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This article explores how contemporary developmental psychology, specifically developmental-contextualism, provides a conceptual framework for practice and research by counseling psychologists who work with schools. Developmentalcontextualism articulates how human development (a) is affected by context, (b) involves bio-psycho-social levels, (c) occurs during the life span, and (d) includes strengths and deficits. The authors delineate how these four developmental principles, in conjunctionwith the traditional strengths of counseling psychology, can guide the application of effective interventions with school-aged children and their families.

We examined variation of attack by mountain pine beetle (MPB) (Dendroctonus ponderosae) (Coleoptera: Scolytidae) in a 20-year-old lodgepole pine open-pollinated (OP) family trial composed of 165 OP parent-trees originating from local and nonlocal provenances. Trees were assessed in the summer of 2005 for traits relating to attack, survival, gallery formation, and infection from the fungi associated with MPB, Ophiostoma sp. Successful initial attack was determined by the presence of dead (i.e., red or gray foliage) crowns and the presence of entrance holes from MPB. Eighty-seven percent of the trees still had green crowns in the fall of 2005 (GC05), with family mean differences ranging from 46 to 100%. The mean number of pitch tubes per tree (PT#05) (in a sampling area of 225 cm 2 at breast height) was 1.5 with a range from 0 to 14 per tree. However, for pitch tubes indicating presence or absence (PTP05) of MPB on each tree, 63% of the trees had pitch tubes and family means ranged from 7 to 100%. Significant levels of genetic variation were found for GC05 and PTP05 with narrow-sense heritabilities of 0.20 (SE=0.11) and 0.26 (SE=0.07), respectively. Provenance differences were also significant, indicating that some population structure is present for these "resistance" attributes. The family breeding value correlations between 10-year height growth and PTP05 was 0.22, indicating that at the population level faster growing families may be slightly more subject to attack. An intensive survey of a subsample of 442 trees in the test (selected from 50 families with a range of attack levels) was conducted, and trees were reassessed for the presence of attack, presence of blue stain in the wood, and presence of galleries and egg chambers/eggs in the gallery. Family means ranged from 0 to 57% for blue stain, 11 to 63% for galleries, and 0 to 57% for egg chambers/eggs; however, due to the relatively small sample sizes and the nature of the binary data, family differences were not highly statistically significant. Further research is underway to improve the quantitative genetic parameters and determine the actual mechanisms at work; however, it is clear the MPB does react differently to host genotypes in terms of initial attack.

Premature infants exposed to hyperoxia suffer acute and long-term pulmonary consequences. Nevertheless, neonates survive hyperoxia better than adults. The factors contributing to neonatal hyperoxic tolerance are not fully elucidated. In contrast to adults, heme oxygenase (HO)-1, an endoplasmic reticulum (ER)-anchored protein, is abundant in the neonatal lung but is not inducible in response to hyperoxia. The latter may be important, because very high levels of HO-1 overexpression are associated with significant oxygen cytotoxicity in vitro. Also, in contrast to adults, HO-1 localizes to the nucleus in neonatal mice exposed to hyperoxia. To understand the mechanisms by which HO-1 expression levels and subcellular localization contribute to hyperoxic tolerance in neonates, lung-specific transgenic mice expressing high or low levels of full-length HO-1 (cytoplasmic, HO-1-FL(H) or HO-1-FL(L)) or C-terminally truncated HO-1 (nuclear, Nuc-HO-1-TR) were generated. In HO-1-FL(L), the lungs had a normal alveolar appearance and lesser oxidative damage after hyperoxic exposure. In contrast, in HO-1-FL(H), alveolar wall thickness with type II cell hyperproliferation was observed as well worsened pulmonary function and evidence of abnormal lung cell hyperproliferation in recovery from hyperoxia. In Nuc-HO-1-TR, the lungs had increased DNA oxidative damage, increased poly (ADP-ribose) polymerase (PARP) protein expression, and reduced poly (ADP-ribose) (PAR) hydrolysis as well as reduced pulmonary function in recovery from hyperoxia. These data indicate that low cytoplasmic HO-1 levels protect against hyperoxia-induced lung injury by attenuating oxidative stress, whereas high cytoplasmic HO-1 levels worsen lung injury by increasing proliferation and decreasing apoptosis of alveolar type II cells. Enhanced lung nuclear HO-1 levels impaired recovery from hyperoxic lung injury by disabling PAR-dependent regulation of DNA repair. Lastly both high cytoplasmic and nuclear expression of HO-1 predisposed to long-term abnormal lung cellular proliferation. To maximize HO-1 cytoprotective effects, therapeutic strategies must account for the specific effects of its subcellular localization and expression levels.

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