Soybeans in family meals

"MP484, 2/76/3M""This publication was originally printed as Home and Garden Bulletin #208 USDA.

New Study Underway to Estimate the Impact of Lesser Scaup on Arkansas’ Baitfish Industry

The baitfish industry is an important economic enterprise for many aquaculture producers in Arkansas. The industry generates approximately $30 million annually in farm-gate sales of these small fish that include fathead minnows, goldfish and golden shiners. Diving ducks known as scaup, or “Bluebills,” spend late fall through early spring in Arkansas and Mississippi on deep water wetlands, rivers, and aquaculture ponds. The notion that scaup are consuming an abundance of baitfish in Arkansas ponds has concerned commercial growers for several years

New Study Underway to Estimate the Impact of Lesser Scaup on Arkansas’ Baitfish Industry

The baitfish industry is an important economic enterprise for many aquaculture producers in Arkansas. The industry generates approximately $30 million annually in farm-gate sales of these small fish that include fathead minnows, goldfish and golden shiners. Diving ducks known as scaup, or “Bluebills,” spend late fall through early spring in Arkansas and Mississippi on deep water wetlands, rivers, and aquaculture ponds. The notion that scaup are consuming an abundance of baitfish in Arkansas ponds has concerned commercial growers for several years

Scaup Depredation on Arkansas Baitfish and Sportfish Aquaculture

Lesser scaup (Aythya affinis) and greater scaup (A. marila), hereafter scaup, consume a variety of aquatic invertebrates, plants, and occasionally small fish. Scaup have foraged on commercial aquaculture farms in the southern United States for decades. However, the types, abundance, and rate of fish exploitation by scaup on baitfish and sportfish farms are not well documented. Thus, information is needed to understand how fish and other foods influence scaup use of aquatic resources, and any potential economic effects of depredation of fish. From November–March in winters 2016–2017 and 2017–2018, we conducted 1,458 pond surveys to estimate the abundance and distribution of scaup on Arkansas baitfish and sportfish farms that commercially produce species such as golden shiners (Notemigonus crysoleucas), fathead minnows (Pimephales promelas), goldfish (Carassius auratus), and sunfish (Lepomis spp.). We also collected and processed 531 foraging scaup and quantified the proportion of scaup consuming fish and the proportion of their diet obtained from fish. Fish consumption was highly variable between years. In our survey area, we estimated total fish consumption at 1,400 kg and 60,500 kg for winters 2016–2017 and 2017–2018, respectively. Sunfish ponds experienced the maximum loss (18,000 fish/ha) during winter 2017–2018, while goldfish ponds experienced a loss of just 2,600 fish/ha during the same winter. The estimates of baitfish and sportfish loss to scaup revealed potential management strategies for minimizing fish loss and can inform economic analysis of the financial impact of scaup on producers

Molecular networks discriminating mouse bladder responses to intravesical bacillus Calmette-Guerin (BCG), LPS, and TNF-α

<p>Abstract</p> <p>Background</p> <p>Despite being a mainstay for treating superficial bladder carcinoma and a promising agent for interstitial cystitis, the precise mechanism of Bacillus Calmette-Guerin (BCG) remains poorly understood. It is particularly unclear whether BCG is capable of altering gene expression in the bladder target organ beyond its well-recognized pro-inflammatory effects and how this relates to its therapeutic efficacy. The objective of this study was to determine differentially expressed genes in the mouse bladder following chronic intravesical BCG therapy and to compare the results to non-specific pro inflammatory stimuli (LPS and TNF-α). For this purpose, C57BL/6 female mice received four weekly instillations of BCG, LPS, or TNF-α. Seven days after the last instillation, the urothelium along with the submucosa was removed from detrusor muscle and the RNA was extracted from both layers for cDNA array experiments. Microarray results were normalized by a robust regression analysis and only genes with an expression above a conditional threshold of 0.001 (3SD above background) were selected for analysis. Next, genes presenting a 3-fold ratio in regard to the control group were entered in Ingenuity Pathway Analysis (IPA) for a comparative analysis in order to determine genes specifically regulated by BCG, TNF-α, and LPS. In addition, the transcriptome was precipitated with an antibody against RNA polymerase II and real-time polymerase chain reaction assay (Q-PCR) was used to confirm some of the BCG-specific transcripts.</p> <p>Results</p> <p>Molecular networks of treatment-specific genes generated several hypotheses regarding the mode of action of BCG. BCG-specific genes involved small GTPases and BCG-specific networks overlapped with the following canonical signaling pathways: axonal guidance, B cell receptor, aryl hydrocarbon receptor, IL-6, PPAR, Wnt/β-catenin, and cAMP. In addition, a specific detrusor network expressed a high degree of overlap with the development of the lymphatic system. Interestingly, TNF-α-specific networks overlapped with the following canonical signaling pathways: PPAR, death receptor, and apoptosis. Finally, LPS-specific networks overlapped with the LPS/IL-1 mediated inhibition of RXR. Because NF-kappaB occupied a central position in several networks, we further determined whether this transcription factor was part of the responses to BCG. Electrophoretic mobility shift assays confirmed the participation of NF-kappaB in the mouse bladder responses to BCG. In addition, BCG treatment of a human urothelial cancer cell line (J82) also increased the binding activity of NF-kappaB, as determined by precipitation of the chromatin by a NF-kappaB-p65 antibody and Q-PCR of genes bearing a NF-kappaB consensus sequence. Next, we tested the hypothesis of whether small GTPases such as LRG-47 are involved in the uptake of BCG by the bladder urothelium.</p> <p>Conclusion</p> <p>As expected, BCG treatment induces the transcription of genes belonging to common pro-inflammatory networks. However, BCG also induces unique genes belonging to molecular networks involved in axonal guidance and lymphatic system development within the bladder target organ. In addition, NF-kappaB seems to play a predominant role in the bladder responses to BCG therapy. Finally, in intact urothelium, BCG-GFP internalizes in LRG-47-positive vesicles.</p> <p>These results provide a molecular framework for the further study of the involvement of immune and nervous systems in the bladder responses to BCG therapy.</p

Foraging Ecology and Distribution of Scaup (Aythya spp.) on Arkansas Commercial Baitfish and Sportfish Farms

Lesser Scaup (Aythya affinis)and Greater Scaup (Aythya marila) have been reported to consume substantial quantities of golden shiners (Notemigonus crysoleucas), fathead minnows (Pimephales promelas), goldfish (Carassius auratus), and sunfish (Lepomis spp.) produced on Arkansas commercial baitfish and sportfish farms. The goals of this study were to investigate foraging ecology and distribution of Scaup at these facilities, and use this information to assist producers in administering bird harassment efforts more efficiently. During typical wintering period for Scaup in Arkansas (November-March), we conducted approximately 1,400 pond surveys to estimate abundance and distribution of scaup on farms in 2016-2017 and 2017-2018. Information related to pond size, fish species, fish size, and stocking density, were also obtained to enable a more detailed analysis of Scaup use. We also collected 561 Scaup from these facilities to quantify the proportion of diet obtained from fish. There was an increase in Scaup abundance and fish consumption between the first to the second winter, likely attributed to cooler temperatures during the second winter. Our distribution model predicted an increased probability of Scaup use on larger ponds containing high densities of fish, while diet analysis indicated increased fish consumption during colder winter periods. Our results can be used by farm managers to designate resources for bird harassment to particular locations and times of the winter when scaup are more likely to negatively impact the fish crop

Depredation Impact of Double-Crested Cormorants (Phalacrocorax auritus) on Commercial Catfish Production in the Mississippi Delta

Double-crested Cormorants (Phalacrocorax auritus) impact United States commercial aquaculture and are considered the greatest avian predators on catfish (Ictalurus spp.) aquaculture facilities. Cormorants are especially problematic in the Delta region in western Mississippi, where catfish production is concentrated providing ideal wintering and foraging areas. Although cormorant/aquaculture dynamics have been studied, recent changes in aquaculture practices, regulatory policies, and decreased overall hectares in production merit contemporary research. Therefore, we estimated abundance and distribution of cormorants at their night roosts and assessed diet related to catfish consumption. Aerial surveys of cormorant night roosts were flown from October through April, 2016-2018. Following each survey, three active night roosts were randomly selected for harvesting cormorants for later necropsy and stomach contents assessment. We completed 25 total surveys and counted an average of 23,379 cormorants (range 5,026 to 40,535) pooled over years (corrected for observer and method bias). A total of 728 cormorants from 27 different night roosts were collected across years. Survey count models estimated 4.2 and 5 million cormorant forage days in the Delta during winters 2016-2017 and 2017-2018, respectively. Throughout the study, catfish comprised 33% of the prey biomass detected; shad (Dorosoma spp.) also were dominant (58%) prey. Evidence suggests that the area of catfish aquaculture surrounding a night roost within a 30.6-km forage buffer is an important predictor for a bird’s relative amount of catfish consumption. These results will inform wildlife managers regarding relationships between cormorant night roost locations in the Delta and disproportionate consumption of catfish, enhancing techniques to reduce fish losses on aquaculture facilities

Transcription factor network downstream of protease activated receptors (PARs) modulating mouse bladder inflammation

<p>Abstract</p> <p>Background</p> <p>All four PARs are present in the urinary bladder, and their expression is altered during inflammation. In order to search for therapeutic targets other than the receptors themselves, we set forth to determine TFs downstream of PAR activation in the C57BL/6 urinary bladders.</p> <p>Methods</p> <p>For this purpose, we used a protein/DNA combo array containing 345 different TF consensus sequences. Next, the TF selected was validated by EMSA and IHC. As mast cells seem to play a fundamental role in bladder inflammation, we determined whether c-kit receptor deficient (Kit^w/Kit^w-v) mice have an abrogated response to PAR stimulation. Finally, TFEB antibody was used for CHIP/Q-PCR assay and revealed up-regulation of genes known to be downstream of TFEB.</p> <p>Results</p> <p>TFEB, a member of the MiTF family of basic helix-loop-helix leucine zipper, was the only TF commonly up-regulated by all PAR-APs. IHC results confirm a correlation between inflammation and TFEB expression in C57BL/6 mice. In contrast, Kit^w/Kit^w-vmice did not exhibit inflammation in response to PAR activation. EMSA results confirmed the increased TFEB binding activity in C57BL/6 but not in Kit^w/Kit^w-vmice.</p> <p>Conclusion</p> <p>This is the first report describing the increased expression of TFEB in bladder inflammation in response to PAR activation. As TFEB belongs to a family of TFs essential for mast cell survival, our findings suggest that this molecule may influence the participation of mast cells in PAR-mediated inflammation and that targeting TFEB/MiTF activity may be a novel approach for the treatment of bladder inflammatory disorders.</p

VEGF signaling mediates bladder neuroplasticity and inflammation in response to BCG

<p>Abstract</p> <p>Background</p> <p>This work tests the hypothesis that increased levels of vascular endothelial growth factor (VEGF) observed during bladder inflammation modulates nerve plasticity.</p> <p>Methods</p> <p>Chronic inflammation was induced by intravesical instillations of Bacillus Calmette-Guérin (BCG) into the urinary bladder and the density of nerves expressing the transient receptor potential vanilloid subfamily 1 (TRPV1) or pan-neuronal marker PGP9.5 was used to quantify alterations in peripheral nerve plasticity. Some mice were treated with B20, a VEGF neutralizing antibody to reduce the participation of VEGF. Additional mice were treated systemically with antibodies engineered to specifically block the binding of VEGF to NRP1 (anti-NRP1^B) and NRP2 (NRP2^B), or the binding of semaphorins to NRP1 (anti-NRP1 ^A) to diminish activity of axon guidance molecules such as neuropilins (NRPs) and semaphorins (SEMAs). To confirm that VEGF is capable of inducing inflammation and neuronal plasticity, another group of mice was instilled with recombinant VEGF₁₆₅or VEGF₁₂₁into the urinary bladder.</p> <p>Results</p> <p>The major finding of this work was that chronic BCG instillation resulted in inflammation and an overwhelming increase in both PGP9.5 and TRPV1 immunoreactivity, primarily in the sub-urothelium of the urinary bladder. Treatment of mice with anti-VEGF neutralizing antibody (B20) abolished the effect of BCG on inflammation and nerve density.</p> <p>NRP1^Aand NRP1^Bantibodies, known to reduce BCG-induced inflammation, failed to block BCG-induced increase in nerve fibers. However, the NRP2^Bantibody dramatically potentiated the effects of BCG in increasing PGP9.5-, TRPV1-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)-immunoreactivity (IR). Finally, instillation of VEGF₁₂₁or VEGF₁₆₅into the mouse bladder recapitulated the effects of BCG and resulted in a significant inflammation and increase in nerve density.</p> <p>Conclusions</p> <p>For the first time, evidence is being presented supporting that chronic BCG instillation into the mouse bladder promotes a significant increase in peripheral nerve density that was mimicked by VEGF instillation. Effects of BCG were abolished by pre-treatment with neutralizing VEGF antibody. The present results implicate the VEGF pathway as a key modulator of inflammation and nerve plasticity, introduces a new animal model for investigation of VEGF-induced nerve plasticity, and suggests putative mechanisms underlying this phenomenon.</p

Mandatory role of proteinase-activated receptor 1 in experimental bladder inflammation

BACKGROUND: In general, inflammation plays a role in most bladder pathologies and represents a defense reaction to injury that often times is two edged. In particular, bladder neurogenic inflammation involves the participation of mast cells and sensory nerves. Increased mast cell numbers and tryptase release represent one of the prevalent etiologic theories for interstitial cystitis and other urinary bladder inflammatory conditions. The activity of mast cell-derived tryptase as well as thrombin is significantly increased during inflammation. Those enzymes activate specific G-protein coupled proteinase-activated receptors (PAR)s. Four PARs have been cloned so far, and not only are all four receptors highly expressed in different cell types of the mouse urinary bladder, but their expression is altered during experimental bladder inflammation. We hypothesize that PARs may link mast cell-derived proteases to bladder inflammation and, therefore, play a fundamental role in the pathogenesis of cystitis. RESULTS: Here, we demonstrate that in addition to the mouse urinary bladder, all four PA receptors are also expressed in the J82 human urothelial cell line. Intravesical administration of PAR-activating peptides in mice leads to an inflammatory reaction characterized by edema and granulocyte infiltration. Moreover, the inflammatory response to intravesical instillation of known pro-inflammatory stimuli such as E. coli lipopolysaccharide (LPS), substance P, and antigen was strongly attenuated by PAR1-, and to a lesser extent, by PAR2-deficiency. CONCLUSION: Our results reveal an overriding participation of PAR1 in bladder inflammation, provide a working model for the involvement of downstream signaling, and evoke testable hypotheses regarding the role of PARs in bladder inflammation. It remains to be determined whether or not mechanisms targeting PAR1 gene silencing or PAR1 blockade will ameliorate the clinical manifestations of cystitis