DOCUMENTING CHANGE AT UPPER HAMBURG BEND: NEBRASKA\u27S FIRST SIDE-CHANNEL RESTORATION

In 1996 a side channel was excavated on 629 hectares of former agricultural land at Upper Hamburg Bend on the Missouri River in Otoe County, NE. This was the first side channel constructed on the Missouri River in an attempt to restore lost aquatic habitat. The initial design was for an approximately 4,200 m long side channel to be constructed with a 3 m bottom width. Development ofthe site was to be dependent on flows diverted from the main channel of the river with a final projected top width of 61 m. The side channel was completed in the spring, and shortly thereafter the site was subjected to a series of flood events. The side channel has been subjected to periods of both high and low water since opening. We documented physical changes at the site with the aid of aerial photography, acoustic Doppler current profiler (ADCP) surveys, and topographic surveys. By 2010 the side channel was 4,342 m long with a mean top width of89.5 m. Channel development has occurred during periods of high and low water. ADCP surveys established that mean depths and velocities have increased since 2001. An increase in the amount of discharge through the side channel since 2001 has resulted in the loss of some of the shallower and lower velocity habitats. Modifications to the site may be necessary to reverse this loss of shallow, slow water habitat that the side channel was designed to provide. Although new off-channel aquatic habitat has been created, channel development has been impacted by the presence of rock control structures throughout the site. Reducing the number of control structures to the minimum necessary to prohibit the side channel from impacting adjacent properties may allow the continued restoration of lost alluvial processes through the ongoing process of bend development and migration

DOCUMENTING CHANGE AT UPPER HAMBURG BEND: NEBRASKA\u27S FIRST SIDE-CHANNEL RESTORATION

In 1996 a side channel was excavated on 629 hectares of former agricultural land at Upper Hamburg Bend on the Missouri River in Otoe County, NE. This was the first side channel constructed on the Missouri River in an attempt to restore lost aquatic habitat. The initial design was for an approximately 4,200 m long side channel to be constructed with a 3 m bottom width. Development ofthe site was to be dependent on flows diverted from the main channel of the river with a final projected top width of 61 m. The side channel was completed in the spring, and shortly thereafter the site was subjected to a series of flood events. The side channel has been subjected to periods of both high and low water since opening. We documented physical changes at the site with the aid of aerial photography, acoustic Doppler current profiler (ADCP) surveys, and topographic surveys. By 2010 the side channel was 4,342 m long with a mean top width of89.5 m. Channel development has occurred during periods of high and low water. ADCP surveys established that mean depths and velocities have increased since 2001. An increase in the amount of discharge through the side channel since 2001 has resulted in the loss of some of the shallower and lower velocity habitats. Modifications to the site may be necessary to reverse this loss of shallow, slow water habitat that the side channel was designed to provide. Although new off-channel aquatic habitat has been created, channel development has been impacted by the presence of rock control structures throughout the site. Reducing the number of control structures to the minimum necessary to prohibit the side channel from impacting adjacent properties may allow the continued restoration of lost alluvial processes through the ongoing process of bend development and migration

Challenge pools of hepatitis C virus genotypes 1-6 prototype strains: replication fitness and pathogenicity in chimpanzees and human liver-chimeric mouse models

Chimpanzees represent the only animal model for studies of the natural history of hepatitis C virus (HCV). To generate virus stocks of important HCV variants, we infected chimpanzees with HCV strains of genotypes 1-6 and determined the infectivity titer of acute-phase plasma pools in additional animals. The courses of first- and second-passage infections were similar, with early appearance of viremia, HCV RNA titers of >10(4.7) IU/mL, and development of acute hepatitis; the chronicity rate was 56%. The challenge pools had titers of 10(3)-10(5) chimpanzee infectious doses/mL. Human liver-chimeric mice developed high-titer infections after inoculation with the challenge viruses of genotypes 1-6. Inoculation studies with different doses of the genotype 1b pool suggested that a relatively high virus dose is required to consistently infect chimeric mice. The challenge pools represent a unique resource for studies of HCV molecular virology and for studies of pathogenesis, protective immunity, and vaccine efficacy in vivo

Genes involved in carnitine synthesis and carnitine uptake are up-regulated in the liver of sows during lactation

BACKGROUND:Convincing evidence exist that carnitine synthesis and uptake of carnitine into cells is regulated by peroxisome proliferator-activated receptor alpha (PPARA), a transcription factor which is physiologically activated during fasting or energy deprivation. Sows are typically in a negative energy balance during peak lactation. We investigated the hypothesis that genes involved in carnitine synthesis and uptake in the liver of sows are up-regulated during peak lactation. FINDINGS:Transcript levels of several PPARalpha target genes involved in fatty acid uptake (FABP4, SLC25A20), fatty acid oxidation (ACOX1, CYP4A24) and ketogenesis (HMGCS2, FGF21) were elevated in the liver of lactating compared to non-lactating sows (P < 0.05). In addition, transcript levels of genes involved in carnitine synthesis (ALDH9A1, TMLHE, BBOX1) and carnitine uptake (SLC22A5) in the liver were greater in lactating than in non-lactating sows (P < 0.05). Carnitine concentrations in liver and plasma were about 20% and 50%, respectively, lower in lactating than in non-lactating sows (P < 0.05), which is likely due to an increased loss of carnitine via the milk. CONCLUSIONS:The results of the present study show that PPARalpha is activated in the liver of sows during lactation which leads to an up-regulation of genes involved in carnitine synthesis and carnitine uptake. The PPARalpha mediated up-regulation of genes involved in carnitine synthesis and uptake in the liver of lactating sows may be regarded as an adaptive mechanism to maintain hepatic carnitine levels at a level sufficient to transport excessive amounts of fatty acids into the mitochondrion

Treatment of lactating sows with clofibrate as a synthetic agonist of PPARalpha does not influence milk fat content and gains of litters

BACKGROUND: In rats, it has been observed that treatment with activators of peroxisome proliferator-activated receptor a (PPARalpha) disturbs metabolic adaptations during lactation, which in turn lead to a reduction of milk fat content and gains of litters during the suckling period. It has not yet been investigated whether agonists of PPARalpha are impairing milk production of lactating sows in a similar manner as in rats. Therefore, the present study aimed to investigate the effect of treatment with clofibrate, a strong synthetic agonist of PPARalpha, on milk composition and litter gains in lactating sows. RESULTS: Twenty lactating sows received either a basal diet (control group) or the same diet with supplementation of 2 g of clofibrate per kg of diet (clofibrate group). In the clofibrate group, mRNA concentrations of various PPARalpha target genes involved in fatty acid utilization in liver and skeletal muscle were moderately up-regulated. Fat and energy content of the milk and gains of litters during the suckling period were not different between the control group and the clofibrate group. CONCLUSIONS: It is shown that treatment with clofibrate induces only a moderate up-regulation of PPARalpha target genes in liver and muscle of lactating sows and in turn might have limited effect on whole body fatty acid utilization. This may be the reason why clofibrate treatment did not influence milk fat content and gains of litters during the suckling period. Thus, the present study indicates that activation of PPARalpha induced either by native agonists such as dietary polyunsaturated fatty acids or a by negative energy balance might be largely uncritical in lactating sows with respect to milk production and litter gains in lactating sows

FINAL REPORT -- Missouri River Fish and Wildlife Mitigation Program: Fish Community Monitoring and Habitat Assessment of Off-channel Mitigation Sites

The Missouri River has been developed for flood control, commercial navigation, irrigation, fish and wildlife conservation, municipal water supply, water quality control and hydropower production through a series of congressional acts. However, prior to development, the lower Missouri River was characterized by a highly sinuous to braided channel with abundant log jams, sand bars, secondary channels and cut-off channels. Construction of the Bank Stabilization and Navigation Project (BSNP) converted the lower Missouri River into a narrow, self scouring channel. The active channel downstream of Sioux City, Iowa was as wide as 1.8 km before river modification, but is now confined to a 91.4 m channel. Total river and floodplain habitat altered or destroyed by the BSNP is estimated at 211,246 hectares. The Missouri River Fish and Wildlife Mitigation Project (Mitigation Project) was established to restore fish and wildlife habitat lost by the construction, operation and maintenance of the BSNP. The Water Resources Development Act of 1986 authorized the United States Army Corps of Engineers (COE) to acquire and develop habitat on 12,100 hectares of non public lands and the development of 7,365 hectares of habitat on existing public lands to mitigate habitat losses. The Water Resources Development Act of 1999 authorized an additional 48,016 hectares to the program. The Final Supplemental Environmental Impact Statement (FSEIS) for the expanded Mitigation Project was issued in March of 2003, and it included a preferred alternative proposing the creation of additional shallow water habitat (defined as areas less than 1.5 m deep with a current velocity of less than 0.76 m/s). The preferred action in the FSEIS for the expanded Mitigation Project included creation of 2,833 to 8,094 hectares of shallow water habitat (SWH). In 2005, the Iowa Department of Natural Resources, Nebraska Game and Parks Commission (NGPC), Missouri Department of Conservation and U.S. Fish and Wildlife Service, Columbia Fisheries Resource Office (renamed to Columbia National Fish and Wildlife Conservation Office) were contracted by the COE to monitor and evaluate fish communities of select off-channel aquatic habitat sites that were constructed through the Mitigation Project. Additionally, the NGPC was contracted to collect physical habitat information from the secondary channels that were selected for biological monitoring in the upper channelized section above Kansas City. Sixteen sites selected for monitoring covered a range of aquatic habitats including backwaters and secondary channels with varying levels of engineering and development. Sites from upstream to downstream included Tieville-Decatur Bend (two backwaters), Louisville Bend (backwater), Tyson Island (backwater), California Bend (chute on the Nebraska bank and a chute with connected backwater on the Iowa bank), Tobacco Island (chute), Upper and Lower Hamburg Bends (one chute each), Kansas Bend (two small chutes, treated as one), Deroin Bend (chute), Lisbon Bottom (natural chute), North Overton Bottoms (chute), Tadpole Island (chute) and Tate Island (chute). The study was designed to include three field sampling seasons, but due to delays implementing contracts in 2005 another complete year of sampling was added. Thus, fish community monitoring and habitat assessment of offchannel mitigation sites began in April, 2006 and concluded in October, 2008. The objective of this project was to determine biological performance and functionality of chutes and backwaters and to compare chutes and backwaters in an effort to identify designs most beneficial to native Missouri River fish species. Additionally, this project was designed to help determine if additional modifications are needed at existing mitigation sites, if existing designs are providing a range of habitats, if these habitats are of value to the biological diversity of the Missouri River and if these habitats are of specific value to species of concern or importance, such as pallid sturgeon

Genes involved in carnitine synthesis and carnitine uptake are up-regulated in the liver of sows during lactation

Abstract Background: Convincing evidence exist that carnitine synthesis and uptake of carnitine into cells is regulated by peroxisome proliferator-activated receptor α (PPARA), a transcription factor which is physiologically activated during fasting or energy deprivation. Sows are typically in a negative energy balance during peak lactation. We investigated the hypothesis that genes involved in carnitine synthesis and uptake in the liver of sows are upregulated during peak lactation. Findings: Transcript levels of several PPARα target genes involved in fatty acid uptake (FABP4, SLC25A20), fatty acid oxidation (ACOX1, CYP4A24) and ketogenesis (HMGCS2, FGF21) were elevated in the liver of lactating compared to non-lactating sows (P &lt; 0.05). In addition, transcript levels of genes involved in carnitine synthesis (ALDH9A1, TMLHE, BBOX1) and carnitine uptake (SLC22A5) in the liver were greater in lactating than in non-lactating sows (P &lt; 0.05). Carnitine concentrations in liver and plasma were about 20% and 50%, respectively, lower in lactating than in non-lactating sows (P &lt; 0.05), which is likely due to an increased loss of carnitine via the milk. Conclusions: The results of the present study show that PPARα is activated in the liver of sows during lactation which leads to an up-regulation of genes involved in carnitine synthesis and carnitine uptake. The PPARα mediated up-regulation of genes involved in carnitine synthesis and uptake in the liver of lactating sows may be regarded as an adaptive mechanism to maintain hepatic carnitine levels at a level sufficient to transport excessive amounts of fatty acids into the mitochondrion

Mitofusin 2 is essential for IP3-mediated SR/Mitochondria metabolic feedback in ventricular myocytes

Aim: Endothelin-1 (ET-1) and angiotensin II (Ang II) are multifunctional peptide hormones that regulate the function of the cardiovascular and renal systems. Both hormones increase the intracellular production of inositol-1,4,5-trisphosphate (IP$_3$) by activating their membrane-bound receptors. We have previously demonstrated that IP$_3$-mediated sarcoplasmic reticulum (SR) Ca$^{2+}$ release results in mitochondrial Ca$^{2+}$ uptake and activation of ATP production. In this study, we tested the hypothesis that intact SR/mitochondria microdomains are required for metabolic IP$_3$-mediated SR/mitochondrial feedback in ventricular myocytes. Methods: As a model for disrupted mitochondrial/SR microdomains, cardio-specific tamoxifen-inducible mitofusin 2 (Mfn2) knock out (KO) mice were used. Mitochondrial Ca$^{2+}$ uptake, membrane potential, redox state, and ATP generation were monitored in freshly isolated ventricular myocytes from Mfn2 KO mice and their control wild-type (WT) littermates. Results: Stimulation of ET-1 receptors in healthy control myocytes increases mitochondrial Ca$^{2+}$ uptake, maintains mitochondrial membrane potential and redox balance leading to the enhanced ATP generation. Mitochondrial Ca$^{2+}$ uptake upon ET-1 stimulation was significantly higher in interfibrillar (IFM) and perinuclear (PNM) mitochondria compared to subsarcolemmal mitochondria (SSM) in WT myocytes. Mfn2 KO completely abolished mitochondrial Ca$^{2+}$ uptake in IFM and PNM mitochondria but not in SSM. However, mitochondrial Ca2+ uptake induced by beta-adrenergic receptors activation with isoproterenol (ISO) was highest in SSM, intermediate in IFM, and smallest in PNM regions. Furthermore, Mfn2 KO did not affect ISO-induced mitochondrial Ca$^{2+}$ uptake in SSM and IFM mitochondria; however, enhanced mitochondrial Ca$^{2+}$ uptake in PNM. In contrast to ET-1, ISO induced a decrease in ATP levels in WT myocytes. Mfn2 KO abolished ATP generation upon ET-1 stimulation but increased ATP levels upon ISO application with highest levels observed in PNM regions. Conclusion: When the physical link between SR and mitochondria by Mfn2 was disrupted, the SR/mitochondrial metabolic feedback mechanism was impaired resulting in the inability of the IP$_3$-mediated SR Ca$^{2+}$ release to induce ATP production in ventricular myocytes from Mfn2 KO mice. Furthermore, we revealed the difference in Mfn2-mediated SR-mitochondrial communication depending on mitochondrial location and type of communication (IP$_3$R-mRyR1 vs. ryanodine receptor type 2-mitochondrial calcium uniporter)

Mitofusin 2 is essential for IP3-mediated SR/mitochondria metabolic feedback in ventricular myocytes

Aim: Endothelin-1 (ET-1) and angiotensin II (Ang II) are multifunctional peptide hormones that regulate the function of the cardiovascular and renal systems. Both hormones increase the intracellular production of inositol-1,4,5-trisphosphate (IP$_3$) by activating their membrane-bound receptors. We have previously demonstrated that IP$_3$-mediated sarcoplasmic reticulum (SR) Ca$^{2+}$ release results in mitochondrial Ca$^{2+}$ uptake and activation of ATP production. In this study, we tested the hypothesis that intact SR/mitochondria microdomains are required for metabolic IP$_3$-mediated SR/mitochondrial feedback in ventricular myocytes. Methods: As a model for disrupted mitochondrial/SR microdomains, cardio-specific tamoxifen-inducible mitofusin 2 (Mfn2) knock out (KO) mice were used. Mitochondrial Ca$^{2+}$ uptake, membrane potential, redox state, and ATP generation were monitored in freshly isolated ventricular myocytes from Mfn2 KO mice and their control wild-type (WT) littermates. Results: Stimulation of ET-1 receptors in healthy control myocytes increases mitochondrial Ca$^{2+}$ uptake, maintains mitochondrial membrane potential and redox balance leading to the enhanced ATP generation. Mitochondrial Ca$^{2+}$ uptake upon ET-1 stimulation was significantly higher in interfibrillar (IFM) and perinuclear (PNM) mitochondria compared to subsarcolemmal mitochondria (SSM) in WT myocytes. Mfn2 KO completely abolished mitochondrial Ca$^{2+}$ uptake in IFM and PNM mitochondria but not in SSM. However, mitochondrial Ca2+ uptake induced by beta-adrenergic receptors activation with isoproterenol (ISO) was highest in SSM, intermediate in IFM, and smallest in PNM regions. Furthermore, Mfn2 KO did not affect ISO-induced mitochondrial Ca$^{2+}$ uptake in SSM and IFM mitochondria; however, enhanced mitochondrial Ca$^{2+}$ uptake in PNM. In contrast to ET-1, ISO induced a decrease in ATP levels in WT myocytes. Mfn2 KO abolished ATP generation upon ET-1 stimulation but increased ATP levels upon ISO application with highest levels observed in PNM regions. Conclusion: When the physical link between SR and mitochondria by Mfn2 was disrupted, the SR/mitochondrial metabolic feedback mechanism was impaired resulting in the inability of the IP$_3$-mediated SR Ca$^{2+}$ release to induce ATP production in ventricular myocytes from Mfn2 KO mice. Furthermore, we revealed the difference in Mfn2-mediated SR-mitochondrial communication depending on mitochondrial location and type of communication (IP$_3$R-mRyR1 vs. ryanodine receptor type 2-mitochondrial calcium uniporter)