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Plasticity in life history traits is commonly used to explain the invasion success of social insects. While intraspecific plasticity is often recognized, interspecific variability is easily overlooked, whereby different species exhibit different strategies. The presence of many queens per colony and the collapse of colony boundaries have favored invasiveness for many ant species. However, these strategies are absent from other successful social invaders. Here, we report that various life-history traits may differentially enhance the invasion success in social insects. We suggest that other aspects of their breeding system, like asexual reproduction, intranidal mating and pre-adaptation to inbreeding may enhance their invasion success. Thorough comparative studies between native and introduced populations or studies of closely related species will help identify additional traits favoring the invasion success of social insects, and ultimately provide a more comprehensive picture of the evolutionary factors enhancing invasiveness across this phylogenetically and ecologically diverse group.
To compare 5-year change in femorotibial cartilage thickness in 121 young, active adults with an acute anterior cruciate ligament (ACL) tear randomized to a strategy of structured rehabilitation plus early ACL reconstruction (ACLR) or structured rehabilitation plus optional delayed ACLR.
62 patients were randomized to early ACLR, 59 to optional delayed ACLR. Magnetic resonance imaging (MRI) was acquired within 4 weeks of injury, at two- and 5-years follow-up. Main outcome was 5-year change in overall femorotibial cartilage thickness. Secondary outcomes included the location-independent cartilage ChangeScore, summarizing thinning and thickening in 16 femorotibial subregions. An exploratory as-treated comparison was performed additionally.
Baseline and at least one follow-up MRI were available for 117 patients. Over 5 years, a comparable increase in overall femorotibial cartilage thickness was observed for patients randomized to early ACLR (n=59) and patients randomized to optional delayed ACLR (n=58, adjusted mean difference-5μm, 95% CI [-118, 108]μm). STZ inhibitor solubility dmso However, the location-independent cartilage ChangeScore was greater in those treated with early ACLR than in patients treated with optional delayed ACLR (adjusted mean difference 403μm [119, 687]μm). As-treated analysis showed no between-group differences for the main outcome, while the location-independent cartilage ChangeScore was greater for patients treated with early (adjusted mean difference 632μm [268, 996]μm) or delayed ACLR (adjusted mean difference 449μm [108, 791]μm) than for patients treated with rehabilitation alone.
In young active adults with acute ACL-injury, choice of treatment strategy for the injured ACL did not modify the magnitude of 5-year change in overall femorotibial cartilage thickness.
ISRCTN84752559.
ISRCTN84752559.Noradrenergic neurotransmission may play an important role in tremor modulation through its innervation of key structures of the central tremor circuits. Here, Parkinson's disease (PD) patients with (PDT+) or without (PDT-) rest tremor had 11C-methylreboxetine(11C-MeNER) positron emission tomography (PET) to test the hypothesis that noradrenaline terminal function was relatively preserved in PDT+ compared to PDT-.
Sixty-five PD patients and 28 healthy controls (HC) were scanned with
C-MeNER PET. Patients were categorized as PD
if subscores in UPDRS-III item 3 or MDS-UPDRS-III item 17 was ≥2; remaining were categorized as PD
. Simplified reference tissue model 2 distribution volume ratios (DVR) for
C-MeNER were calculated for thalamus, dorsal and median raphe, locus coeruleus (LC) and red nucleus using time activity curves (TACs) obtained from volumes of interest (VOI). Data were statistically interrogated with a general linear mixed model using 'region', and 'group' as factors and the interaction of 'nd thalamus compared with PDT+ is in line with earlier in-vitro studies and could potentially contribute to their tremor negative phenotype.Finely-tuned gamma (FTG) oscillations can be recorded from cortex or the subthalamic nucleus (STN) in patients with Parkinson's disease (PD) on dopaminergic medication, and have been associated with dyskinesias. When recorded during deep brain stimulation (DBS) on medication the FTG is entrained to half the stimulation frequency. We investigated whether these characteristics are shared off medication by recording local field potentials (LFP) from the STN from externalised DBS leads in 14 PD patients after overnight withdrawal of medication. FTG was induced de-novo by DBS in the absence of dyskinesias in a third of our cohort. The FTG could outlast stimulation or arise only after DBS ceased. FTG frequencies decreased during and across consecutive DBS blocks, but did not shift with changing stimulation frequency off medication. Together with the sustained after-effects this argues against simple entrainment by DBS in the off medication state. We also found significant coherence between STN-LFP and electroencephalogram (EEG) signals at FTG frequencies. We conclude that FTG is a network phenomenon that behaves differently in the off medication state, when it is neither associated with dyskinesias nor susceptible to entrainment.Despite concerted efforts to identify CNS regeneration strategies, an incomplete understanding of how the needed molecular machinery is regulated limits progress. Here we use models of lateral compression and FEJOTA clip contusion-compression spinal cord injury (SCI) to identify the thrombin receptor (Protease Activated Receptor 1 (PAR1)) as an integral facet of this machine with roles in regulating neurite growth through a growth factor- and cholesterol-dependent mechanism. Functional recovery and signs of neural repair, including expression of cholesterol biosynthesis machinery and markers of axonal and synaptic integrity, were all increased after SCI in PAR1 knockout female mice, while PTEN was decreased. Notably, PAR1 differentially regulated HMGCS1, a gene encoding a rate-limiting enzyme in cholesterol production, across the neuronal and astroglial compartments of the intact versus injured spinal cord. Pharmacologic inhibition of cortical neuron PAR1 using vorapaxar in vitro also decreased PTEN and promoted neurite outgrowth in a cholesterol dependent manner, including that driven by suboptimal brain derived neurotrophic factor (BDNF).
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