Sea-level change and storm surges in the context of climate change

This paper reviews the latest research in New Zealand surrounding the issues of sea-level rise and extreme sea levels in the context of global warming and variability in the Pacific-wide El Nino– Southern Oscillation (ENSO). Past records of climate, sea level (excluding tides) and sea and air temperatures have shown that they are continuously fluctuating over various long-term timescales of years, decades and centuries. This has made it very difficult to determine whether the anthropogenic effects such as increased levels of “greenhouse” gases are having an accelerating effect on global sea levels or an increased incidence of extreme storms. Over the past century, global sea level has risen by 10–25 cm, and is in line with the rise in relative sea level at New Zealand’s main ports of +1.7 mm yr –1. What has become very clear is the need to better understand interannual (year-to-year) and decadal variability in sea-level, as these larger signals of the order of 5–15 cm in annual-mean sea level have a significant “flow-on” effect on the long-term trend in sea level. The paper describes sea level variability in northern New Zealand—both long- and short-term—involved in assessing the regional trends in sea level. The paper also discusses the relative contributions of tides, barometric pressure and wind set-up in causing extreme sea levels during storm surges. Some recent research also looked at a related question—Is there any sign of increased storminess, and hence storm surge, in northern New Zealand due to climate change? The paper concludes that, while no one can be completely sure how sea-level and the degree of storminess will respond in the near future, what is clear is that interannual and decadal variability in sea level is inextricably linked with Pacific-wide ENSO response and longer inter-decadal shifts in the Pacific climate regime, such as the latest shift in 1976

Regional diversity in the murine cortical vascular network is revealed by synchrotron X-ray tomography and is amplified with age

Cortical bone is permeated by a system of pores, occupied by the blood supply and osteocytes. With ageing, bone mass reduction and disruption of the microstructure are associated with reduced vascular supply. Insight into the regulation of the blood supply to the bone could enhance the understanding of bone strength determinants and fracture healing. Using synchrotron radiation-based computed tomography, the distribution of vascular canals and osteocyte lacunae was assessed in murine cortical bone and the influence of age on these parameters was investigated. The tibiofibular junction from 15-week- and 10-month-old female C57BL/6J mice were imaged post-mortem. Vascular canals and three-dimensional spatial relationships between osteocyte lacunae and bone surfaces were computed for both age groups. At 15 weeks, the posterior region of the tibiofibular junction had a higher vascular canal volume density than the anterior, lateral and medial regions. Intracortical vascular networks in anterior and posterior regions were also different, with connectedness in the posterior higher than the anterior at 15 weeks. By 10 months, cortices were thinner, with cortical area fraction and vascular density reduced, but only in the posterior cortex. This provided the first evidence of age-related effects on murine bone porosity due to the location of the intracortical vasculature. Targeting the vasculature to modulate bone porosity could provide an effective way to treat degenerative bone diseases, such as osteoporosis

Metabolic Energy Correlates of Heart Rate Variability Spectral Power Associated with a 900-Calorie Challenge

We studied healthy males challenged with a 900 Cal test beverage and correlated EE with the raw (ms2) and normalized units (nu) of total power (TP), low frequency/high frequency (LF/HF) and VLF spectral power of heart rate variability (HRV). The correlations were evaluated during 20 min of normal breathing (NB, control) and 20 min of paced breathing (PB) at 12 breaths·min−1 (0.2 Hz). EE was not significantly correlated with any of the HRV variables before the metabolic challenge. After the challenge, EE was positively correlated with LF/HF and with VLF; VLF was also positively correlated with LF/HF during both NB and PB. These findings suggest that EE may be a correlate of LF/HF and of VLF spectral power of HRV in healthy adolescent/young adult males. The association of lower resting energy expenditure with lower amounts of VLF spectral power may occur in individuals with predilections for obese phenotypes

Twenty Thousand-Year-Old Huts at a Hunter-Gatherer Settlement in Eastern Jordan

Ten thousand years before Neolithic farmers settled in permanent villages, hunter-gatherer groups of the Epipalaeolithic period (c. 22–11,600 cal BP) inhabited much of southwest Asia. The latest Epipalaeolithic phase (Natufian) is well-known for the appearance of stone-built houses, complex site organization, a sedentary lifestyle and social complexity—precursors for a Neolithic way of life. In contrast, pre-Natufian sites are much less well known and generally considered as campsites for small groups of seasonally-mobile hunter-gatherers. Work at the Early and Middle Epipalaeolithic aggregation site of Kharaneh IV in eastern Jordan highlights that some of these earlier sites were large aggregation base camps not unlike those of the Natufian and contributes to ongoing debates on their duration of occupation. Here we discuss the excavation of two 20,000-year-old hut structures at Kharaneh IV that pre-date the renowned stone houses of the Natufian. Exceptionally dense and extensive occupational deposits exhibit repeated habitation over prolonged periods, and contain structural remains associated with exotic and potentially symbolic caches of objects (shell, red ochre, and burnt horn cores) that indicate substantial settlement of the site pre-dating the Natufian and outside of the Natufian homeland as currently understood

Whole genome sequence data implicate RBFOX1 in epilepsy risk in baboons

Background: Baboons exhibit a genetic generalized epilepsy (GGE) that resembles juvenile myoclonic epilepsy and may represent a suitable genetic model for human epilepsy. The genetic underpinnings of epilepsy were investigated in a baboon colony at the Southwest National Primate Research Center (San Antonio, TX) through the analysis of whole-genome sequence (WGS) data. Methods: Baboon WGS data were obtained for 38 cases and 19 healthy controls from the NCBI Sequence Read Archive and, after standard QC filtering, two subsets of variants were examined: (1) 20,881 SNPs from baboon homologs of 19 candidate GGE genes; and (2) 36,169 protein-altering SNPs. Association tests were conducted in SOLAR, and gene set enrichment analyses (GSEA) and protein-protein interaction (PPI) network construction were performed on genome-wide significant association results (Pn= 441 genes). Results: Heritability for epileptic seizure in the pedigreed baboon sample was estimated at 0.76 (SE=0.77; P=0.07). A significant association was detected for an intronic SNP in RBFOX1 (P=5.92 × 10-6; adjusted P=0.016). For protein-altering variants, GSEA revealed significant positive enrichment for genes involved in the extracellular matrix structure (ECM; FDR=0.0072) and collagen formation (FDR=0.017). Conclusions: SNP association results implicate RBFOX1 in baboon epilepsy, a gene that plays a key role in neuronal excitation and transcriptomic regulation, and has been previously linked to human epilepsy, both focal and generalized. Moreover, protein-damaging variants from across the baboon genome exhibit a wider pattern of association that links collagen-containing ECM to epilepsy risk. These findings suggest a shared genetic etiology between baboon and human forms of GGE

Influence of age, sex and genetic factors on the human brain

We report effects of age, age(2), sex and additive genetic factors on variability in gray matter thickness, surface area and white matter integrity in 1,010 subjects from the Genetics of Brain Structure and Function Study. Age was more strongly associated with gray matter thickness and fractional anisotropy of water diffusion in white matter tracts, while sex was more strongly associated with gray matter surface area. Widespread heritability of neuroanatomic traits was observed, suggesting that brain structure is under strong genetic control. Furthermore, our findings indicate that neuroimaging-based measurements of cerebral variability are sensitive to genetic mediation. Fundamental studies of genetic influence on the brain will help inform gene discovery initiatives in both clinical and normative samples

Penal Agnosis and Historical Denial: Problematising ‘Common Sense’ Understandings of Prison Officers and Violence in Prison

The aim of this chapter is to consider if the much-publicised ‘causal relationship’ between prison officer numbers and prisoner violence is a form of ‘penal agnosis’: the cultural production of penal ignorance (Proctor, Agnotology: a missing term to describe the cultural production of ignorance. In R. Proctor & L. Schiebinger (Eds.), Agnotology: the making and unmaking of ignorance. Stanford: Stanford University Press, 2008). My use of penal agnosis draws directly from the writings of Cohen (States of denial. Cambridge: Polity, 2001) and Mathiesen (Silently silenced. Winchester: Waterside Press, 2004). Silencing techniques deployed in everyday life help to keep people quiet and neutralise criticism. Whilst these are varied, of particular concern here is when an event becomes “isolated in the present” (Mathiesen, Silently silenced. Winchester: Waterside Press, 2004: 42), specifically contemporary media and political discussions of prison officers and prison violence. This chapter provides a theoretical context to the invisibility of historical evidence regarding the deeply embedded harms and violence of penal confinement. It focuses on how the narrative of prison staffing levels is not only time-locked but also how the current understandings of the relationship with violence are derived primarily from the perspective of prison officers. Through critique of this approach an alternative space is opened for thinking differently about how to best respond to the current harms and violence of incarceration

Genetic basis of neurocognitive decline and reduced white-matter integrity in normal human brain aging

Identification of genes associated with brain aging should markedly improve our understanding of the biological processes that govern normal age-related decline. However, challenges to identifying genes that facilitate successful brain aging are considerable, including a lack of established phenotypes and difficulties in modeling the effects of aging per se, rather than genes that influence the underlying trait. In a large cohort of randomly selected pedigrees (n = 1,129 subjects), we documented profound aging effects from young adulthood to old age (18-83 y) on neurocognitive ability and diffusion-based white-matter measures. Despite significant phenotypic correlation between white-matter integrity and tests of processing speed, working memory, declarative memory, and intelligence, no evidence for pleiotropy between these classes of phenotypes was observed. Applying an advanced quantitative gene-by-environment interaction analysis where age is treated as an environmental factor, we demonstrate a heritable basis for neurocognitive deterioration as a function of age. Furthermore, by decomposing gene-by-aging (G × A) interactions, we infer that different genes influence some neurocognitive traits as a function of age, whereas other neurocognitive traits are influenced by the same genes, but to differential levels, from young adulthood to old age. In contrast, increasing white-matter incoherence with age appears to be nongenetic. These results clearly demonstrate that traits sensitive to the genetic influences on brain aging can be identified, a critical first step in delineating the biological mechanisms of successful aging