To determine if surgery to repair a perilymphatic fistula (PLF) has any significant morbidity and to determine the outcome of the surgery in regards to hearing and vertiginous symptoms. MATERIALS AND METHODS: A retrospective study was performed with all patients undergoing PLF repair at a tertiary medical center. Each patient was assessed for comparison of their pre- and postoperative hearing levels, vertiginous complaints, and recurrences. RESULTS: One hundred sixty ears were operated on for PLF over a 13-year period. Of the 103 ears positive for PLF, 92% either stabilized or improved their hearing and 3% noticed a decrease, but this was well after surgery and not believed to be related. These results were similar in the non-PLF ears in which 95% had stabilized or improved hearing and again 3% had a much delayed decrease. Of the children who had vertiginous complaints before surgery, 91% were improved or stable. Only 1 child felt somewhat worse, but, as in the hearing loss, this was greater than 6 months after the surgery. CONCLUSIONS: Surgical repair of PLF does not result in a significant risk for postoperative hearing loss or additional vertiginous complaints. Surgical repair may prevent further deterioration of hearing loss even in those patients in whom a PLF was not identified at the time of surgery.

Adolescent↗
PubMedDate not supplied

Use of Alloderm in the neurotologic setting.

PURPOSE: To determine whether Alloderm (Life Cell Corporation, The Woodlands, TX) can be used to cover canal wall down mastoid defects, as well as repair dural defects from translabyrinthine and transpetrosal approaches to the skull base. METHODS: A retrospective analysis was performed at an academic tertiary care medical center. Eighteen patients were operated on with canal wall down mastoidectomies, and Alloderm was used to reconstruct the tympanic membrane and line the mastoid cavity. Eleven patients had dural defects reconstructed after skull base approach surgery. We wanted to determine whether the Alloderm graft healed in canal wall down mastoidectomy procedures with good epithelialization. For the skull base approaches, we determined whether a cerebrospinal fluid leak had occurred. RESULTS: The 18 patients who were reconstructed with an Alloderm graft after a canal wall down mastoidectomy all had good epithelialization. As with fascia reconstruction, some granulation tissue occurred, but this was easily controlled in the office setting. Of the 11 patients who underwent reconstruction for skull base surgery approaches, none developed a cerebrospinal fluid leak. CONCLUSION: Alloderm may provide a suitable grafting material when fascia is either not readily available, or the size of the defect precludes the use of fascia.

Adolescent↗