36 research outputs found
Reconfigurable Photonic Crystal Cavities
Photonic crystals are optical structures that contain a periodic modulation of their refractive index, allowing them to control light in recent years of an unprecedented capacity. Photonic crystals may take on a variety of configurations, in particular the photonic crystal cavity, which may “hold” light in small volumes comparable to the light’s wavelength. This capability to spatially confine light opens up countless possibilities to explore for research in telecommunications, quantum electrodynamics experiments and high-resolution sensor applications. However, the vast functionality potentially made available by photonic crystal cavities is limited due to the difficulty in redefining photonic crystal components once they are formed in their (typically) solid material. The work presented in this thesis investigates several approaches to overcome this issue by reconfiguring photonic crystal cavities
The toxicity of very prolonged courses of PEGasparaginase or Erwinia asparaginase in relation to asparaginase activity, with a special focus on dyslipidemia
Aggravated bone density decline following symptomatic osteonecrosis in children with acute lymphoblastic leukemia
Osteonecrosis and decline of bone density are serious side effects during and after treatment of childhood acute lymphoblastic leukemia. It is unknown whether osteonecrosis and low bone density occur together in the same patients, or whether these two osteogenic side-effects can mutually influence each other's development. Bone density and the incidence of symptomatic osteonecrosis were prospectively assessed in a national cohort of 466 patients with acute lymphoblastic leukemia (4-18 years of age) who were treated according to the dexamethasone-based Dutch Child Oncology Group-ALL9 protocol. Bone mineral density of the lumbar spine (BMDLS) (n= 466) and of the total body (BMDTB) (n=106) was measured by dual X-ray absorptiometry. Bone density was expressed as age-and gender-matched standard deviation scores. Thirty patients (6.4%) suffered from symptomatic osteonecrosis. At baseline, BMDLS and BMDTB did not differ between patients who did or did not develop osteonecrosis. At cessation of treatment, patients with osteonecrosis had lower mean BMDLS and BMDTB than patients without osteonecrosis (respectively, with osteonecrosis: -2.16 versus without osteonecrosis: -1.21, P</p
Aggravated bone density decline following symptomatic osteonecrosis in children with acute lymphoblastic leukemia
Intragraft platelet-derived growth factor-alpha and transforming growth factor-beta1 during the development of accelerated graft vascular disease after clinical heart transplantation
Cyclosporine A downregulates intragraft platelet-derived growth factor-alpha mRNA expression after clinical heart transplantation
Intragraft platelet-derived growth factor-alpha and transforming growth factor-beta1 during the development of accelerated graft vascular disease after clinical heart transplantation
This study was to determine whether the growth factors platelet-derived growth factor-alpha (PDGF-alpha) and transforming growth factor-beta1 (TGF-beta1) contribute to the development of graft vascular disease (GVD) after clinical heart transplantation. We analysed intragraft PDGF-alpha and TGF-beta1 messenger RNA (mRNA) expression levels by competitive template reverse transcriptase polymerase chain reaction (RT-PCR). Endomyocardial biopsies (EMB) were obtained at 1 and 9 months post-transplant from cardiac allograft recipients with (n = 11) and without (n = 11) angiographic evidence of GVD at 1 year. In 1-month EMB, comparable TGF-beta1 mRNA levels were found in patients with and without GVD at 1 year (p = 0.84, Mann-Whitney U-test). In contrast, in 9-month EMB during the development of GVD, intragraft mRNA levels of both PDGF-alpha (p = 0.08) and TGF-beta1 (p = 0.03) were higher in patients with GVD after the first year compared to patients without GVD. These results suggest that intragraft PDGF-alpha and TGF-beta1 play a role in the pathogenesis of accelerated GVD after clinical heart transplantation