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The eastern Australia coastline is characterized by impressive coastal landforms and an extensive northward-moving longshore drift system that have been influenced by a stable, long-term tectonic history over the Quaternary period. However, the timing and drivers of the formation of two conspicuous landscape features—Fraser Island (K’gari) and the Great Barrier Reef—remain poorly understood. Here we use optically stimulated luminescence and palaeomagnetic dating to constrain the formation of the extensive dunes that make up Fraser Island, the world’s largest sand island, and adjacent Cooloola Sand Mass in southeastern Queensland. We find that both formed between 1.2 Ma and 0.7 Ma, during a global climate reconfiguration across the Middle Pleistocene transition. They formed as a direct result of increased amplitude of sea-level fluctuations associated with increasing global ice volume that redistributed previously stored sediment across the continental shelf. The development of Fraser Island dramatically reduced sediment supply to the continental shelf north of the island. This facilitated widespread coral reef formation in the southern and central Great Barrier Reef and was a necessary precondition for its development. This major reorganization of the coastal sedimentary system is probably not unique to eastern Australia and should be investigated in other passive-margin coastlines.

Stream restoration, such as channel reconfiguration and riparian zone revegetation, is increasing in response to aquatic impairment in agroecosystems. Though riparian zones effectively remove nitrogen (N), conditions that foster nitrate (NO3−) removal (e.g., soil saturation, low oxygen, available carbon) may facilitate the release of soluble reactive phosphorus (SRP) and greenhouse gases (GHGs—carbon dioxide [CO2], methane [CH4], and nitrous oxide [N2O]). In this study, water quality and GHG fluxes were quantified seasonally at agricultural restored, unrestored, and forested riparian zones via networks of wells and static chambers. Carbon dioxide comprised the majority of GHG emissions, and CO2 fluxes were lower at the restored site than the forested site (medians: 0.71 g C m−2 day−1 and 1.29 g C m−2 day−1, respectively). The restored site was a net CH4 source (median: 1.20 mg C m−2 day−1), while the other sites were net CH4 sinks (medians: − 1.00 to − 1.76 mg C m−2 day−1). Sites had comparable N2O emissions. Subsurface SRP was lower at the restored than unrestored agricultural sites, while median NO3− removal efficiency was higher (restored: 91%, unrestored: 35–66%). Over time, NO3− removal and CO2 fluxes increased post-restoration. Methane emissions were elevated when the restored riparian zone was a CO2 and N2O sink and NO3− removal was high. Despite variability within and between sites, seasonal conditions (temperature, water table height, precipitation) and site characteristics (geomorphology, soils) remained key explanatory variables for riparian N removal and GHG release. Overall, riparian restoration may promote N removal without increasing total GHG emissions.

The abdominal wall and musculoskeletal tendons share many anatomic, physiologic, and functional characteristics. This review aims to highlight these similar characteristics and to present a rationale why the treatment principles of successful musculoskeletal tendon reconstruction, including principles of surgical technique and physical therapy, can be used in the treatment of complex abdominal wall reconstruction or ventral hernia repair. The MEDLINE/PubMed database was used to identify published literature relevant to the purpose of this review. There are several anatomical and functional similarities between the linea alba and musculoskeletal tendons. Because of this reason, many of the surgical principles for musculoskeletal tendon repair and ventral hernia repair overlap. Distribution of tension is the main driving principle for both procedures. Suture material and configuration are chosen to maximize tension distribution among the tissue edges, as seen in the standard of care multistrand repairs for musculoskeletal tendons, as well as in the small bites for laparotomy technique described in the STITCH trial. Physical therapy is also one of the mainstays of tendon repair, but surprisingly, is not routine in ventral hernia repair. The evidence surrounding physical therapy prehabilitation and rehabilitation protocols in other disciplines is significant. This review challenges the fact that these protocols are not routinely implemented for ventral hernia repair, and presents the rationale and feasibility for the routine practice of physical therapy in ventral hernia repair.

While the influence of stream restoration on vertical and lateral hyporheic exchange has been documented, impacts on broader riparian zone hydrology have not been thoroughly investigated. We quantified riparian water table dynamics, hydraulic gradient, and groundwater flow paths and fluxes across a range of hydrologic conditions following natural channel design restoration (riparian regrading, in-channel cross-vane structure installation). Water table measurements were collected at least once per season for 2.5 years to capture water levels during baseflow conditions from networks of wells and piezometers at sites with different stream morphology (created riffle-cross-vane-scour pool complexes versus natural pools and riffles), restoration status (agricultural restored, unrestored, forested reference), and riparian characteristics (slope, soils, topography) in North Carolina, USA. The regraded riparian zone had higher near-stream water tables (< 0.5 m below ground surface) than the unrestored site. Riffle-cross-vane complexes induced a zone of low hydraulic gradient that spanned 30–40% of the riparian area, similar to groundwater dynamics near beaver dams. This effect persisted regardless of hydrologic condition (wet or dry) or scour pool status (functioning or filled-in). Riffles also promoted a lower near-stream hydraulic gradient at the forested site. Conversely, the influence of stream features on riparian groundwater was minimal at the unrestored site, where groundwater fluxes were controlled by hillslope inputs and riparian geomorphology. Overall, restoration enhanced stream-riparian zone hydrologic interaction beyond the immediate hyporheic zone. Our work stresses that cross-vanes, even when partially buried by sediments post-restoration, impact whole floodplain hydrology in a more significant way than shown by prior stream restoration studies.

The suprachiasmatic nucleus (SCN) is the master circadian pacemaker in the mammalian brain, responsible for coordinating circadian (ca 24 h) rhythms throughout the body. When individual SCN neurons are dispersed in low density culture, they generate independent circadian oscillations in neuronal firing rate. This observation has led to the widely accepted conclusion that single SCN neurons are autonomous circadian oscillators. More recent studies using bioluminescence imaging to monitor rhythms of clock gene expression have indicated that fibroblasts, too, are autonomous circadian oscillators. But does this mean that the fibroblast should “replace the SCN as the in vitro model of choice”? On the contrary, the SCN is much more than a population of independent cellular oscillators. SCN function depends on important network interactions that allow for cell synchrony, enhanced pacemaker precision, reinforcement of rhythm amplitude, and robustness against genetic perturbations. The distribution of phases of cells within the SCN network also permits variously phased rhythmic output signals, as well as the encoding of seasonal changes in photoperiod and other features of environmental lighting history. Thus, unlike fibroblasts, SCN neurons are designed to be “team players,” and SCN network interactions are integral to the normal function of the SCN as a circadian pacemaker.

This study was designed to investigate the use and impact of a continuous glucose monitoring system (the FreeStyle Navigator) under home-use conditions in the self-management of type 1 diabetes.A 20 day masked phase, when real-time data and alarms were not available, was compared with a subsequent 40 day unmasked phase for a number of specified measures of glycaemic variability. HbA(1c) (measured by DCA 2000) and a hypoglycaemia fear survey were recorded at the start and end of the study.The study included 48 patients with type 1 diabetes (mean age 35.7 +/- 10.9, range 18-61 years; diabetes duration 17.0 +/- 9.5 years). Two patients did not complete the study for personal reasons. Comparing masked (all 20 days) and unmasked (last 20 days) phases, the following reductions were seen: time outside euglycaemia from 11.0 to 9.5 h/day (p = 0.002); glucose SD from 3.5 to 3.2 mmol/l (p0.001); hyperglycaemic time (10.0 mmol/l) from 10.3 to 8.9 h/day (p = 0.0035); mean amplitude of glycaemic excursions (peak to nadir) down by 10% (p0.001); high blood glucose index down by 18% (p = 0.0014); and glycaemic risk assessment diabetes equation score down by 12% (p = 0.0013). Hypoglycaemic time (3.9 mmol/l) decreased from 0.70 to 0.64 h/day without statistical significance (p0.05). Mean HbA(1c) fell from 7.6 +/- 1.1% at baseline to 7.1 +/- 1.1% (p0.001). In the hypoglycaemia fear survey, the patients tended to take less snacks at night-time after wearing the sensor.Home use of a continuous glucose monitoring system has a positive effect on the self-management of diabetes. Thus, continuous glucose monitoring may be a useful tool to decrease glycaemic variability.

As concentrations of greenhouse gases (GHG: N2O, CO2, CH4) continue to increase in the earth’s atmosphere, there is a need to further quantify the contribution of natural systems to atmospheric GHG concentrations. Within this context, characterizing GHG contributions of riparian zones following storms events is especially important. This study documents soil GHG effluxes in a North Carolina riparian zone in the days following both a natural 2.5-cm precipitation event, and that same event associated with the addition of 8.7 cm artificial rainwater in select static chambers. No significant differences in CO2, CH4, and N2O fluxes in response to increased moisture were observed between a depression, a sand bar, and an upland forested area. However, in this water-limited riparian zone, less negative CH4 fluxes (i.e., methane oxidation decreased) and higher CO2 fluxes (i.e., aerobic respiration increased) were observed following precipitation. A short-term burst in N2O emission was observed in the hours after precipitation occurred, but elevated N2O emissions did not persist long enough to turn the site from the N2O sink to a N2O source in the 3 days following the beginning of the experiment. Our results are in contrast with riparian GHG studies in wetter environments and illustrate the importance of water limitation in regulating riparian soil response to precipitation with respect to GHG emissions. More studies should be conducted in water-limited environments (e.g., US southeast/southwest) before management strategies commonly applied in wetter environments (e.g., US Northeast/Midwest) are applied in these regions.

Recent research indicates that riparian zones have the potential to contribute significant amounts of greenhouse gases (GHG: N2O, CO2, CH4) to the atmosphere. Yet, the short-term spatial and temporal variability in GHG emission in these systems is poorly understood. Using two transects of three static chambers at two North Carolina agricultural riparian zones (one restored, one unrestored), we show that estimates of the average GHG flux at the site scale can vary by one order of magnitude depending on whether the mean or the median is used as a measure of central tendency. Because the median tends to mute the effect of outlier points (hot spots and hot moments), we propose that both must be reported or that other more advanced spatial averaging techniques (e.g., kriging, area-weighted average) should be used to estimate GHG fluxes at the site scale. Results also indicate that short-term temporal variability in GHG fluxes (a few days) under seemingly constant temperature and hydrological conditions can be as large as spatial variability at the site scale, suggesting that the scientific community should rethink sampling protocols for GHG at the soil-atmosphere interface to include repeated measures over short periods of time at select chambers to estimate GHG emissions in the field. Although recent advances in technology provide tools to address these challenges, their cost is often too high for widespread implementation. Until technology improves, sampling design strategies will need to be carefully considered to balance cost, time, and spatial and temporal representativeness of measurements.

We examined psychological functioning in siblings of children with Attention Deficit Hyperactivity Disorder (ADHD). Siblings of children diagnosed with ADHD (n = 45) between the ages of 9 and 13 and a control group (n = 46) within the same age range composed of siblings of children with no diagnosed disorders completed measures of psychological functioning. A significant multivariate difference was observed on these measures across groups. Post hoc investigation of the univariate means revealed one significant group difference, which occurred on a measure of Trait Anger. This finding suggests that future research on family members of children with ADHD may be warranted.

Direct evidence for the requirement of transcriptional feedback repression in circadian clock function has been elusive. Here, we developed a molecular genetic screen in mammalian cells to identify mutants of the circadian transcriptional activators CLOCK and BMAL1, which were uncoupled from CRYPTOCHROME (CRY)-mediated transcriptional repression. Notably, mutations in the PER-ARNT-SIM domain of CLOCK and the C terminus of BMAL1 resulted in synergistic insensitivity through reduced physical interactions with CRY. Coexpression of these mutant proteins in cultured fibroblasts caused arrhythmic phenotypes in population and single-cell assays. These data demonstrate that CRY-mediated repression of the CLOCK/BMAL1 complex activity is required for maintenance of circadian rhythmicity and provide formal proof that transcriptional feedback is required for mammalian clock function.

Many psychiatric disorders are characterized by circadian rhythm abnormalities, including disturbed sleep/wake cycles, changes in locomotor activity, and abnormal endocrine function. Animal models with mutations in circadian "clock genes" commonly show disturbances in reward processing, locomotor activity and novelty seeking behaviors, further supporting the idea of a connection between the circadian clock and psychiatric disorders. However, if circadian clock dysfunction is a common risk factor for multiple psychiatric disorders, it is unknown if and how these putative clock abnormalities could be expressed differently, and contribute to multiple, distinct phenotypes. One possible explanation is that the circadian clock modulates the biological responses to stressful environmental factors that vary with an individual's experience. It is known that the circadian clock and the stress response systems are closely related: Circadian clock genes regulate the physiological sensitivity to and rhythmic release of glucocorticoids (GC). In turn, GCs have reciprocal effects on the clock. Since stressful life events or increased vulnerability to stress are risk factors for multiple psychiatric disorders, including post-traumatic stress disorder (PTSD), attention deficit hyperactivity disorder (ADHD), bipolar disorder (BD), major depressive disorder (MDD), alcohol use disorder (AUD) and schizophrenia (SCZ), we propose that modulation of the stress response is a common mechanism by which circadian clock genes affect these illnesses. Presently, we review how molecular components of the circadian clock may contribute to these six psychiatric disorders, and present the hypothesis that modulation of the stress response may constitute a common mechanism by which the circadian clock affects multiple psychiatric disorders.

Recently, developmental neurobiologists have identified multipotential stem cells in the mature nervous systems of vertebrates. The identification of these progenitor cells, which perdure into adulthood, may have important implications for how we think about brain tumor pathology, as we must now consider the possibility that some tumors may arise from these multipotential precursor cells. Currently, neuropathological classification systems are based primarily upon morphological criteria. While these classification systems provide important information regarding prognosis, they have thus far provided little insight into how, from where, and why any given tumor arises. Even prior to having the knowledge that stem cells are present in the adult central nervous system (CNS), several investigators began to explore the idea that antigenic markers, which have proven invaluable to our understanding of what constitutes the normal repertoire of behaviors and lineages of CNS cells, may provide insights into the basic biology of brain tumors. In the following exegesis, we first highlight two papers that review some of the exciting recent advances in developmental neurobiology and point out what implications this may have on our understanding of brain malignancies. We then present several studies in which the investigators sought to test the hypothesis that the antigenic markers that have proved so useful for the developmental neurobiologist may also prove useful in trying to understand the similarities and differences in various categories of brain tumors. While none of these studies demonstrate definitively that brain tumors can or do arise from the aberrant behavior of CNS stem cells, they do provide enough circumstantial evidence that this may be the case to warrant further serious investigation of this hypothesis.

In each circadian cycle, a mouse begins its major activity period with discrete wake onset and activity onset events. The precision with which these events are timed in constant darkness was analyzed using the approach outlined by Pittendrigh and Daan (1976). 1. Negative serial correlations of observed circadian period values (mean r1=−0.471 for wake data, −0.409 for activity data) imply that deviations in period tend to be compensated by opposite deviations in the following cycle. 2. As a result, precision of the circadian pacemaker must be better than that of observed rhythms. Standard deviation of the pacemaker periodσ(Τ) was estimated at 5.1 min. Some individual data series had estimates s(Τ)=0, implying a nearly perfect pacemaker. 3. Previous speculation was that wake onset would be under more direct pacemaker control than activity onset, and would therefore be timed more precisely (Pittendrigh and Daan 1976; Richardson et al. 1985). Contrary to this prediction, intervals between successive wake onsets exhibited significantly greater variance than intervals between successive activity onsets. Two possible interpretations of this finding were proposed.

SINCE the discovery of the large dielectric absorption in aliphatic secondary alcohols1, there have been several papers2–4 published on this subject. The only definite conclusion about the mechanism is that the presence of some lattice defect or arrangement of defects is required for this large absorption3,4.