Tributary use and large-scale movements of grass carp in Lake Erie

Infrequent captures of invasive, non-native grass carp (Ctenopharyngodon idella) have occurred in Lake Erie over the last 30+ years, with recent evidence suggesting wild reproduction in the lake’s western basin (WB) is occurring. Information on grass carp movements in the Laurentian Great Lakes is lacking, but an improved understanding of large-scale movements and potential areas of aggregation will help inform control strategies and risk assessment if grass carp spread to other parts of Lake Erie and other Great Lakes. Twenty-three grass carp captured in Lake Erie’s WB were implanted with acoustic transmitters and released. Movements were monitored with acoustic receivers deployed throughout Lake Erie and elsewhere in the Great Lakes. Grass carp dispersed up to 236 km, with approximately 25% of fish dispersing greater than 100 km from their release location. Mean daily movements ranged from <0.01 to 2.49 km/day, with the highest daily averages occurring in the spring and summer. The Sandusky, Detroit, and Maumee Rivers, and Plum Creek were the most heavily used WB tributaries. Seventeen percent of grass carp moved into Lake Erie’s central or eastern basins, although all fish eventually returned to the WB. One fish emigrated from Lake Erie through the Huron-Erie Corridor and into Lake Huron. Based on our results, past assessments may have underestimated the potential for grass carp to spread in the Great Lakes. We recommend focusing grass carp control efforts on Sandusky River and Plum Creek given their high use by tagged fish, and secondarily on Maumee and Detroit Rivers.     

Spatial ecology of common carp (Cyprinus carpio) in Lake Winnipeg and its potential for management actions

Common carp feeding and spawning behaviours negatively impact the functioning of marsh ecosystems. In the Netley-Libau Marsh, situated on the southern end of Lake Winnipeg, water level regulations, nonpoint source nutrient pollution, and the non-native common carp are thought to be the main contributors to the degradation of the marsh habitat. Using acoustic telemetry, we analysed the movement rate, frequency and timing of suspected spawning migrations, spatial ecology, and aggregation of common carp in the Lake Winnipeg drainage over a three year time period. Common carp moved the farthest during the open water period when water temperature was >5 °C. Their annual migration into Netley-Libau Marsh was correlated to ordinal date. Common carp left the marsh in late spring/early summer, presumably feeding in Lake Winnipeg, before moving to overwintering sites situated in Traverse Bay and Lake Winnipeg, where they arrived typically by October and formed aggregations. These findings will inform habitat and fisheries managers in the effort to undertake evidence-based management actions. The predictability of the movements and the tendency for common carp to aggregate indicates that exclusion techniques and commercial fishing may represent viable management solutions.     

A probabilistic fire-protection siting model with joint vehicle reliability requirements

A probabilistic fire-protection siting model is described that places capacitated stations, engine companies, and truck companies in such a way that the population or calls covered by an engineand a truck with a joint reliability of at least is maximized. Probabilistic constraints are developed and numerical equivalents are found for the probability requirement for proximate server presence. The multiple co-location of servers at stations and the use of stations with a limited capacity are also investigated. Structures are utilized that preserve the integer properties when the model is solved by linear programming relaxation.An earlier version of this paper was presented at the 37th North American Meetings, Boston, November 1990.     

The Neurovascular Unit Dysfunction in Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. Histopathologically, AD presents with two hallmarks: neurofibrillary tangles (NFTs), and aggregates of amyloid β peptide (Aβ) both in the brain parenchyma as neuritic plaques, and around blood vessels as cerebral amyloid angiopathy (CAA). According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia. Hypoxia may reduce Aβ clearance from the brain and increase its production, leading to both parenchymal and vascular accumulation of Aβ. An increase in Aβ amplifies neuronal dysfunction, NFT formation, and accelerates neurodegeneration, resulting in dementia. In recent decades, therapeutic approaches have attempted to decrease the levels of abnormal Aβ or tau levels in the AD brain. However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition. Here, we review the pathogenesis and potential therapeutic targets associated with dysfunction of the NVU in AD.     

Insoluble Vascular Amyloid Deposits Trigger Disruption of the Neurovascular Unit in Alzheimer’s Disease Brains

Alzheimer’s disease (AD) is a neurodegenerative disease, characterized histopathologically by intra-neuronal tau-related lesions and by the accumulation of amyloid β-peptide (Aβ) in the brain parenchyma and around cerebral blood vessels. According to the vascular hypothesis of AD, an alteration in the neurovascular unit (NVU) could lead to Aβ vascular accumulation and promote neuronal dysfunction, accelerating neurodegeneration and dementia. To date, the effects of insoluble vascular Aβ deposits on the NVU and the blood–brain barrier (BBB) are unknown. In this study, we analyze different Aβ species and their association with the cells that make up the NVU. We evaluated post-mortem AD brain tissue. Multiple immunofluorescence assays were performed against different species of Aβ and the main elements that constitute the NVU. Our results showed that there are insoluble vascular deposits of both full-length and truncated Aβ species. Besides, insoluble aggregates are associated with a decrease in the phenotype of the cellular components that constitute the NVU and with BBB disruption. This approach could help identify new therapeutic targets against key molecules and receptors in the NVU that can prevent the accumulation of vascular fibrillar Aβ in AD.     

Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7

Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with congenital fiber type disproportion and muscle weakness. The molecular mechanisms underlying muscle dysfunction in this disease remain unclear. Here, we observed that this mutation causes an abnormally high Ca²⁺-sensitivity of myofilaments in vitro and in muscle fibers. To determine the critical conformational changes that myosin, actin, and tropomyosin undergo during the ATPase cycle and the alterations in these changes caused by R90P replacement in Tpm3.12, we used polarized fluorimetry. It was shown that the R90P mutation inhibits the ability of tropomyosin to shift towards the outer domains of actin, which is accompanied by the almost complete depression of troponin’s ability to switch actin monomers off and to reduce the amount of the myosin heads weakly bound to F-actin at a low Ca²⁺. These changes in the behavior of tropomyosin and the troponin–tropomyosin complex, as well as in the balance of strongly and weakly bound myosin heads in the ATPase cycle may underlie the occurrence of both abnormally high Ca²⁺-sensitivity and muscle weakness. BDM, an inhibitor of myosin ATPase activity, and W7, a troponin C antagonist, restore the ability of tropomyosin for Ca²⁺-dependent movement and the ability of the troponin–tropomyosin complex to switch actin monomers off, demonstrating a weakening of the damaging effect of the R90P mutation on muscle contractility.     

A STUDY ON THE PERFORMANCE OF THE CATALYTIC POROUS-WALL THREE-PHASE REACTOR

A theoretical investigation of a catalytic porous-wall reactor in which gaseous and liquid reactants approach each other from opposite sides of the catalyst is undertaken. Equations for the annular liquid-channel are coupled with those for the catalytic wall and solved numerically and analytically using a simplified model. For the model reaction under study, the main design and operation parameters which affect reactor performance are the Thiele modulus, Peclet number, width of the liquid channel and the inlet concentration of the reactant in the liquid phase.

The effect of reactor configuration is peculiar to the cylindrical geometry because the thickness and relative location of the catalytic wall as well as the selection of the liquid and gas channels can influence the reactor performance. Thin-walled catalyst tubes have larger effectiveness factors and as the tube radius approaches that of the reactor, conversion in the reactor increases especially when the liquid is saturated with the gaseous reactant. Concentration of the liquid reactant in the feed has a significant effect if the reactant is depleted at some point inside the catalyst wall. Since the reaction zone width can be adjusted by changing the feed composition, this might have important implications with respect to selectivity.     

Inactivation of Giardia muris Using Ozone and Ozone-Hydrogen Peroxide

The disinfection effects of the ozone molecule alone and that of ozone decomposition products when inactivating Giardia muris cysts were investigated at bench-scale using two different ozone demand-free laboratory buffer systems. The first water was a 0.05 M phosphate buffer with hydrogen peroxide added at a 10:1 weight ratio. The second water was a 0.05 M phosphate – 0.01 M bicarbonate buffer which quickly scavenged radical species from ozone decomposition. The C3H/HeN mouse model was used to assess the infectivity of ozone treated cysts.

The phosphate-bicarbonate buffer system had significantly greater (P ≤ 0.05) inactivation of G. muris cysts than that observed in the phosphate buffer – peroxide system where ozone was completely decomposed in less than 120 s. Consequently, the design of ozone disinfection processes should maintain ozone residual for disinfection prior to the addition of hydrogen peroxide for the oxidation of other compounds.