Paraoxonase gene polymorphisms and haplotype analysis in a stroke population

Peer reviewedPublisher PD

A Pilot investigation into the assessment of changes in the psycholinguistic abilities of new-entrant Māori school children using the Illinois Test of Psycholinguistic Abilities

The role of language as the principal medium of instruction within the New Zealand (N .Z.) educational system has recently received increasing attention both from researchers and those responsible for the formulation of our national educational policy. In particular, much attention has been directed toward the Maori pupil and the use of the English language as the medium for his instruction. The range of literature on this question includes controlled research studies on English usage by Maori children, educational policy statements concerning the - medium of instruction to be employed in New Zealand schools and writings of a more speculative, and potentially political nature, questioning educational policy and the role of language in "Maori education"

A novel formulation for the explicit discretisation of evolving boundaries with application to topology optimisation

Evolving boundaries are an intrinsic part of many physical processes and numerical methods. Most efforts to model evolving boundaries rely on implicit schemes, such as the level-set method (LSM). LSM provides the means to efficiently model the evolution of a boundary, but lacks the ability to transmit information or provide information directly at the boundary. Explicit alternatives based on remeshing or partial-remeshing are often computationally expensive and inherently complex to implement. This work proposes a solution to this dichotomy: a novel finite element method (FEM) based formulation capable of explicitly discretising moving boundaries in an accurate and numerically-efficient way. It couples the floating node method (FNM) with LSM for the first time, which yield a methodology suitable for implementation as user-element in a generic FEM package. The explicitly discretised boundary allows for a new velocity-extension methodology, and a new LSM-reinitialisation procedure, which show benefits in accuracy and efficiency. The potential of this formulation is showcased within topology optimisation, showing greater geometrical accuracy and improvements in the optimum solution attained when compared to implicit methods

Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2

Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-α expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the β-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17β-estradiol (E2) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E2 was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E2 suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E2 inhibition. E2 increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E2 was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GH/JAK/STAT pathway, in which SOCS-2 plays a central mechanistic role

Hypothermic retrograde venous perfusion with adenosine cools the spinal cord and reduces the risk of paraplegia after thoracic aortic clamping

AbstractObjective: We evaluated the utility of retrograde venous perfusion to cool the spinal cord and protect neurologic function during aortic clamping. We hypothesized that hypothermic adenosine would preserve the spinal cord during ischemia. Methods: Six swine (group I) underwent thoracic aortic occlusion for 30 minutes at normothermia. Group II animals underwent spinal cooling by retrograde perfusion of the paravertebral veins with hypothermic (4°C) saline solution during aortic occlusion. The spinal cords of group III animals were cooled with a hypothermic adenosine solution in a similar fashion. Intrathecal temperature was monitored and somatosensory evoked potentials assessed the functional status of spinal pathways. Results: Spinal cooling without systemic hypothermia significantly improved neurologic Tarlov scores in group III (4.8 ± 0.2) and group II (3.8 ± 0.4) when compared with group I scores (1.3 ± 0.6) (P < .001). Furthermore, 5 of the 6 animals in group III displayed completely normal neurologic function, whereas only one animal in group II and no animals in group I did (P = .005). Somatosensory evoked potentials were lost 10.6 ± 1.4 minutes after ischemia in group I. In contrast, spinal cooling caused rapid cessation of neural transmission with loss of somatosensory evoked potentials at 6.9 ± 1.2 minutes in group II and 7.0 ± 0.8 minutes in group III (P = .06). Somatosensory evoked potential amplitudes returned to 85% of baseline in group III and 90% of baseline in group II compared with only 10% of baseline in group I (P = .01). Conclusions: We conclude that retrograde cooling of the spinal cord is possible and protects against ischemic injury and that adenosine enhances this effect. The efficacy of this method may be at least partly attributed to a more rapid reduction in metabolic and electrical activity of the spinal cord during ischemia. (J Thorac Cardiovasc Surg 2000;119:588-95