The effects of hydrocarbon pollution from a two‐stroke outboard engine on the feeding behaviour of Lythrypnus dalli (Perciformes: Gobidae)

Feeding behaviour (time of attack on flake fish food) in Lythrypnus dalli was measured under pollution concentrations of 2.1 and 4.01mgl^?1 total extractable material produced by a two‐stroke outboard engine. The variance of the times increased in pollution versus control treatments for both concentrations. No significant difference was found between the mean times of the control and 2.1 mgl^?1 pollution treatments. A significant difference was found between the mean times of the control and pollution treatments for two different tests at 4.01 mgl^?1. The combination of the increase in mean time of food attack and the increase of variance indicates that pollution concentrations lower than LD50 levels change feeding behaviour, and thus may indirectly effect the survival of the organism.     

Passive and facilitated transport in nuclear pore complexes is largely uncoupled

Nuclear pore complexes provide the sole gateway for the exchange of material between nucleus and cytoplasm of interphase eukaryotic cells. They support two modes of transport: passive diffusion of ions, metabolites, and intermediate-sized macromolecules and facilitated, receptor-mediated translocation of proteins, RNA, and ribonucleoprotein complexes. It is generally assumed that both modes of transport occur through a single diffusion channel located within the central pore of the nuclear pore complex. To test this hypothesis, we studied the mutual effects between transporting molecules utilizing either the same or different modes of translocation. We find that the two modes of transport do not interfere with each other, but molecules utilizing a particular mode of transport do hinder motion of others utilizing the same pathway. We therefore conclude that the two modes of transport are largely segregated.     

Aging-associated reductions in AMP-activated protein kinase activity and mitochondrial biogenesis

Recent studies have demonstrated a strong relationship between aging-associated reductions in mitochondrial function, dysregulated intracellular lipid metabolism, and insulin resistance. Given the important role of the AMP-activated protein kinase (AMPK) in the regulation of fat oxidation and mitochondrial biogenesis, we examined AMPK activity in young and old rats and found that acute stimulation of AMPK-alpha(2) activity by 5'-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and exercise was blunted in skeletal muscle of old rats. Furthermore, mitochondrial biogenesis in response to chronic activation of AMPK with beta-guanidinopropionic acid (beta-GPA) feeding was also diminished in old rats. These results suggest that aging-associated reductions in AMPK activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular lipid metabolism associated with aging.     

Neuroligin-1 loss is associated with reduced tenacity of excitatory synapses

Neuroligins (Nlgns) are postsynaptic, integral membrane cell adhesion molecules that play important roles in the formation, validation, and maturation of synapses in the mammalian central nervous system. Given their prominent roles in the life cycle of synapses, it might be expected that the loss of neuroligin family members would affect the stability of synaptic organization, and ultimately, affect the tenacity and persistence of individual synaptic junctions. Here we examined whether and to what extent the loss of Nlgn-1 affects the dynamics of several key synaptic molecules and the constancy of their contents at individual synapses over time. Fluorescently tagged versions of the postsynaptic scaffold molecule PSD-95, the AMPA-type glutamate receptor subunit GluA2 and the presynaptic vesicle molecule SV2A were expressed in primary cortical cultures from Nlgn-1 KO mice and wild-type (WT) littermates, and live imaging was used to follow the constancy of their contents at individual synapses over periods of 8-12 hours. We found that the loss of Nlgn-1 was associated with larger fluctuations in the synaptic contents of these molecules and a poorer preservation of their contents at individual synapses. Furthermore, rates of synaptic turnover were somewhat greater in neurons from Nlgn-1 knockout mice. Finally, the increased GluA2 redistribution rates observed in neurons from Nlgn-1 knockout mice were negated by suppressing spontaneous network activity. These findings suggest that the loss of Nlgn-1 is associated with some use-dependent destabilization of excitatory synapse organization, and indicate that in the absence of Nlgn-1, the tenacity of excitatory synapses might be somewhat impaired.     

Predation by gulls on crabs in rocky intertidal and shallow subtidal zones of the Gulf of Maine

Most organisms in intertidal areas are marine in origin; many have distributions that extend into the subtidal zone. Terrestrial predators such as mammals and birds may exploit these animals during low tide and can have considerable effects on intertidal food webs. Several studies have shown that avian predators are capable of reducing densities of sessile and slow-moving intertidal invertebrates but very few studies have considered avian predation on mobile invertebrate predators such as crabs. In this study, we investigated predation by Great Black-backed Gulls (Larus marinus Linnaeus) on three species of crabs (Cancer borealis Stimpson, Cancer irroratus Say, and Carcinus maenas Linnaeus). The study was at Appledore Island, ME (a gull breeding island) and 8 other sites throughout the Gulf of Maine, including breeding islands and mainland sites. On Appledore Island, intertidal and subtidal zones provided over one-third of prey remains found at gull nests, and crabs were a substantial proportion (∼ 30% to 40%) of the total remains. Similarly, collections of prey remains from intertidal areas indicated that crabs were by far the most common marine prey. C. borealis was eaten far more often and C. irroratus and C. maenas less often than expected at each site. Comparing numbers of carapaces to densities of crabs in low intertidal and shallow subtidal zones at each site, we estimated that gulls remove between 15% and 64% of C. borealis during diurnal low tides. The proportion of C. borealis eaten by gulls was independent of proximity to a gull colony. Approximately 97% of the outer coast of Maine is within 20 km of a breeding island. Thus, a lot of gull predation on crabs may occur throughout the Gulf of Maine during summer months. Crabs are important predators of other invertebrates; if predation by gulls reduces the number of crabs in intertidal and shallow subtidal areas, gulls may have important indirect effects on intertidal food webs.     

ICAMs Are Not Obligatory for Functional Immune Synapses between Naive CD4 T Cells and Lymph Node DCs

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Semaphorins as Mediators of Neuronal Apoptosis

Shrinkage and collapse of the neuritic network are often observed during the process of neuronal apoptosis. However, the molecular and biochemical basis for the axonal damage associated with neuronal cell death is still unclear. We present evidence for the involvement of axon guidance molecules with repulsive cues in neuronal cell death. Using the differential display approach, an up-regulation of collapsin response mediator protein was detected in sympathetic neurons undergoing dopamine-induced apoptosis. A synchronized induction of mRNA of the secreted collapsin-1 and the intracellular collapsin response mediator protein that preceded commitment of neurons to apoptosis was detected. Antibodies directed against a conserved collapsin-derived peptide provided marked and prolonged protection of several neuronal cell types from dopamine-induced apoptosis. Moreover, neuronal apoptosis was inhibited by antibodies against neuropilin-1, a putative component of the semaphorin III/collapsin-1 receptor. Induction of neuronal apoptosis was also caused by exposure of neurons to semaphorin III-alkaline phosphatase secreted from 293EBNA cells. Anti-collapsin-1 antibodies were effective in blocking the semaphorin III-induced death process. We therefore suggest that, before their death, apoptosis-destined neurons may produce and secrete destructive axon guidance molecules that can affect their neighboring cells and thus transfer a "death signal" across specific and susceptible neuronal populations.     

Spondylodiskitis and endocarditis due to <Emphasis Type="Italic">Streptococcus gordonii</Emphasis>

Background

Streptococcus gordonii is an infrequent cause of infective endocarditis (IE); associated spondylodiskitis has not yet been described in the literature.

Purpose

We describe 2 patients who presented with new-onset, severe back pain; blood cultures revealed S. gordonii bacteremia, which led to the diagnosis of spondylodiskitis and IE. We review our 2-decade experience with S. gordonii bacteremia to describe the clinical and epidemiological characteristics of these patients.

Results

In our hospital over the last 20 years (1998–2017), a total of 15 patients with S. gordonii bacteremia were diagnosed, including 11 men and 4 women, and the mean age was 65 ± 22 (range 23–95). The most common diagnosis was IE (9 patients), spondylodiskitis (the presented 2 patients, who in addition were diagnosed with endocarditis), necrotizing fasciitis (1), sternitis (1), septic arthritis (1) and pneumonia (1). The 11 patients with IE were treated with penicillin ± gentamicin, or ceftriaxone for 6 weeks, 5 required valve surgery and 10/11 (91%) attained complete cure. The 2 patients with diskitis required 2–3 months of intravenous antibiotics to achieve complete cure.

Conclusion

Spondylodiskitis was the presenting symptom of 2/11 (18%) patients with S. gordonii endocarditis. Spondylodiskitis should probably be looked for in patients diagnosed with S. gordonii endocarditis and back pain as duration of antibiotic treatment to achieve complete cure may be considerably longer.