Shaping a Bright Future for Montana Tech: Developing State, National and Global Leaders in Resource Sectors

Presentation by Leigh W. Freeman. Rachel Carson's book Silent Spring published in 1962 marked the birth of concepts leading to the development of mineral resources with a balance of economic, environmental and social imperatives. Montana plays a special role in this story. It is 'the last best place.' As such it can serve as a bell-weather state for Carson's revelations. Consider: Butte as a poster child for legacy problems resulting from resource development under solely economic imperatives; and Montana as a first-adapter in 1971 of state environmental laws based on imperatives heralded with Silent Spring. What better place is there to educate and develop leaders and incubate the future of resource development in global sustainability?

Coronary artery disease is common in asymptomatic patients with signs of myocardial ischemia

BACKGROUND: The incidence of coronary artery disease (CAD) in totally asymptomatic patients with myocardial ischemia during stress testing is unknown. METHODS: 54 patients with asymptomatic myocardial ischemia participated in the Swiss Interventional Study on Silent Ischemia type I (SWISSI I). Asymptomatic myocardial ischemia was verified by bicycle ergometry and stress imaging (echocardiography or scintigraphy). Findings from coronary angiographies in the course of the study constituted the main outcome. RESULTS: Of the 54 study participants, 29 patients (53.7%) underwent coronary angiography. CAD was found in 27 of 29 patients (93.1%). In those 27 patients with CAD, 9 patients (33.3%) suffered from single vessel disease, 9 patients (33.3%) from two vessel disease, and 9 patients (33.3%) from triple vessel disease. Two patients showed left main coronary artery stenosis. CONCLUSION: This study shows a high incidence of relevant CAD among totally asymptomatic patients with myocardial ischemia during stress testing. Previously healthy subjects with exercise-induced ST-segment depression at check-up examinations, even if asymptomatic, should have further diagnostic evaluation.

Corticospinal output and loss of force during motor fatigue

The objective of this study was to analyze central motor output changes in relation to contraction force during motor fatigue. The triple stimulation technique (TST, Magistris et al. in Brain 121(Pt 3):437-450, 1998) was used to quantify a central conduction index (CCI = amplitude ratio of central conduction response and peripheral nerve response, obtained simultaneously by the TST). The CCI removes effects of peripheral fatigue from the quantification. It allows a quantification of the percentage of the entire target muscle motor unit pool driven to discharge by a transcranial magnetic stimulus. Subjects (n = 23) performed repetitive maximal voluntary contractions (MVC) of abductor digiti minimi (duration 1 s, frequency 0.5 Hz) during 2 min. TST recordings were obtained every 15 s, using stimulation intensities sufficient to stimulate all cortical motor neurons (MNs) leading to the target muscle, and during voluntary contractions of 20% of the MVC to facilitate the responses. TST was also repetitively recorded during recovery. This basic exercise protocol was modified in a number of experiments to further characterize influences on CCI of motor fatigue (4 min exercise at 50% MVC; delayed fatigue recovery during local hemostasis, "stimulated exercise" by 20 Hz trains of 1 s duration at 0.5 Hz during 2 min). In addition, the cortical silent period was measured during the basic exercise protocol. Force fatigued to approximately 40% of MVC in all experiments and in all subjects. In all subjects, CCI decreased during exercise, but this decrease varied markedly between subjects. On average, CCI reductions preceded force reductions during exercise, and CCI recovery preceded force recovery. Exercising at 50% for 4 min reduced muscle force more markedly than CCI. Hemostasis induced by a cuff delayed muscle force recovery, but not CCI recovery. Stimulated exercise reduced force markedly, but CCI decreased only marginally. Summarized, force reduction and reduction of the CCI related poorly quantitatively and in time, and voluntary drive was particularly critical to reduce the CCI. The fatigue induced reduction of CCI may result from a central inhibitory phenomenon. Voluntary muscle activation is critical for the CCI reduction, suggesting a primarily supraspinal mechanism.

Simulating in vivo-like Synaptic Input Patterns in Multicompartmental Models

In the laboratory of Dr. Dieter Jaeger at Emory University, we use computer simulations to study how the biophysical properties of neurons—including their three-dimensional structure, passive membrane resistance and capacitance, and active membrane conductances generated by ion channels—affect the way that the neurons transfer synaptic inputs into the action potential streams that represent their output. Because our ultimate goal is to understand how neurons process and relay information in a living animal, we try to make our computer simulations as realistic as possible. As such, the computer models reflect the detailed morphology and all of the ion channels known to exist in the particular neuron types being simulated, and the model neurons are tested with synaptic input patterns that are intended to approximate the inputs that real neurons receive in vivo. The purpose of this workshop tutorial was to explain what we mean by ‘in vivo-like’ synaptic input patterns, and how we introduce these input patterns into our computer simulations using the freely available GENESIS software package (http://www.genesis-sim.org/GENESIS). The presentation was divided into four sections: first, an explanation of what we are talking about when we refer to in vivo-like synaptic input patterns

Die Flüsterkette – Geräuschreduzierung an Fördersystemen

Um die in einem Kunststoffkettenfördersystem auftretenden Geräusche zu reduzieren, wurde ein spezielles Bauteil der Kette im Zweikomponenten-Spritzguss aus einem thermoplastischen Elastomer (TPE) und kettentypischen Kunststoffen gefertigt. Im Rahmen der Entwicklung wurden u. a. Voruntersuchungen zur Haftung zwischen den Werkstoffen durchgeführt. Die neu geschaffene Kette bewirkt eine Verringerung des Schalldruckpegels um 3 4 dB[A] gegenüber herkömmlichen Kunststoffketten im Fördersystem. Das ermöglicht eine Steigerung der Fördergeschwindigkeit um bis zu 30% ohne zusätzliche Lärmbelastung.

Iowa State Daily (January 25, 2012)

ContentsPresident: U.S. is 'built to last'Silent voices no moreCity makes investment in remodel of areaHill: policies must be 'balanced'Wrestlers struggle through season with concussionsPlacement testing would benefit allGrilled cheese recipes offer grown-up twist

Learning by the Dendritic Prediction of Somatic Spiking

Recent modeling of spike-timing-dependent plasticity indicates that plasticity involves as a third factor a local dendritic potential, besides pre- and postsynaptic firing times. We present a simple compartmental neuron model together with a non-Hebbian, biologically plausible learning rule for dendritic synapses where plasticity is modulated by these three factors. In functional terms, the rule seeks to minimize discrepancies between somatic firings and a local dendritic potential. Such prediction errors can arise in our model from stochastic fluctuations as well as from synaptic input, which directly targets the soma. Depending on the nature of this direct input, our plasticity rule subserves supervised or unsupervised learning. When a reward signal modulates the learning rate, reinforcement learning results. Hence a single plasticity rule supports diverse learning paradigms.

The cam-type deformity - what is it: SCFE, osteophyte, or a new disease?

Cam-type deformity of the proximal femur is a risk factor for the development of cam-type femoroacetabular impingement and a prearthrotic condition of the hip. The etiology of cam-type deformity remains unclear. There are a number of causes of cam-type deformity including sequellae of slipped capital femoral epiphysis, Legg-Calvé-Perthes disease or Perthes-like deformities, postinfectious, and traumatic. However, the majority of cam-type deformities arise without any apparent preexisting hip disease. These "idiopathic" cam-type deformities likely represent a majority of cases, and show clear racial and sex differences, as well as developmental and genetic influences. Idiopathic cam-type deformity also seems to be a distinct entity from residual or silent slipped capital femoral epiphysis, as well as osteoarthritis-induced osteophytes. In this paper we examine the different pathogenetic aspects of the proximal femur that contribute to cam-type deformity and/or symptomatic cam-type femoroacetabular impingement.

Natural history of optical coherence tomography-detected non-flow-limiting edge dissections following drug-eluting stent implantation

Aims: Angiographic evidence of edge dissections has been associated with a risk of early stent thrombosis. Optical coherence tomography (OCT) is a high-resolution technology detecting a greater number of edge dissections -particularly non-flow-limiting- compared to angiography. Their natural history and clinical implications remain unclear. The objectives of the present study were to assess the morphology, healing response, and clinical outcomes of OCT-detected edge dissections using serial OCT imaging at baseline and at one year following drug-eluting stent (DES) implantation. Methods and results: Edge dissections were defined as disruptions of the luminal surface in the 5 mm segments proximal and distal to the stent, and categorised as flaps, cavities, double-lumen dissections or fissures. Qualitative and quantitative OCT analyses were performed every 0.5 mm at baseline and one year, and clinical outcomes were assessed. Sixty-three lesions (57 patients) were studied with OCT at baseline and one-year follow-up. Twenty-two non-flow-limiting edge dissections in 21 lesions (20 patients) were identified by OCT; only two (9%) were angiographically visible. Flaps were found in 96% of cases. The median longitudinal dissection length was 2.9 mm (interquartile range [IQR] 1.6-4.2 mm), whereas the circumferential and axial extensions amounted to 1.2 mm (IQR: 0.9-1.7 mm) and 0.6 mm (IQR: 0.4-0.7 mm), respectively. Dissections extended into the media and adventitia in seven (33%) and four (20%) cases, respectively. Eighteen (82%) OCT-detected edge dissections were also evaluated with intravascular ultrasound which identified nine (50%) of these OCT-detected dissections. No stent thrombosis or target lesion revascularisation occurred up to one year. At follow-up, 20 (90%) edge dissections were completely healed on OCT. The two cases exhibiting persistent dissection had the longest flaps (2.81 mm and 2.42 mm) at baseline. Conclusions: OCT-detected edge dissections which are angiographically silent in the majority of cases are not associated with acute stent thrombosis or restenosis up to one-year follow-up.

Linkage in narratives: A comparison between monolingual speakers of French and Italian, and early and late French-Italian bilinguals

In the course of language acquisition learners have to deal with the task of producing narrative texts that are coherent across a range of conceptual domains (space, time, entities) -- both within as well as across utterances. The organization of information is analyzed in this study, on the basis of retellings of a silent film, in terms of devices used in the coordination and subordination of events within the narrative sequence. The focus on subordination reflects a core grammatical difference between Italian and French, as Italian is a null-subject language while French is not. The implications of this contrast for information structure include differences in topic management within the sequence of events. The present study investigates in how far Italian-French bilingual speakers acquire the patterns of monolingual speakers of Italian. It compares how early and late bilinguals of these two languages proceed when linking information in narratives in Italian.

Matching Recall and Storage in Sequence Learning with Spiking Neural Networks

Storing and recalling spiking sequences is a general problem the brain needs to solve. It is, however, unclear what type of biologically plausible learning rule is suited to learn a wide class of spatiotemporal activity patterns in a robust way. Here we consider a recurrent network of stochastic spiking neurons composed of both visible and hidden neurons. We derive a generic learning rule that is matched to the neural dynamics by minimizing an upper bound on the Kullback–Leibler divergence from the target distribution to the model distribution. The derived learning rule is consistent with spike-timing dependent plasticity in that a presynaptic spike preceding a postsynaptic spike elicits potentiation while otherwise depression emerges. Furthermore, the learning rule for synapses that target visible neurons can be matched to the recently proposed voltage-triplet rule. The learning rule for synapses that target hidden neurons is modulated by a global factor, which shares properties with astrocytes and gives rise to testable predictions.

Post-translational regulation of an Aplysia glutamate transporter during long-term facilitation.

Regulation of glutamate transporters accompanies plasticity of some glutamatergic synapses. The regulation of glutamate uptake at the Aplysia sensorimotor synapse during long-term facilitation (LTF) was investigated. Previously, increases in levels of ApGT1 (Aplysia glutamate transporter 1) in synaptic membranes were found to be related to long-term increases in glutamate uptake. In this study, we found that regulation of ApGT1 during LTF appears to occur post-translationally. Serotonin (5-HT) a transmitter that induces LTF did not increase synthesis of ApGT1. A pool of ApGT1 appears to exist in sensory neuron somata, which is transported to the terminals by axonal transport. Blocking the rough endoplasmic reticulum-Golgi-trans-Golgi network (TGN) pathway with Brefeldin A prevented the 5-HT-induced increase of ApGT1 in terminals. Also, 5-HT produced changes in post-translational modifications of ApGT1 as well as changes in the levels of an ApGT1-co-precipitating protein. These results suggest that regulation of trafficking of ApGT1 from the vesicular trafficking system (rough endoplasmic reticulum-Golgi-TGN) in the sensory neuron somata to the terminals by post-translational modifications and protein interactions appears to be the mechanism underlying the increase in ApGT1, and thus, glutamate uptake during memory formation.

Quantitation of contacts among sensory, motor, and serotonergic neurons in the pedal ganglion of aplysia.

Present models of long-term sensitization in Aplysia californica indicate that the enhanced behavioral response is due, at least in part, to outgrowth of sensory neurons mediating defensive withdrawal reflexes. Presumably, this outgrowth strengthens pre-existing connections by formation of new synapses with follower neurons. However, the relationship between the number of sensorimotor contacts and the physiological strength of the connection has never been examined in intact ganglia. As a first step in addressing this issue, we used confocal microscopy to examine sites of contact between sensory and motor neurons in naive animals. Our results revealed relatively few contacts between physiologically connected cells. In addition, the number of contact sites was proportional to the amplitude of the EPSP elicited in the follower motor neuron by direct stimulation of the sensory neuron. This is the first time such a correlation has been observed in the central nervous system. Serotonin is the neurotransmitter most closely examined for its role in modulating synaptic strength at the sensorimotor synapse. However, the structural relationship of serotonergic processes and sensorimotor synapses has never been examined. Surprisingly, serotonergic processes usually made contact with sensory and motor neurons at sites located relatively distant from the sensorimotor synapse. This result implies that heterosynaptic regulation is due to nondirected release of serotonin into the neuropil.

The ubiquitin-proteasome system is necessary for long-term synaptic depression in Aplysia.

The neuropeptide Phe-Met-Arg-Phe-NH(2) (FMRFa) can induce transcription-dependent long-term synaptic depression (LTD) in Aplysia sensorimotor synapses. We investigated the role of the ubiquitin-proteasome system and the regulation of one of its components, ubiquitin C-terminal hydrolase (ap-uch), in LTD. LTD was sensitive to presynaptic inhibition of the proteasome and was associated with upregulation of ap-uch mRNA and protein. This upregulation appeared to be mediated by CREB2, which is generally regarded as a transcription repressor. Binding of CREB2 to the promoter region of ap-uch was accompanied by histone hyperacetylation, suggesting that CREB2 cannot only inhibit but also promote gene expression. CREB2 was phosphorylated after FMRFa, and blocking phospho-CREB2 blocked LTD. In addition to changes in the expression of ap-uch, the synaptic vesicle-associated protein synapsin was downregulated in LTD in a proteasome-dependent manner. These results suggest that proteasome-mediated protein degradation is engaged in LTD and that CREB2 may act as a transcription activator under certain conditions.

TGF-beta1 in Aplysia: role in long-term changes in the excitability of sensory neurons and distribution of TbetaR-II-like immunoreactivity.

Exogenous recombinant human transforming growth factor beta-1 (TGF-beta1) induced long-term facilitation of Aplysia sensory-motor synapses. In addition, 5-HT-induced facilitation was blocked by application of a soluble fragment of the extracellular portion of the TGF-beta1 type II receptor (TbetaR-II), which presumably acted by scavenging an endogenous TGF-beta1-like molecule. Because TbetaR-II is essential for transmembrane signaling by TGF-beta, we sought to determine whether Aplysia tissues contained TbetaR-II and specifically, whether neurons expressed the receptor. Western blot analysis of Aplysia tissue extracts demonstrated the presence of a TbetaR-II-immunoreactive protein in several tissue types. The expression and distribution of TbetaR-II-immunoreactive proteins in the central nervous system was examined by immunohistochemistry to elucidate sites that may be responsive to TGF-beta1 and thus may play a role in synaptic plasticity. Sensory neurons in the ventral-caudal cluster of the pleural ganglion were immunoreactive for TbetaR-II, as well as many neurons in the pedal, abdominal, buccal, and cerebral ganglia. Sensory neurons cultured in isolation and cocultured sensory and motor neurons were also immunoreactive. TGF-beta1 affected the biophysical properties of cultured sensory neurons, inducing an increase of excitability that persisted for at least 48 hr. Furthermore, exposure to TGF-beta1 resulted in a reduction in the firing threshold of sensory neurons. These results provide further support for the hypothesis that TGF-beta1 plays a role in long-term synaptic plasticity in Aplysia.