The impact of polycyclic aromatic hydrocarbons and fine particles on pregnancy outcome

The relationship between intrauterine growth retardation (IUGR) and exposure to particulate matter [less than/equal to] 10 microm (PM(10)) and particulate matter [less than and equal to] 2.5 microm (PM(2.5))( )in early pregnancy was recently studied in the highly polluted district of Teplice (Northern Bohemia). From this observation rose the question about the possible role of the carcinogenic fraction of polycyclic aromatic hydrocarbons (c-PAHs), which are usually bound to fine particles. The impact of c-PAHs and fine particles on IUGR was analyzed in Teplice and in Prachatice, a region with similarly high c-PAH but low particle levels. All European, single live births occurring in a 4-year period in Teplice (n = 3,378) and Prachatice (n = 1,505) were included. Detailed personal data were obtained via questionnaires and medical records. Mean PM(10), PM(2.5,) and c-PAHs levels during the 9 gestational months (GM) were estimated for each mother. Adjusted odds ratios (AORs) of IUGR for three levels of c-PAHs (low, medium, and high) and for continuous data were estimated after adjustment for a range of covariates using logistic regression models. In the present 4-year sample from Teplice, previously published results about increasing IUGR risk after exposure to particles in the first GM were fully confirmed, but no such effects were found in Prachatice. The AOR of IUGR for fetuses from Teplice exposed to medium levels of c-PAHs in the first GM was 1.60 [confidence interval (CI), 1.06-2. 15], and to high levels 2.15 (CI, 27-3.63). An exposure-response relationship was established by analyzing the continuous data. For each 10 ng increase of c-PAHs in the first GM, the AOR was 1.22 (CI, 1.07-1.39). About the same relationship was observed in Prachatice in spite of the low particle levels. The results prove that exposure to c-PAHs in early gestation may influence fetal growth. The particulate matter-IUGR association observed earlier may be at least partly explained by the presence of c-PAHs on particle surfaces.     

Comparing health inequalities among men aged 18-65 years in Australia and England using the SF-36

OBJECTIVE: To compare the distribution of the domains and summary scores of the SF-36 health survey by occupation-related social classes in England and Australia for employed males age 18-65 years. METHOD: Relative and absolute measures of inequality based on the concentration index were used to examine the distribution of indicators of reported health based on domains and summary scores of the SF-36 across occupation-related social classes in both countries. RESULTS: The degree of inequality is most pronounced in the domains and summary scores of the SF-36 representing aspects of physical health. In regard to comparisons between these countries, there is no significant difference in the distribution of summary scores for physical health. Although there are differences in the summary scores for mental health, there is no evidence of significant inequality in Australia in this aspect of health. CONCLUSIONS: There is a similar pattern of occupation-related health inequality in the physical health dimensions of the SF-36 health survey for employed males age 18-65 years. Implications: Given the similarities in the distribution of measures of physical health in the two countries, it would be useful to assess recent English policy initiatives aimed at reducing health inequalities when developing interventions to tackle inequalities in Australia.     

Heat-shock protein 90 inhibitors as novel cancer chemotherapeutic agents

Heat-shock protein 90 (Hsp90) is a molecular chaperone whose association is required for the stability and function of multiple mutated, chimeric and overexpressed signalling proteins that promote cancer cell growth and/or survival. Hsp90 client proteins include mutated p53, Bcr-Abl, Raf-1, Akt, HER2/Neu (ErbB2) and hypoxia inducible factor-1alpha (HIF-1alpha). Through specific interaction with a single molecular target, Hsp90 inhibitors cause the destabilisation and eventual degradation of Hsp90 client proteins, and they have shown promising antitumour activity in preclinical model systems. One Hsp90 inhibitor, 17-allylamino-geldanamycin (17-AAG), is currently in Phase I clinical trials. Hsp90 inhibitors are unique in that, although they are directed towards a specific molecular target, they simultaneously inhibit multiple signalling pathways on which cancer cells depend for growth and survival. Further, because of the unique effect that Hsp90 inhibition has on cancer cells, combination of an Hsp90 inhibitor with standard chemotherapeutic agents may dramatically increase the in vivo efficacy of the standard agent.     

Brittle nail syndrome: treatment options and the role of the nurse

Dermatology nurses are uniquely positioned to assess brittle nail syndrome, a multifactoral disorder, in conjunction with a physician, and to help develop a therapeutic plan. Once underlying causes are identified, dermatology nurses can support patients in nail care and assist the dermatologist in promoting treatment compliance.     

Grandparents as Parents: Research Findings and Policy Recommendations

This article presents an overview of research on grandparenthood in the latter decades of the twentieth century. Theories contributing to understanding of the grandparenting role are discussed, and significant factors affecting the grandparenting experience—including sex, age, retirement status, race, and ethnicity—are reviewed. The special case of grandparents raising grandchildren is explored through a review of demographics, outcomes for children in grandparent foster care, and the impact of raising grandchildren on grandparents. Interventions supporting custodial grandparents and the grandchildren in their care are examined. Drawing on the findings and implications of this overview, recommendations for policy, clinical practice, professional education, and future research are offered.     

Localization of brain-derived neurotrophic factor and TrkB receptors to postsynaptic densities of adult rat cerebral cortex

Although neurotrophins are critical for neuronal survival and differentiation, recent studies suggest that they also regulate synaptic plasticity. Brain-derived neurotrophic factor (BDNF) rapidly increases synaptic transmission in hippocampal neurons, and enhances long-term potentiation (LTP), a cellular and molecular model of learning and memory. Loci and precise mechanisms of BDNF action remain to be defined: evidence supports both pre- and postsynaptic sites of action. To help elucidate the synaptic mechanisms of BDNF action, we used antisera directed against the extracellular and intracellular domains of trkB receptors, anti-trkBout and anti-trkBin, respectively, to localize the receptors in relation to synapses. Synaptic localization of BDNF was examined in parallel using anti-BDNF antisera. By light microscopy, trkBin and trkBout immunoreactivities were localized to hippocampal neurons and all layers of the overlying visual cortex. Immunoelectron microscopic analysis of the cerebral cortex revealed that trkB and BDNF localize discretely to postsynaptic densities (PSD) of axo-spinous asymmetric synaptic junctions, that are the morphological correlates of excitatory, glutamatergic synapses. TrkB immunoreactivity was also detected in the nucleoplasm by light and electron microscopy. Western blot analysis indicated that both anti-trkBout and anti-trkBin antisera react with a protein band in the PSD corresponding to the molecular weight expected for trkB; however, molecular species distinct from that for trkB were recognized in the nuclear fraction by both anti-trkBin and anti-trkBout antisera, indicating that the nuclear immunoreactivity, seen by immunocytochemistry, reflects cross-reactivity with proteins closely related to, but distinct from, trkB. The PSD localization of both BDNF and trkB supports the contention that this receptor/ligand pair participates in postsynaptic plasticity.