Monitoring and Evaluation of Smolt Migration in the Columbia Basin : Volume XVI : Survival and Transportation Effects for Migrating Snake River Hatchery Chinook Salmon and Steelhead: Historical Estimates from 1996-2003.

In 2005, the University of Washington developed a new statistical model to analyze the combined juvenile and adult detection histories of PIT-tagged salmon migrating through the Federal Columbia River Power System (FCRPS). This model, implemented by software Program ROSTER (River-Ocean Survival and Transportation Effects Routine), has been used to estimate survival and transportation effects on large temporal and spatial scales for PIT-tagged hatchery spring and summer Chinook salmon and steelhead released in the Snake River Basin from 1996 to 2003. Those results are reported here. Annual estimates of the smolt-to-adult return ratio (SAR), juvenile inriver survival from Lower Granite to Bonneville, the ocean return probability from Bonneville to Bonneville, and adult upriver survival from Bonneville to Lower Granite are reported. Annual estimates of transport-inriver (T/I) ratios and differential post-Bonneville mortality (D) are reported on both a systemwide basis, incorporating all transport dams analyzed, and a dam-specific basis. Transportation effects are estimated only for dams where at least 5,000 tagged smolts were transported from a given upstream release group. Because few tagged hatchery steelhead were transported in these years, no transportation effects are estimated for steelhead. Performance measures include age-1-ocean adult returns for steelhead, but not for Chinook salmon. Annual estimates of SAR from Lower Granite back to Lower Granite averaged 0.71% with a standard error (SE) of 0.18% for spring Chinook salmon from the Snake River Basin for tagged groups released from 1996 through 2003, omitting age-1-ocean (jack) returns. For summer Chinook salmon from the Snake River Basin, the estimates of annual SAR averaged 1.15% (SE=0.31%). Only for the release years 1999 and 2000 did the Chinook SAR approach the target value of 2%, identified by the NPCC as the minimum SAR necessary for recovery. Annual estimates of SAR for hatchery steelhead from the Snake River Basin averaged 0.45% (SE=0.11%), including age-1-ocean returns, for release years 1996 through 2003. For release years when the ocean return probability from Bonneville back to Bonneville could be estimated (i.e., 1999 through 2003), it was estimated that on average approximately 86% of the total integrated mortality for nontransported, tagged hatchery spring and summer Chinook, and 74% for steelhead, occurred during the ocean life stage (i.e., from Bonneville to Bonneville). This suggests that additional monitoring and research efforts should include the ocean and estuary environment. Annual estimates of the systemwide T/I are weighted averages of the dam-specific T/I ratios for each transport dam (with {ge} 5,000 tagged fish transported), weighted by the probabilities of being transported at each dam. The systemwide T/I compares the observed SAR under the existing transportation system with the expected SAR if the transportation system had not been operated. Estimates of 1.0 indicate that the systemwide transportation program has no effect on SAR, while estimates > 1.0 indicate that the transportation program increases SAR. Excluding the 2001 release group, the geometric mean of the systemwide T/I estimates for hatchery spring Chinook salmon from the Snake River Basin was 1.15 (SE=0.03) for release years 1997 through 2003. The geometric mean of the systemwide T/I estimates for hatchery summer Chinook salmon from the Snake River Basin was 1.28 (SE=0.13) for release years 1997 through 2000 and 2003. Estimates were much higher for the 2001 release groups. These estimates reflect transportation from Lower Granite and/or Little Goose for most release years, depending on the number of tagged smolts actually transported at each dam during each release year. Differential post-Bonneville mortality (D) is the ratio of post-Bonneville survival to Lower Granite Dam of transported fish to that of nontransported ('inriver') fish. Excluding the 2001 release year, the geometric mean of the D estimates for hatchery spring Chinook salmon from the Snake River Basin was 1.00 (SE=0.09) for release years 1997 through 2003. For hatchery summer Chinook salmon from the Snake River Basin, the geometric mean of the D estimates was 1.32 (SE=0.27) for release years 1997 through 2000 and 2003. These estimates reflect transportation from Lower Granite and/or Little Goose, depending on the number of tagged smolts actually transported at each dam during each release year. Approximately half the point estimates of D for both spring and summer Chinook salmon were 1.0 or greater, indicating that for those release groups, transported fish did not have lower ocean and adult survival than nontransported fish. For those years with estimates of D < 1.0, the systemwide T/I estimates were always {ge} 1.0, indicating that despite lower ocean and adult survival of transported fish, transportation did not lower SAR overall

Monitoring and Evaluation of Smolt Migration in the Columbia Basin : Volume XVIII: Survival and Transportation Effects of Migrating Snake River Wild Chinook Salmon and Steelhead: Historical Estimates From 1996-2004 and Comparison to Hatchery Results. Draft.

The combined juvenile and adult detection histories of PIT-tagged wild salmonids migrating through the Federal Columbia River Power System (FCRPS) were analyzed using the ROSTER (River-Ocean Survival and Transportation Effects Routine) statistical release-recapture model. This model, implemented by software Program ROSTER, was used to estimate survival on large temporal and spatial scales for PIT-tagged wild spring and summer Chinook salmon and steelhead released in the Snake River Basin upstream of Lower Granite Dam from 1996 to 2004. In addition, annual results from wild salmonids were compared with results from hatchery salmonids, which were presented in a previous report in this series (Buchanan, R. A., Skalski, J. R., Lady, J. L., Westhagen, P., Griswold, J., and Smith, S. 2007, 'Survival and Transportation Effects for Migrating Snake River Hatchery Chinook Salmon and Steelhead: Historical Estimates from 1996-2003', Technical report, Bonneville Power Administration, Project 1991-051-00). These results are reported here. Annual estimates of the smolt-to-adult return ratio (SAR), juvenile inriver survival from Lower Granite to Bonneville, the ocean return probability from Bonneville to Bonneville, and adult upriver survival from Bonneville to Lower Granite are reported. Annual estimates of transport-inriver (T/I) ratios and differential post-Bonneville mortality (D) are reported on a dam-specific basis for release years with sufficient numbers of wild PIT-tagged smolts transported. Transportation effects are estimated only for dams where at least 1,000 tagged wild smolts were transported from a given upstream release group. Because few wild Chinook salmon and steelhead tagged upstream of Lower Granite Dam were transported before the 2003 release year, T/I and D were estimated only for the 2003 and 2004 release years. Performance measures include age-1-ocean adult returns for steelhead, but not for Chinook salmon. Spring and summer Chinook salmon release groups were pooled across the entire Snake River Basin upstream of Lower Granite Dam for this report. Annual estimates of SAR from Lower Granite back to Lower Granite averaged 0.92% with an estimated standard error (dSE) of 0.25% for wild spring and summer Chinook salmon for tagged groups released from 1996 through 2004, omitting age-1-ocean (jack) returns. Only for the 1999 and 2000 release years did the wild Chinook SAR approach the target value of 2%, identified by the NPCC as the minimum SAR necessary for recovery. Annual estimates of SAR for wild steelhead from the Snake River Basin averaged 0.63% (dSE = 0.15%), including age-1-ocean returns, for release years 1996 through 2004. For release years when the ocean return probability from Bonneville back to Bonneville could be estimated (i.e., 1999 through 2004), it was estimated that on average approximately 83% of the total integrated mortality for nontransported, tagged wild spring and summer Chinook, and 78% for steelhead (omitting the 2001 release year), occurred during the ocean life stage (i.e., from Bonneville to Bonneville). This suggests that additional monitoring and research efforts should include the ocean and estuary environment. Annual estimates of the dam-specific T/I for Lower Granite Dam were available for the 2003 and 2004 release years for both wild Chinook salmon and wild steelhead. The estimated T/I for Lower Granite was significantly > 1.0 for Chinook in 2004 (P < 0.0001) and for steelhead in both 2003 (P < 0.0001) and 2004 (P < 0.0001), indicating that for these release years, wild fish transported at Lower Granite returned there in higher proportions than fish that were returned to the river at Lower Granite, or that passed Lower Granite without detection as juveniles. Annual estimates of the dam-specific T/I for Little Goose Dam were available for wild Chinook salmon for both 2003 and 2004. The estimated T/I for Little Goose was significantly > 1.0 for wild Chinook in 2004 (P = 0.0024), but not in 2003 (P = 0.1554). Differential post-Bonneville mortality (D) is the ratio of post-Bonneville survival to Lower Granite Dam of transported fish to that of nontransported ('inriver') fish. Estimates of D were available for transportation from Lower Granite and Little Goose dams in 2003 and 2004 for wild Chinook, and from Lower Granite Dam in 2003 and 2004 for wild steelhead. Point estimates ranged from 0.74 (dSE = 0.29) for transportation of wild Chinook salmon from Lower Granite Dam in 2003 to 1.91 (dSE = 0.61) for transportation of wild steelhead from Lower Granite Dam in 2003. Small transport groups resulted in high uncertainty on the point estimates, and only for 2003 steelhead transported from Lower Granite Dam did transported fish have significantly greater post-Bonneville survival than nontransported fish (P = 0.0213)

Meox2 Haploinsufficiency Accelerates Axonal Degeneration in DBA/2J Glaucoma.

Purpose: Glaucoma is a complex disease with major risk factors including advancing age and increased intraocular pressure (IOP). Dissecting these earliest events will likely identify new avenues for therapeutics. Previously, we performed transcriptional profiling in DBA/2J (D2) mice, a widely used mouse model relevant to glaucoma. Here, we use these data to identify and test regulators of early gene expression changes in DBA/2J glaucoma. Methods: Upstream regulator analysis (URA) in Ingenuity Pathway Analysis was performed to identify potential master regulators of differentially expressed genes. The function of one putative regulator, mesenchyme homeobox 2 (Meox2), was tested using a combination of genetic, biochemical, and immunofluorescence approaches. Results: URA identified Meox2 as a potential regulator of early gene expression changes in the optic nerve head (ONH) of DBA/2J mice. Meox2 haploinsufficiency did not affect the characteristic diseases of the iris or IOP elevation seen in DBA/2J mice but did cause a significant increase in the numbers of eyes with axon damage compared to controls. While young mice appeared normal, aged Meox2 haploinsufficient DBA/2J mice showed a 44% reduction in MEOX2 protein levels. This correlated with modulation of age- and disease-specific vascular and myeloid alterations. Conclusions: Our data support a model whereby Meox2 controls IOP-dependent vascular remodeling and neuroinflammation to promote axon survival. Promoting these earliest responses prior to IOP elevation may be a viable neuroprotective strategy to delay or prevent human glaucoma

Enhancing face validity of mouse models of Alzheimer\u27s disease with natural genetic variation.

Classical laboratory strains show limited genetic diversity and do not harness natural genetic variation. Mouse models relevant to Alzheimer\u27s disease (AD) have largely been developed using these classical laboratory strains, such as C57BL/6J (B6), and this has likely contributed to the failure of translation of findings from mice to the clinic. Therefore, here we test the potential for natural genetic variation to enhance the translatability of AD mouse models. Two widely used AD-relevant transgenes, APPswe and PS1de9 (APP/PS1), were backcrossed from B6 to three wild-derived strains CAST/EiJ, WSB/EiJ, PWK/PhJ, representative of three Mus musculus subspecies. These new AD strains were characterized using metabolic, functional, neuropathological and transcriptional assays. Strain-, sex- and genotype-specific differences were observed in cognitive ability, neurodegeneration, plaque load, cerebrovascular health and cerebral amyloid angiopathy. Analyses of brain transcriptional data showed strain was the greatest driver of variation. We identified significant variation in myeloid cell numbers in wild type mice of different strains as well as significant differences in plaque-associated myeloid responses in APP/PS1 mice between the strains. Collectively, these data support the use of wild-derived strains to better model the complexity of human AD

Assessment of protein allergenicity on the basis of immune reactivity: animal models.

Because of the public concern surrounding the issue of the safety of genetically modified organisms, it is critical to have appropriate methodologies to aid investigators in identifying potential hazards associated with consumption of foods produced with these materials. A recent panel of experts convened by the Food and Agriculture Organization and World Health Organization suggested there is scientific evidence that using data from animal studies will contribute important information regarding the allergenicity of foods derived from biotechnology. This view has given further impetus to the development of suitable animal models for allergenicity assessment. This article is a review of what has been achieved and what still has to be accomplished regarding several different animal models. Progress made in the design and evaluation of models in the rat, the mouse, the dog and in swine is reviewed and discussed

Are Small Effects the Indispensable Foundation for a Cumulative Psychological Science? A Reply to Götz et al. (2022).

Götz et al. (2022) argue that small effects are “the indispensable foundation for a cumulative psychological science”. They support their argument by claiming that (i) psychology, like genetics, consists of complex phenomena explained by additive small effects, (ii) psychological research culture rewards large effects, which means small effects are being ignored, and (iii) small effects become meaningful at scale and over time. We rebut these claims with three objections: (i) the analogy between genetics and psychology is misleading, (ii) p-values are the main currency for publication in psychology, meaning that any biases in the literature are (currently) caused by a pressure to publish statistically significant results and not large effects, and (iii) claims regarding small effects as important and consequential must be supported by empirical evidence or, at least, a falsifiable line of reasoning. If accepted uncritically, we believe the arguments of Götz et al. (2022) could be used as a blanket justification for the importance of any and all ‘small’ effects, thereby undermining best practices in effect size interpretation. We end with guidance on evaluating effect sizes in relative, not absolute terms

Survival of Juvenile Chinook Salmon Passing the Bonneville Dam Spillway in 2007

The U.S. Army Corps of Engineers Portland District (CENWP) funds numerous evaluations of fish passage and survival on the Columbia River. In 2007, the CENWP asked Pacific Northwest National Laboratory to conduct an acoustic telemetry study to estimate the survival of juvenile Chinook salmon passing the spillway at Bonneville Dam. This report documents the study results which are intended to be used to improve the conditions juvenile anadromous fish experience when passing through the dams that the Corps operates on the river

Associations of β-Amyloid and Vascular Burden With Rates of Neurodegeneration in Cognitively Normal Members of the 1946 British Birth Cohort

OBJECTIVE: To quantify the independent and interactive associations of amyloid-β (Aβ) and white matter hyperintensity volume (WMHV) - a marker of presumed cerebrovascular disease (CVD) - with rates of neurodegeneration, and to examine the contributions of APOE ε4 and vascular risk measured at different stages of adulthood in cognitively normal members of the 1946 British birth cohort. METHODS: Participants underwent brain MRI and florbetapir-Aβ positron emission tomography as part of Insight 46, an observational population-based study. Changes in whole brain, ventricular and hippocampal volume were directly measured from baseline and repeat volumetric T1 MRI using the Boundary Shift Integral. Linear regression was used to test associations with: baseline Aβ deposition; baseline WMHV; APOE ε4; and office-based Framingham heart study-cardiovascular risk scores (FHS-CVS) and systolic blood pressure (BP) at ages 36, 53 and 69 years. RESULTS: 346 cognitively normal participants (mean [SD] age at baseline scan 70.5 [0.6] years; 48% female) had high-quality T1 MRI data from both time-points (mean [SD] scan interval 2.4 [0.2] years). Being Aβ positive at baseline was associated with 0.87 ml/year faster whole brain atrophy (95% CI 0.03, 1.72), 0.39 ml/year greater ventricular expansion (95% CI 0.16, 0.64) and 0.016 ml/year faster hippocampal atrophy (95% CI 0.004, 0.027), while each 10 ml additional WMHV at baseline was associated with 1.07 ml/year faster whole brain atrophy (95% CI 0.47, 1.67), 0.31 ml/year greater ventricular expansion (95% CI 0.13, 0.60) and 0.014 ml/year faster hippocampal atrophy (95% CI 0.006, 0.022). These contributions were independent and there was no evidence that Aβ and WMHV interacted in their effects. There were no independent associations of APOE ε4 with rates of neurodegeneration after adjusting for Aβ status and WMHV, and no clear relationships between FHS-CVS or systolic BP and rates of neurodegeneration when assessed across the whole sample, nor any evidence that they acted synergistically with Aβ. CONCLUSIONS: Aβ and presumed CVD have distinct and additive effects on rates of neurodegeneration in cognitively normal elderly. These findings have implications for the use of MRI measures as biomarkers of neurodegeneration and emphasize the importance of risk management and early intervention targeting both pathways