Field Measurement of Bridges for Long-term Structural Movement, HR-295, 1988

This report describes the field application of the tilt sensing method for monitoring movement of the Black Hawk and Karl King Bridges. The study objectives were: to design a data acquisition system for tilt sensing equipment utilizing a telephone telemetry system; to monitor possible movement of the main span pier, Pier No. 2, on the Black Hawk Bridge in Lansing and the possible long-term movement of Pier No. 4 on the Karl King Bridge in Fort Dodge; and to assess the feasibility, reliability, and accuracy of the instrumentation system used in this study.

Long-Term Structural Movement, HR-275, 1986

This report describes the field application of the tilt sensing method for monitoring movement of the Black Hawk and Karl King Bridges. The study objectives were: to design a data acquisition system for tilt sensing equipment utilizing a telephone telemetry system; to monitor possible movement of the main span pier, Pier No. 2, on the Black Hawk Bridge in Lansing and the possible long-term movement of Pier No. 4 on the Karl King Bridge in Fort Dodge; and to assess the feasibility, reliability, and accuracy of the instrumentation system used in this study.

The role of the δ-opioid receptor in skin homeostasis and wound healing

Au regard des agressions environnementales constantes que la peau doit endurer, l'équilibre fragile entre l'expression et la répression des gènes épidermiques, nécessaire à la différentiation et la prolifération des kératinocytes, pourrait facilement être perturbé en l'absence des mécanismes de stabilisation robustes. La présence d'un système neuroendocrinien local est donc importante afin de coordonner une réponse aux éventuelles irritations. En effet, l'expression de plusieurs neurohormones, des neurotransmetteurs et des neuropeptides, y compris des dérivés pro-opiomélanocortine comme la ß-endorphine et [Met5]-enképhaline, ainsi que l'expression du récepteur 8-opioïde (DOR) a été démontré dans la peau. Cependant, les mécanismes moléculaires par lesquels ils modulent la fonction des kératinocytes sont mal connus. Le présent travail démontre que la voie de signalisation DOR active spécifiquement la voie ERK 1/2 MAPK dans les lignées cellulaires de kératinocytes humains, inhibant la prolifération des cellules et entraîne une diminution de l'épaisseur épidermique dans un modèle organotypique de peau. De plus, l'expression de DOR retarde nettement l'induction de la kératine 10 (KRT 10) et la kératine 1 (KRT 1) dans une modèle 2D de différentiation in vitro, et supprime l'induction de KRT 10 dans un modèle organotypique de peau. Ceci est accompagné de la dérégulation de l'involucrine (IVL), la loricrine (LOR) et la fïlaggrin (FLG), résultant en une induction nettement réduite de leur expression lors de l'initiation de la différentiation in vitro. De plus, POU2F3 a été identifié comme un facteur de transcription régulant les gènes de différentiation des kératinocytes modulés par DOR. Il a été démontré que la régulation négative de POU2F3 via la voie DOR-ERK affecte les principaux aspects de la fonction des kératinocytes. Toutefois, il est évident que des facteurs supplémentaires influencent la fonctionnalité de la voie DOR elle-même. Le calcium et le contact cellule-cellule augmentent la quantité des récepteurs à la surface cellulaire des kératinocytes. Les kératinocytes dont les récepteurs sont internalisés ne répondent pas de la même manière que ceux possédant des récepteurs fonctionnels localisée à la membrane. Ce travail suggère que lors de signaux intrinsèques ou extrinsèques spécifiques, les kératinocytes sont capable de répondre via le système opioïdergique neuro-epidermique. Cette réponse doit être spatialement et temporairement contrôlée afin d'éviter un déséquilibre de l'homéostasie épidermique et un retard de cicatrisation. La compréhension de ce processus très complexe pourrait permettre à terme le développement de meilleurs traitements des affections cutanées pathologiques. En complément des études précédentes sur des souris DOR-défïcientes, ces données suggèrent que l'activation de DOR dans les kératinocytes humains influence la morphogenèse et l'homéostasie de l'épiderme, et pourrait jouer un rôle lors du processus de cicatrisation. - In view of the constant environmental assaults that the skin must endure, the delicate balance of an eloquent sequence of epidermal gene expression and repression, that is required for appropriate differentiation and proliferation of keratinocytes, might easily become derailed in the absence of robust stabilizing mechanisms. The presence of a local neuroendocrine system is thereby important to coordinate a response towards irritations. In fact, the expression of several neurohormones, neurotransmitters, and neuropeptides, including proopiomelanocortin derivatives, such as ß- endorphin and [Met5]-enkephalin has been shown in skin, as well as expression of the 6-opioid receptor (DOR). However, there is currently a lack of understanding of the molecular mechanisms by which their signalling modulates keratinocyte function. The present work demonstrates that DOR signalling specifically activates the ERK 1/2 MAPK pathway in human keratinocyte cell lines. This activation inhibits cell proliferation, resulting in decreased epidermal thickness in an organotypic skin model. Furthermore, DOR expression markedly delays induction of keratin intermediate filament Keratin 10 (KRT 10) and KRT 1 during in vitro differentiation, and abolishes the induction of KRT 10 in the organotypic skin model. This is accompanied by deregulation of involucrin (IVL), loricrin (LOR), and filaggrin (FLG), illustrated by a markedly reduced induction of their expression upon initiation of differentiation in vitro. Additionally, POU2F3 was identified as a transcription factor mediating the DOR induced regulation of keratinocyte differentiation related genes. It was revealed that DOR-mediated ERK-dependent downregulation of this factor affects key aspects of keratinocyte function. However, it is evident that additional triggers influence the functionality of the DOR itself. Calcium at concentrations above 0.1 mM and cell-cell contact both enhance the presence of receptor molecules on the keratinocytes cell surface. Keratinocytes with internalized receptor do not respond to DOR ligands in the same way as keratinocytes with a functional membrane localized receptor.

Psychomotor retardation in depression: bradykinesia or paucity of movement?

Objectives: Psychomotor retardation is part of Major Depression (MD) diagnosis criteria and has been assimilated to bradykinesia, even though there is a clear lack of objective measurement of motor activity in MD. We conducted a study to evaluate bradykinesia, posture and gait parameters in MD patients with an ambulatory system, allowing continuous motor measurements. Methods: Patients with DSM-IV MD and healthy controls matched for age and sex were asked to carry on with their usual activities while being recorded for 6 hours by a wireless autonomous ambulatory system, containing miniature gyroscopes, data-logger, battery and flash memory. allowing continuous recording of upper limbs movements (speed, amplitude and activity (% of time with movement)), posture (% of time standing, walking, lying or sitting) and gait parameters (speed, cadence, stance, double support, stride). Results: Hands activity was significantly lower in depressed patients, as compared to controls (MD: 40%, controls: 60%; p<0.05). Speed of hand movements (p= 0.13) and their amplitude (p=0.71) were similar to controls. MD patients had a trend to spend more time lying or sitting than controls (p=0.06) but did not differ in terms of any gait parameters. Conclusion: Patients with MD displayed less hand movements than controls and tended to spend more time lying or sitting over 6 hours, but did not differ in terms of speed and amplitude of movement, nor in gait parameters. These results suggest that psychomotor retardation classically described in MD might be the expression of a paucity of movement rather than a bradykinesia as observed in parkinsonism and might involved different (nondopaminergic) mechanisms.

Résultats préliminaires de l'enclouage rétrograde de l'humérus [Preliminary results of retrograde nailing of the humerus]

A group of nine patients with a diaphyseal fracture of the humerus and treated with retrograde nailing were studied with a mean follow-up of 15.3 months. Six patients with a humeral fracture without neurological deficit showed a good shoulder and elbow mobility at the last visit. Three patients with neurological lesion preoperatively suffer from a diminished range of movement not related to the surgical procedure. During the operation and postoperatively we found no complication related to the implant and more precisely we could not find a iatrogenic fracture or nervous lesion except one intraoperative lesion of the radial nerve probably related to an important traction movement during reduction with complete remission. Consolidation has been achieved for all fractures but one. This patient suffers from a lesion of the brachial plexus with complete plegia of the arm and a vascular lesion. This patient had to be reoperated for an atrophic non-union by bone grafting and plate fixation. The retrograde nail is a good implant and must be considered in our treatment plans as much as conservative treatment or surgical treatment with plating, anterograde nailing or the use of an external fixator. Only then will we be able to give to the patient the most adapted treatment for his fracture.

Remorin, a solanaceae protein resident in membrane rafts and plasmodesmata, impairs potato virus X movement.

Remorins (REMs) are proteins of unknown function specific to vascular plants. We have used imaging and biochemical approaches and in situ labeling to demonstrate that REM clusters at plasmodesmata and in approximately 70-nm membrane domains, similar to lipid rafts, in the cytosolic leaflet of the plasma membrane. From a manipulation of REM levels in transgenic tomato (Solanum lycopersicum) plants, we show that Potato virus X (PVX) movement is inversely related to REM accumulation. We show that REM can interact physically with the movement protein TRIPLE GENE BLOCK PROTEIN1 from PVX. Based on the localization of REM and its impact on virus macromolecular trafficking, we discuss the potential for lipid rafts to act as functional components in plasmodesmata and the plasma membrane.

Study of the Regulatory Issues Affecting Truck Freight Movement in the Midwest, RB29-013, 2014

This project investigated regulatory issues that may affect or limit freight movement in Iowa and other Midwest states: Illinois, Kansas, Minnesota, Missouri, Nebraska, South Dakota, and Wisconsin. Current state regulations for the following are reviewed and summarized: - Vehicle dimensions - Vehicle weights - Speed limits - Weight compliance enforcement - Fees and taxes - Driver qualifications - Medical certification - Hours of service - Oversize-overweight permits

Mouvements anormaux et accident vasculaire cérébral [Movement disorders in stroke]

Dyskinesias are infrequent presentations in acute stroke (1%). They can be found more frequently as delayed presentations after a stroke, but the prevalence is not available from the literature. The full spectrum of hyper- and hypo-akinetic syndromes has been described, but three main pictures are rather specific of an acute stroke: limb shaking, hemichorea-hemiballism and unilateral asterixis. Besides limb shaking, that seems to reflect a transient diffuse ischemia of the frontosubcortical motor pathway, lesions are described at all levels of the frontosubcortical motor circuit including the sensorimotor frontoparietal cortex, the striatum, the pallidum, the thalamic nuclei, the subthalamic nucleus, the substantia nigra, the cerebellum, the brainstem and their interconnecting pathways, as ischemic or hemorrhagic strokes. The preferentially late development of dyskinesia could reflect the return to a more ancestral motor control level, the most functional possible with the remaining configuration of structures, elaborated by brain plasticity after stroke.

Lake dwellers occupation gap in Lake Geneva (France-Switzerland) possibly explained by an earthquake-mass movement-tsunami event during Early Bronze Age

High-resolution seismic and sediment core data from the 'Grand Lac' basin of Lake Geneva reveal traces of repeated slope instabilities with one main slide-evolved mass-flow (minimum volume 0.13 km3) that originated from the northern lateral slope of the lake near the city of Lausanne. Radiocarbon dating of organic remains sampled from the top of the main deposit gives an age interval of 1865-1608 BC. This date coincides with the age interval for a mass movement event described in the 'Petit Lac' basin of Lake Geneva (1872-1622 BC). Because multiple mass movements took place at the same time in different parts of the lake, we consider the most likely trigger mechanism to be a strong earthquake (Mw 6) that occurred in the period between 1872 and 1608 BC. Based on numerical simulations, we show the major deposit near Lausanne would have generated a tsunami with local wave heights of up to 6 m. The combined effects of the earthquake and the following tsunami provide a possible explanation for a gap in lake dwellers occupation along the shores of Lake Geneva revealed by dendrochronological dating of two palafitte archaeological sites.

Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing.

Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that binds to partners to mediate responses to environmental signals. To investigate its role in the innate immune system, floxed ARNT mice were bred with lysozyme M-Cre recombinase animals to generate lysozyme M-ARNT (LAR) mice with reduced ARNT expression. Myeloid cells of LAR mice had altered mRNA expression and delayed wound healing. Interestingly, when the animals were rendered diabetic, the difference in wound healing between the LAR mice and their littermate controls was no longer present, suggesting that decreased myeloid cell ARNT function may be an important factor in impaired wound healing in diabetes. Deferoxamine (DFO) improves wound healing by increasing hypoxia-inducible factors, which require ARNT for function. DFO was not effective in wounds of LAR mice, again suggesting that myeloid cells are important for normal wound healing and for the full benefit of DFO. These findings suggest that myeloid ARNT is important for immune function and wound healing. Increasing ARNT and, more specifically, myeloid ARNT may be a therapeutic strategy to improve wound healing.

Influence of triamcinolone intravitreal injection on retinochoroidal healing processes.

To analyze the effects of triamcinolone intravitreal injection on the wound healing processes after argon laser retinal photocoagulation, wild type C57BL/6J mice, 8-12 weeks old underwent a standard argon laser photocoagulation protocol. After pentobarbital anesthesia and pupil dilatation, argon laser lesions were induced (50microm, 400mW, 0.05s). Two photocoagulation impacts created two disc diameters from the optic nerve in both eyes. The photocoagulated mice were divided into four groups: Group I (n=12), photocoagulation controls, did not receive any intravitreous injection. Group II (n=12), received an intravitreous injection of 1microl of balanced salt solution (BSS). Group III (n=12), received an intravitreous injection of 1microl containing 15microg of triamcinolone acetonide (TAAC) in BSS. Two mice from each of these three groups were sacrificed at 1, 3, 7, 14 days and 2 and 4 months after photocoagulation. Group IV (n=10) received 1.5, 3, 7.5, 15, or 30microg of TAAC and were all sacrificed on day 14. The enucleated eyes were subjected to systematic analysis of the cellular remodeling processes taking place within the laser lesion and its vicinity. To this purpose, specific antibodies against GFAP, von Willebrand factor, F4/80 and KI67 were used for the detection of astrocytes, activated Müller cells, vascular endothelial cells, infiltrating inflammatory cells and actively proliferating cells. TUNEL reaction was also carried out along with nuclear DAPI staining. Temporal and spatial observations of the created photocoagulation lesions demonstrate that 24h following the argon laser beam, a localized and well-delineated affection of the RPE cells and choroid is observed in mice in Groups I and II. The inner retinal layers in these mice eyes are preserved while TUNEL positive (apoptotic) cells are observed at the retinal outer nuclear layer level. At this stage, intense staining with GFAP is associated with activated retinal astrocytes and Müller cells throughout the laser path. From day 3 after photocoagulation, dilated new choroidal capillaries are detected on the edges of the laser lesion. These processes are accompanied by infiltration of inflammatory cells and the presence of proliferating cells within the lesion site. Mice in Group III treated with 15microg/mul of triamcinolone showed a decreased number of infiltrating inflammatory cells and proliferating cells, which was not statistically significant compared to uninjected laser treated controls. The development of new choroidal capillaries on the edges of the laser lesion was also inhibited during the first 2 months after photocoagulation. However, on month 4 the growth of new vessels was observed in these mice treated with TAAC. Mice of Group IV did not show any development of new capillaries even with small doses. After argon laser photocoagulation of the mouse eye, intravitreal injection of triamcinolone markedly influenced the retina and choroid remodeling and healing processes. Triamcinolone is a powerful inhibitor of the formation of neovessels in this model. However, this inhibition is transient. These observations should provide a practical insight for the mode of TAAC use in patients with wet AMD.

Caveolin expression changes in the neurovascular unit after juvenile traumatic brain injury: signs of blood-brain barrier healing?

Traumatic brain injury (TBI) is one of the major causes of death and disability in pediatrics, and results in a complex cascade of events including the disruption of the blood-brain barrier (BBB). A controlled-cortical impact on post-natal 17 day-old rats induced BBB disruption by IgG extravasation from 1 to 3 days after injury and returned to normal at day 7. In parallel, we characterized the expression of three caveolin isoforms, cav-1, cav-2 and cav-3. While cav-1 and cav-2 are expressed on endothelial cells, both cav-1 and cav-3 were found to be present on reactive astrocytes, in vivo and in vitro. Following TBI, cav-1 expression was increased in blood vessels at 1 and 7 days in the perilesional cortex. An increase of vascular cav-2 expression was observed 7 days after TBI. In contrast, astrocytic cav-3 expression decreased 3 and 7 days after TBI. Activation of eNOS (via its phosphorylation) was detected 1 day after TBI and phospho-eNOS was detected both in association with blood vessels and with astrocytes. The molecular changes involving caveolins occurring in endothelial cells following juvenile-TBI might participate, independently of eNOS activation, to a mechanism of BBB repair while, they might subserve other undefined roles in astrocytes.