Modeling impacts of sea-level rise, oil price, and management strategy on the costs of sustaining Mississippi delta marshes with hydraulic dredging.

Over 25% of Mississippi River delta plain (MRDP) wetlands were lost over the past century. There is currently a major effort to restore the MRDP focused on a 50-year time horizon, a period during which the energy system and climate will change dramatically. We used a calibrated MRDP marsh elevation model to assess the costs of hydraulic dredging to sustain wetlands from 2016 to 2066 and 2016 to 2100 under a range of scenarios for sea level rise, energy price, and management regimes. We developed a subroutine to simulate dredging costs based on the price of crude oil and a project efficiency factor. Crude oil prices were projected using forecasts from global energy models. The costs to sustain marsh between 2016 and 2100 changed from $128,000/ha in the no change scenario to ~$1,010,000/ha in the worst-case scenario for sea level rise and energy price, an ~8-fold increase. Increasing suspended sediment concentrations, which is possible using managed river diversions, raised created marsh lifespan and decreased long term dredging costs. Created marsh lifespan changed nonlinearly with dredging fill elevation and suspended sediment level. Cost effectiveness of marsh creation and nourishment can be optimized by adjusting dredging fill elevation to the local sediment regime. Regardless of management scenario, sustaining the MRDP with hydraulic dredging suffered declining returns on investment due to the convergence of energy and climate trends. Marsh creation will likely become unaffordable in the mid to late 21st century, especially if river sediment diversions are not constructed before 2030. We recommend that environmental managers take into consideration coupled energy and climate scenarios for long-term risk assessments and adjust restoration goals accordingly.

Depletion of colonic detoxication enzyme activity in mice with dextran sulphate sodium-induced colitis.

BACKGROUND: The increased risk of colonic malignancies in individuals with ulcerative colitis has prompted a search for early biomarkers of disease progression. AIM: To characterize Phase II detoxication enzyme expression during acute and chronic colitis. The mouse model of dextran sulphate sodium (DSS)-induced colitis represents a relevant system with which to sequentially evaluate the spectrum of biochemical changes associated with colorectal cancer risk. METHODS: Acute and chronic colitis were induced in Swiss Webster mice by administering DSS in the drinking water (5%) for 1-4 cycles. Each cycle consisted of 7 days DSS and 14 days of water. The glutathione S-transferase (GST) activity, gamma-glutamylcysteine synthetase (gamma-GCS) activity and glutathione content of the colonic tissues were determined at various time points throughout the experiment. Alterations in GST isozyme expression were confirmed by Western and Northern blot. RESULTS: GST activity was reduced significantly in the colon by the end of Cycle 1 (84% of control values). Specific activities continued to decrease with subsequent cycles of DSS exposure. By the end of Cycle 4, glutathione levels and gamma-GCS activity had reached 29% and 56% of control, respectively. CONCLUSIONS: These data suggest that detoxication enzyme depletion is associated with both acute and chronic colitis and may be an important event in the progression of ulcerative colitis to colon cancer.

Experimental analysis of the relationship between charge movement components in skeletal muscle of Rana temporaria.

Experiments were performed to ascertain whether the monotonic (q beta) and delayed (q gamma) components of non-linear charge in skeletal muscle membranes form a sequential system, or are the result of separate, independent processes. The non-linear capacitance studied in a large number of fibres increased with fibre diameter. This dependence was attributable to tetracaine-sensitive (q gamma) but not to tetracaine-resistant (q beta and q alpha) charge. The kinetics and total quantity of q gamma charge moving in response to voltage steps from varying pre-pulse potentials to a fixed probe potential remained constant despite variations in the size of the early q beta decay. The kinetics of the delayed (q gamma) charging current obtained from a single 20 mV depolarizing step were compared with the sum of the responses to two 10 mV steps adding to the same voltage excursion. The respective transients superimposed only if one of the 10 mV steps did not reach the voltage at which q gamma first appears. In the two preceding experiments, total charge was conserved. These results are consistent with separate and functionally independent q beta and q gamma systems of potential-dependent charge, with q gamma residing in the transverse tubules and q beta on surface membrane. The findings can be discussed in terms of a contractile 'activator' with a steep sensitivity to voltage that begins only with depolarization beyond a level close to the actual mechanical threshold.

Charge movements near the mechanical threshold in skeletal muscle of Rana temporaria.

Charge movement was investigated over a range of potentials close to the mechanical threshold in voltage-clamped frog skeletal muscle. The delayed (q gamma) component of the charging currents appeared with a time course lasting well over 100 ms at around -50 to -40 mV, but the currents became larger and faster with further depolarization. The slow charging current was investigated using a 10 mV probe step intercepting the time course of these currents. This procedure showed that the charging currents could last as long as 100-300 ms. The total charge was conserved when the charging current was small and prolonged. The results can be related directly to earlier findings concerning contractile activation of muscle by applied voltage steps to potentials near threshold ( Adrian , Chandler & Hodgkin, 1969).

Charge movement and membrane capacity in frog muscle.

1. The transient current required to impose a step charge of potential has a complex time course especially in the region of internal potential between -50 and -40 mV. 2. Examination of non-linear transient current in this voltage range suggests two components of charge movement: (a) an initial more-or-less exponential movement, and (b) a slower component with a complex time course. 3. Measurements of membrane capacity support such a division and confirm the steeper voltage dependence of the slower charge movement. 4. Permanent depolarization to 40 mV appears to immobilize the slowly moving charge. Depolarization to -20 mV immobilizes both charge movements, and uncovers the presence of a third charge which seems to correspond to Charge 2 (cf. Adrian & Almers, 1976b; Adrian, Chandler & Rakowski, 1976).

Reactivation of membrane charge movement and delayed potassium conductance in skeletal muscle fibres.

1. Intramembrane charge movement has been measured in striated muscle subjected to prolonged depolarization but repolarized to -100 mV for up to 100 sec. The method of measurement allows identification of charge or charges which are 'reprimed' by repolarization. 2. Charge 'reprimed' by repolarization appears to differ in its voltage distribution from charge detected in a permanently polarized fibre. The difference is probably due to the different pulse sequences used in the two measurements and to the fact that there appear to be several species of intramembrane charges with different transition potentials and different steepness of voltage distribution (V and k in eqn. (14): see below). 3. Potassium conductance is reprimed by repolarization following inactivation by depolarization. When the repriming potential is -100 mV the process appears to be in two stages; repriming to a value rather less than half the final value takes place exponentially with a time constant of approximately 40 sec; subsequently repriming to the final value is very slow. At a repriming potential of -140 mV repriming to the final value )1--2 mmho/microF) takes place exponentially with a time constant of approximately 17 sec.

Charge movement in the membrane of striated muscle.

This account of charge movement in striated muscle membrane must be regarded as essentially tentative. I have tried to present, within a simplified descriptive scheme, one way in which the present confusion of results can be resolved into a self-consistent account. But I am sure that as more complete and more accurate measurements are made, the deficiencies of this account will become even clearer. Nevertheless I believe that any successful description of the dielectric properties of biological membranes will have to take account of slow and nonlinear polarization of numerous membrane constituents and of the improbability of finding within the experimentally available range any finite potential region where polarization is linear.

Sodium currents in mammalian muscle.

1. A method is described which allows the approximate computation of membrane current from measurements with three electrodes in the mid-region of a muscle fibre.2. Measurements of inward sodium current in frog muscle are compared with the results of previous clamping studies to test the validity of the new method.3. Sodium current in rat muscle (extensor digitorum longus) is in general similar to sodium current in frog muscle. Two differences in detail have been found between sodium current in rat and frog muscle: (a) at the same temperature (in the range 0-20 degrees C) inactivation is slower in the rat than in the frog; (b) in rat the steady-state activation is shifted negatively on the voltage axis by some 10-15 mV.4. Delayed outward current and charge movement (Schneider & Chandler, 1973) are present in rat muscle.5. Rat muscle fibres are more resistant than frog muscle fibres to the action of tetrodotoxin. Inward current is still detectable in rat muscle at 100 nM tetrodotoxin. We found no evidence to suggest the existence in rat muscle of two kinds of sodium channel, one sensitive and one less sensitive to tetrodotoxin.

Action potentials reconstructed in normal and myotonic muscle fibres.

1. Muscle fibres from goats with myotonia congenita show characteristic responses to stimulation with intracellular currents (Adrian & Bryant, 1974). To test whether the reduced surface chloride conductance can account for these myotonic discharges, we have calculated responses of a model 'muscle fibre' to intracellular current of long duration (greater than 100 msec), assuming that the current is applied at the end of the fibre, that the fibre is of finite length, that a regenerative action potential occurs in the transverse tubular system as well as the surface, and that the potassium current in the wall of the transverse tubular system raises the potassium in the tubular lumen. In the absence of information about the kinetic parameters of the ionic currents in mammalian muscle we have used numerical values from frog muscle (Adrian, Chandler & Hodgkin, 1970). 2. In calculations with a normal surface chloride conductance a long maintained current gives only one action potential. Reduction of the chloride conductance to a half produces repetitive firing during the current; reduction to a tenth produces repetitive firing during and a small number of action potentials after the end of the current. Elimination of the tubular potassium accumulation from the calculation reduces the number but does not eliminate action potentials arising after the end of the applied current. 3. With a tenth of the normal chloride conductance calculated responses show maintained firing following a constant current if the deactivating rate of the sodium channels (betam) is reduced by 25%. As before, eliminating potassium accumulation reduces the number of post-stimulus action potentials, but it does not eliminate them altogether. 4. We conclude that in the absence of a surface chloride conductance tubular potassium accumulation could certainly contribute to the instability of the membrane, but it is clear that potassium accumulation is not the only reason for the instability of myotonic muscle fibres. The kinetics of the sodium channels are important and we do not know that they are the same in normal and myotonic fibres. Nevertheless the presence of a surface chloride conductance does stabilize the response of a fibre to constant current or to repetitive stimulation, and its absence could be a sufficient condition for myotonic behaviour.

The voltage dependence of membrane capacity.

1. Membrane capacity of sartorius muscle fibres has been measured at membrane potentials between -200 and +50 mV. Within this potential range the capacity is not independent of potential. Dielectric saturation is present at large negative and at positive internal potentials, indicating the presence in the membrane of permanent dipoles or movable charges. 2. In normally polarized fibres there is a sharp peak in the capacity-potential relation of about -50 mV; the capacity at this peak is 50% larger than the capacity at -90 mV. 3. In depolarized fibres this sharp peak of capacity is not present. Over the range -200 to +50 mV the capacity variation is about 10% with a broad maximum at about -80 mV. 4. The dielectric behaviour of muscle membrane is most simply explained by postulating two species of permanent dipoles or mobile charges: Charge 1 present in normally polarized fibres, but neutralized or immobilized in depolarized fibres; Charge 2 present in both polarized and depolarized fibres. The distribution of Charge 1 is more steeply voltage-dependent than is the distribution of Charge 2. 5. Movement of Charge 1 from one fully saturated configuration to the other involves a charge transfer across the membrane of between 20 and 30 nC/muF. Movement of Charge 2 in depolarized fibres requires a similar transfer of charge.

Charge movement in the membrane of striated muscle.

1. Non-linear polarization currents apparently due to permanent dipoles or mobile charges in the membrane can be measured by appropriate comparison of the transient currents required to produce small and large steps of membrane potential. Integration of these transient polarization currents estimates the charge transfer associated with the movement of membrane dipoles or charges. 2. Depolarization from -100 to 0 mV requires a charge transfer of 35 nC/muF in addition to the charge transfer predicted by linear extrapolation of the charge required for a small depolarization from -100 mV. Depolarizations of varying size give a charge-voltage relation which is sigmoid saturating beyond o mV and with a midpoint at about -50 mV. The ratnged depolarization reduces or removes charge movement detected by comparing currents for small and large voltage steps from -100 mV (Charge 1). However in depolarized fibres comparison of currents from a small potential step at +40 mV and a large hyperpolarizing potential step from -20 mV reveals large movements of a second charge (Charge 2). Movement of Charge 2 is less steeply dependent on voltage than movement of Charge 2 both in magnitude and in rate. 4. In size and voltage dependence these two kinds of charge movement correspond to measured voltage dependence of capacity in normally polarized and depolarized fibres (Adrian & Almers, 1976).

Charge movement and mechanical repriming in skeletal muscle.

1. Muscles were placed in a solution which depolarized the membrane to -30 to -20 mV so that mechanical activation was made refractory. Mechanical repriming and the recovery of voltage dependent charge movement were studied using a voltage clamp technique. 2. Mechanical repriming was investigated by determining the duration of a hyperpolarizing pulse required to elicit a just-visible contraction for various post-pulse potentials. As the post-pulse potential was made more positive shorter repriming times were required to produce a threshold contraction. The relationship approached a minimum repriming time for very positive post-pulse potentials. 3. These results suggest that hyperpolarization gradually removes some component of the activation mechanism from a refractory state and that the effectiveness of the amount which has recovered depends on the post-pulse potential. A quantitative explanation is given using a simple model in which the essential component is assumed to be the charge movement process. 4. The rate of repriming contraction is voltage dependent; at -160 mV the rate is about twice that at -120 mV. Between 4 and 10 degrees C the rate has a Q10 of about 9. 5. Recovery of charge movement was studied using a repriming duration less than that required to produce a threshold contraction. The observed charge movement increased linearly with repriming time, consistent with the approximately linear initial segment of a slow exponential recovery process. Extrapolation of the recovery curve indicated that 2-5 n/CmuF of charge is reprimed in the time necessary to reprime a threshold contraction. 6. The charge which recovers during a subthreshold repriming pulse is distributed according to membrane potential in the same way as a fully reprimed charge. 7. These results are consistent with the hypothesis that voltage dependent charge movement is an intermediate step in excitation-contraction coupling. 8. The characteristics of a second type of charge movement are also described.

Charge movements in skeletal muscle.

In twitch muscle, an action potential propagating along the surface can lead to mechanical contraction of the entire cross section of the fibre. The processes involve a depolarization of the membranes of the transverse tubular system which, in turn, causes a release of calcium from its intracellular storage location, the sarcoplasmic reticulum. It seems that a change in potential across the first structure can trigger the release from the second, adjacent structure. If the time and voltage dependent ionic currents are blocked, small movements of charge can be detected when a fibre is depolarized from a normal resting potential to a potential at which contraction is activated. These charge movements, which do not behave as currents passing through ionic channels, may be part of a trigger mechanism.

On the repetitive discharge in myotonic muscle fibres.

1. Muscle fibres from myotonic goats respond to injected constant currents with a train of action potentials. If the number of action potentials in an evoked train exceeds 10-15, stopping the current does not stop the repetitive firing of action potentials.2. Normal muscle fibres (goat) in a chloride-free Ringer respond in the same way to constant current.3. In the absence of self-maintained activity both myotonic fibres and normal fibres in chloride-free Ringer show an after-depolarization which is proportional to the number of driven impulses. The half-time for the decay of this after-potential is about 0.5 sec.4. Tubular potassium accumulation resulting from the initially driven activity and the known low chloride conductance of myotonic muscle fibres appear to account for the initiation of the myotonic discharge.