Influence of a high‐head dam as a dispersal barrier to fish community structure of the Upper Mississippi River

In river systems, high‐head dams may increase the distance‐decay of fish community similarity by creating nearly impermeable dispersal barriers to certain species from upstream reaches. Substantial evidence suggests that migratory species are impacted by dams, and most previous studies in stream/river networks have focused on small streams and headwaters. Here, we assess whether a high‐head dam (Lock and Dam 19; LD 19) on a large river, the Upper Mississippi River (UMR), substantially alters fish community structure relative to variability expected to occur independent of the dam's effect as a fish dispersal barrier. Using fish catch per unit effort data, we modelled the distance‐decay function for the UMR fish community and then estimated the similarity that would be expected to occur across LD19 and compared it with measured similarity. Measured similarity in the fish community above and below LD19 was close to the expected value based on the distance‐decay function, suggesting LD19 does not create an abrupt transition in the fish community. Although some migratory fish species no longer occur above LD19 (e.g., skipjack herring, Alosa chrysochloris), these species do not occur in high abundance below the dam and so do not drive variation in fish community structure. Instead, much of the variation in species structure is driven by the loss/gain of species across the latitudinal gradient. Lock and Dam 19 does not appear to be a clear transition point in the river's fish community, although it may function as a meaningful barrier for particular species (e.g., invasive species) and warrant future attention from a management perspective.     

Characterisation of flucloxacillin and 5-hydroxymethyl flucloxacillin haptenated HSA in vitro and in vivo

Flucloxacillin is a synthetic penicillin used in the treatment of Staphylococcal infections. Adverse reactions to the drug are believed to arise through covalent modification of proteins, with tissue damage occurring secondary to an immune reaction. Serum proteins have been shown by adduct-specific antibodies to be modified by flucloxacillin, but the nature and sites of modification have not been characterised. Here, in vitro studies on HSA have shown by MS that the modification of protein lysine residues occurs in a dose-, time- and site-dependent manner. Affinity, cation exchange and reversed phase chromatography prior to MS revealed in vivo modification of HSA with flucloxacillin in tolerant patients, with up to nine modified lysine residues being detected in each patient, and with modification of Lys190 and Lys212 being detected in 8/8 patients. It was also revealed for the first time that plasma proteins could be modified with the 5-hydroxymethyl metabolite of flucloxacillin, and that essentially the same Lys residues were targeted by both the parent drug and its metabolite. This study provides a detailed characterisation of sites of chemical modification of an endogenous target and reveals candidate peptides for T-cell and antibody assays of flucloxacillin hypersensitivity.     

The role of anergy in peripheral T cell unresponsiveness

When a T cell's encounter with specific antigen results in good signaling through the T cell antigen receptor yet does not lead to a proliferative response, the T cell enters a state of nonresponsiveness, or anergy. Anergy induction can result from a number of different situations, including antigen presentation by costimulation-deficient or "non-professional" antigen presenting cells, pharmacological blocking of T cell proliferation, or chronic stimulation of the T cell receptor by antigen. Anergy is a long-lived but temporary state characterized by a profound inability of the T cell to produce IL-2. Other effector functions may be affected to variable degrees. Anergy has been characterized most carefully under in vitro conditions, but several experimental models have demonstrated that T cells can also become anergic in vivo. This mechanism for tolerance induction may help to ensure that any mature autoreactive T cells which escape thymic deletion are unable to respond to host tissues. Furthermore, an understanding of the mechanism of anergy induction will most certainly lead to beneficial clinical applications, including improving graft acceptance and avoiding such deleterious immune responses as autoimmunity and allergy.     

An integrated behavioral medicine approach to improving care of patients with diabetes mellitus

A detailed approach to integrating behavioral techniques into patient education, case management, and treatment evaluation of persons with diabetes mellitus is offered. The author asks a series of "what if" questions to stimulate new thinking about ways to improve patient-physician relations in overcoming problems in managing the condition, citing recent research findings in the field. Adherence to regimens, self-management, goals of an integrated diabetes program and steps along the way to achieving it, psychophysiologic mechanisms in glucose metabolism, and the function of social support are among the topics covered.     

Electrophysiological assessment of primary cortical neurons genetically engineered using iron oxide nanoparticles

The development of safe technologies to genetically modify neurons is of great interest in regenerative neurology,for both translational and basic science applications.Such approaches have conventionally been heavily reliant on viral transduction methods,which have safety and production limitations.Magnetofection (magnet-assisted gene transfer using iron oxide nanoparticles as vectors) has emerged as a highly promising non-viral alternative for safe and reproducible genetic modification of neurons.Despite the high potential of this technology,there is an important gap in our knowledge of the safety of this approach,namely,whether it alters neuronal function in adverse ways,such as by altering neuronal excitability and signaling.We have investigated the effects of magnetofection in primary cortical neurons by examining neuronal excitability using the whole cell patch clamp technique.We found no evidence that magnetofection alters the voltage-dependent sodium and potassium ionic currents that underpin excitability.Our study provides important new data supporting magnetofection as a safe technology for bioengineering of neuronal cell populations.     

Evolution or revolution: where next for impact assessment?

Impact assessment (IA) has become one of the most prevalent environmental policy instruments today. Its introduction under the National Environmental Policy Act (US) in 1969 was revolutionary. Perhaps it is not surprising, then, that such a widely used tool has received its share of criticism, including that it fails to meet some of its fundamental goals. Over the last fifty years, IA has broadened in scope and application and embraced new techniques. It has followed evolved, but has not changed fundamentally.

We believe that IA must continue to change to meet the societal and environmental challenges of the 21^st century. But will it be enough for IA to progress through incremental change (evolution), or is a complete overhaul of impact assessment (revolution) needed? We provide some ideas as to what ‘evolution’ and ‘revolution’ may look like, but rather then offering a definitive way forward now, we invite stakeholders to present their thoughts and suggestions at the IAIA19 Annual Conference in Brisbane, which carries the same theme as the title of this article.     

Photo‐stimulatory effect of LLLT on the proliferation rate of human monocytic leukaemia cells

Low‐level laser therapy (LLLT) is a form of phototherapy used to promote cell proliferation. This study investigates the potential role of LLLT in cellular proliferation of human monocytic leukaemia cells Tamm‐Horsfall Protein 1 (THP‐1) under in vitro conditions. Cells were irradiated with an 850 nm diode laser and exposed to doses ranging from 0 to 26.8 J/cm². After irradiation, cells were incubated for 12 and 24 h to allow time for proliferation. Comet assay was conducted to evaluate genotoxicity of the irradiated cells. Trypan blue was used to estimate cytotoxicity, which peaked at the highest dose as expected. Preliminary results suggest that cell counts increase at low doses, whereas a decrease in cell number at high doses was noted compared with controls. Comet assay showed no significant difference between irradiated and non‐irradiated cells at low doses. In contrast, DNA damage increased at doses ≥8.9 J/cm² and was comparable with the 100 μM hydrogen peroxide positive control at the highest fluence. It could be concluded that LLLT has the ability to stimulate the THP‐1 cell line to proliferate if supplied with the correct energy and dose.Inspec keywords: photodynamic therapy, laser applications in medicine, cellular effects of radiation, biological effects of laser radiation, DNA, diseases, semiconductor lasersOther keywords: photo‐stimulatory effect, LLLT, human monocytic leukaemia cells, cell proliferation rate, low‐level laser therapy, phototherapy, THP‐1, Comet assay, Trypan blue, cytotoxicity, DNA damage, wavelength 850 nm, time 12 h, time 24 h     

Acute vasoconstriction after subarachnoid hemorrhage

OBJECTIVE: Decreased cerebral blood flow (CBF) and cerebral ischemia occurring immediately after subarachnoid hemorrhage (SAH) may be caused by acute microvascular constriction. However, CBF can also be influenced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the significance of acute vasoconstriction after SAH and its relationship to changes in CBF, ICP, CPP, and extracellular glutamate concentrations. METHODS: Three experiments were performed using the endovascular filament technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated with the 24-hour mortality rate. In the second experiment, rats undergoing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of the internal carotid and anterior cerebral arteries and correlation with CBF, ICP, and CPP. In the third experiment (n = 11), extracellular glutamate concentrations determined by hippocampal and cortical microdialysis and high performance liquid chromatography were correlated with physiological changes. RESULTS: CBF reductions to less than 40% of baseline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define "lethal" SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate. The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracellular glutamate concentration increased to 600% of baseline after lethal SAH in both hippocampus and cortex and was inversely correlated with CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. CONCLUSION: Acute vasoconstriction after SAH occurs independently of changes in ICP and CPP and is associated with decreased CBF, larger hemorrhage size, persistent elevations of extracellular glutamate, and poor outcome. Acute vasoconstriction seems to contribute directly to ischemic brain injury after SAH. Further evaluations of pharmacological agents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.