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Biomedical subjects

John Carroll

Publications and source records attributed to John Carroll.

At least 37 records · Page 2Linked to original sources
PubMed2005

An increase in [Ca2+]i is sufficient but not necessary for driving mitosis in early mouse embryos.

An increase in intracellular Ca2+ concentration ([Ca2+]i) has been shown to drive sea-urchin embryos and some fibroblasts through nuclear-envelope breakdown (NEBD) and the metaphase-to-anaphase transition. Mitotic Ca2+ transients can be pan-cellular global events or localized to the perinuclear region. It is not known whether Ca2+ is a universal regulator of mitosis or whether its role is confined to specific cell types. To test the hypothesis that Ca2+ is a universal regulator of mitosis, we have investigated the role of Ca2+ in mitosis in one-cell mouse embryos. Fertilized embryos generate Ca2+ transients during the first mitotic division. Imposing a Ca2+ transient by photorelease of inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] resulted in acceleration of mitosis entry, suggesting that a [Ca2+]i increase is capable of triggering mitosis. Mitotic Ca2+ transients were inhibited using three independent approaches: injection of intracellular Ca2+ buffers; downregulation of Ins(1,4,5)P3 receptors; and removal of extracellular Ca2+. None of the interventions had any effects on the timing of NEBD or cytokinesis. The possibility that NEBD is driven by localized perinuclear Ca2+ transients was examined using two-photon microscopy but no Ca2+-dependent increases in fluorescence were found to precede NEBD. Finally, the second mitotic division took place in the absence of any detectable [Ca2+]i increase. Thus, although an induced [Ca2+]i increase can accelerate mitosis entry, neither cytosolic nor perinuclear [Ca2+] increases appear to be necessary for progression through mitosis in mouse embryos.

Animals↗
PubMed2005

Impact of stenting and abciximab in patients with diabetes mellitus undergoing primary angioplasty in acute myocardial infarction (the CADILLAC trial).

We sought to determine the benefits of stent implantation and abciximab in patients with diabetes mellitus and acute myocardial infarction (AMI) who underwent primary angioplasty. In a 2-by-2 factorial design, 2,082 patients with AMI were randomly assigned to balloon angioplasty versus stenting, with or without abciximab. Diabetes was present in 346 patients (16.6%). The primary end point was the composite incidence of death, disabling stroke, reinfarction, and ischemic target vessel revascularization (TVR). The primary end point at 1 year occurred significantly more frequently in diabetic than nondiabetic patients (21.9% vs 16.8%, p <0.02), driven by increased rates of death (6.1% vs 3.9%, p = 0.04) and TVR (16.4% vs 12.7%, p = 0.07). Among patients with diabetes, TVR at 1 year was significantly reduced with routine stenting compared with balloon angioplasty (10.3% vs 22.4%, p = 0.004), with no differences in death, reinfarction, or stroke. Angiographic restenosis was also greatly reduced in diabetics randomized to stenting (21.1% vs 47.6%, p = 0.009). No beneficial effects were apparent with abciximab in diabetic patients at 1 year. Despite the improved outcomes with stenting in patients with diabetes, 1-year mortality remained increased in diabetic patients who received stents compared with nondiabetics (8.2% vs 3.6%, p = 0.005). Thus, routine stent implantation in diabetic patients with AMI significantly reduces restenosis and enhances survival free from TVR, independent of abciximab use, although survival remains reduced compared with survival in nondiabetic patients regardless of reperfusion modality.

Abciximab↗