Nutrient Restoration of a Large, Impounded, Ultra-Oligotrophic Western River to Recover Declining Native Fishes

Declines in many fish populations in large, western rivers have been primarily attributed to the anthropogenic reduction of nutrient inputs and subsequent impacts to the food web. The largest known river fertilization program was implemented starting in 2005 on the Kootenai River in northern Idaho to restore resident fisheries. Annual electrofishing surveys were conducted at multiple sites in Idaho and Montana before and during nutrient addition to evaluate assemblage and population-level responses. Although few responses in fish assemblage structure were observed, the addition of liquid ammonium polyphosphate fertilizer (3 μg/L) to the Kootenai River increased fish abundance and biomass over the 20-km stretch of river downstream of the treatment site. Increases were most notable in Largescale Suckers Catostomus macrocheilus, Mountain Whitefish Prosopium williamsoni, and Rainbow Trout Oncorhynchus mykiss populations, although increases in catch and biomass were detected for nearly all fish species. The Kootenai River is approximately 30 times larger in discharge than other rivers that have been experimentally fertilized and provides compelling evidence that the mitigation of nutrient declines in rivers of similar size can result in positive influences on the fish populations where primary and secondary production are limiting growth, survival, and recruitment. However, results from our study also highlight the importance of completing evaluations across varying levels of biological organization (e.g., assemblage and population) and over biologically relevant timeframes

Loss of Potential Aquatic-Terrestrial Subsidies Along the Missouri River Floodplain

The floodplains of large rivers have been heavily modified due to riparian development and channel modifications, both of which can eliminate shallow off-channel habitats. The importance of these habitats for aquatic organisms like fishes is well studied. However, loss of off-channel habitat also eliminates habitats for the production of emerging aquatic insects, which subsidize riparian consumers in terrestrial food webs. We used field collections of insect emergence, historical mapping, and statistical modeling to estimate the loss of insect emergence due to channel modifications along eight segments of the Missouri River (USA), encompassing 1566 river km, between 1890 and 2012. We estimate annual production of emerging aquatic insects declined by a median of 36,000 kgC (95% CrI: 3000 to 450,000) between 1890 and 2012 (a 34% loss), due to the loss of surface area in backwaters and related off-channel habitats. Under a conservative assumption that riparian birds obtain 24% of their annual energy budget from adult aquatic insects, this amount of insect loss would be enough to subsidize approximately 790,000 riparan woodland birds during the breeding and nesting period (May to August; 95% CrI: 57,000 to 10,000,000). Most of the loss is concentrated in the lower reaches of the Missouri River, which historically had a wide floodplain, a meandering channel, and a high density of off-channel habitats, but which were substantially reduced due to channelization and bank stabilization. Our results indicate that the loss of off-channel habitats in large river floodplains has the potential to substantially affect energy availability for riparian insectivores, further demonstrating the importance of maintaining and restoring these habitats for linked aquatic-terrestrial ecosystems

Loss of Potential Aquatic-Terrestrial Subsidies Along the Missouri River Floodplain

The floodplains of large rivers have been heavily modified due to riparian development and channel modifications, both of which can eliminate shallow off-channel habitats. The importance of these habitats for aquatic organisms like fishes is well studied. However, loss of off-channel habitat also eliminates habitats for the production of emerging aquatic insects, which subsidize riparian consumers in terrestrial food webs. We used field collections of insect emergence, historical mapping, and statistical modeling to estimate the loss of insect emergence due to channel modifications along eight segments of the Missouri River (USA), encompassing 1566 river km, between 1890 and 2012. We estimate annual production of emerging aquatic insects declined by a median of 36,000 kgC (95% CrI: 3000 to 450,000) between 1890 and 2012 (a 34% loss), due to the loss of surface area in backwaters and related off-channel habitats. Under a conservative assumption that riparian birds obtain 24% of their annual energy budget from adult aquatic insects, this amount of insect loss would be enough to subsidize approximately 790,000 riparan woodland birds during the breeding and nesting period (May to August; 95% CrI: 57,000 to 10,000,000). Most of the loss is concentrated in the lower reaches of the Missouri River, which historically had a wide floodplain, a meandering channel, and a high density of off-channel habitats, but which were substantially reduced due to channelization and bank stabilization. Our results indicate that the loss of off-channel habitats in large river floodplains has the potential to substantially affect energy availability for riparian insectivores, further demonstrating the importance of maintaining and restoring these habitats for linked aquatic-terrestrial ecosystems

Extraocular ectoderm triggers dorsal retinal fate during optic vesicle evagination in zebrafish

AbstractDorsal retinal fate is established early in eye development, via expression of spatially restricted dorsal-specific transcription factors in the optic vesicle; yet the events leading to initiation of dorsal fate are not clear. We hypothesized that induction of dorsal fate would require an extraocular signal arising from a neighboring tissue to pattern the prospective dorsal retina, however no such signal has been identified. We used the zebrafish embryo to determine the source, timing, and identity of the dorsal retina-inducing signal.Extensive cell movements occur during zebrafish optic vesicle morphogenesis, however the location of prospective dorsal cells within the early optic vesicle and their spatial relationship to early dorsal markers is currently unknown. Our mRNA expression and fate mapping analyses demonstrate that the dorsolateral optic vesicle is the earliest region to express dorsal specific markers, and cells from this domain contribute to the dorsal retinal pole at 24hpf.We show that three bmp genes marking dorsal retina at 25hpf are also expressed extraocularly before retinal patterning begins. We identified gdf6a as a dorsal initiation signal acting from the extraocular non-neural ectoderm during optic vesicle evagination. We find that bmp2b is involved in dorsal retina initiation, acting upstream of gdf6a. Together, this work has identified the nature and source of extraocular signals required to pattern the dorsal retina

Zebrafish foxP2 zinc finger nuclease mutant has normal axon pathfinding.

foxP2, a forkhead-domain transcription factor, is critical for speech and language development in humans, but its role in the establishment of CNS connectivity is unclear. While in vitro studies have identified axon guidance molecules as targets of foxP2 regulation, and cell culture assays suggest a role for foxP2 in neurite outgrowth, in vivo studies have been lacking regarding a role for foxP2 in axon pathfinding. We used a modified zinc finger nuclease methodology to generate mutations in the zebrafish foxP2 gene. Using PCR-based high resolution melt curve analysis (HRMA) of G0 founder animals, we screened and identified three mutants carrying nonsense mutations in the 2(nd) coding exon: a 17 base-pair (bp) deletion, an 8bp deletion, and a 4bp insertion. Sequence analysis of cDNA confirmed that these were frameshift mutations with predicted early protein truncations. Homozygous mutant fish were viable and fertile, with unchanged body morphology, and no apparent differences in CNS apoptosis, proliferation, or patterning at embryonic stages. There was a reduction in expression of the known foxP2 target gene cntnap2 that was rescued by injection of wild-type foxP2 transcript. When we examined axon pathfinding using a pan-axonal marker or transgenic lines, including a foxP2-neuron-specific enhancer, we did not observe any axon guidance errors. Our findings suggest that foxP2 is not necessary for axon pathfinding during development

Cataract Surgery in Patients with a Previous History of KAMRA Inlay Implantation: A Case Series

<p><b>Article full text</b></p> <p><br></p> <p>The full text of this article can be found here<b>.</b> <a href="https://link.springer.com/article/10.1007/s40123-017-0088-4">https://link.springer.com/article/10.1007/s40123-017-0088-4</a></p> <p><br></p> <p><b>Provide enhanced content for this article</b></p> <p><br></p> <p>If you are an author of this publication and would like to provide additional enhanced content for your article then please contact <a href="http://www.medengine.com/Redeem/”mailto:[email protected]”"><b>[email protected]</b></a>.</p> <p><br></p> <p>The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content.</p> <p><br></p> <p>Other enhanced features include, but are not limited to:</p> <p><br></p> <p>• Slide decks</p> <p>• Videos and animations</p> <p>• Audio abstracts</p> <p>• Audio slides</p

<i>foxP2</i> does not affect neuron specification, apoptosis, or proliferation, but does affect <i>cntnap2</i> expression levels.

<p>Confocal z-stack images, rostral to the top, scale bars 50 μm. (A, B, E-H, K-L) ventral views. (C, D) dorsal views. (<i>A</i>, <i>B</i>) TH immunohistochemistry at 72hpf shows no difference in WT and mutants in diencephalic dopaminergic neuron pattern or number. (C, D) Calbindin immunohistochemistry in the dorsal hindbrain at 72hpf shows similar patterns and numbers of Purkinje neurons in WT and mutants. (E, F) TUNEL staining for apoptotic cells at 26hpf in the brain shows no difference in pattern or number of cells between WT and mutants. (G, H) Detection of proliferation by H3P staining is similar in WT and mutants at 48hpf. (I, J) Neuropil distribution and intensity visualized with anti-SV2 synaptic vesicle protein antibody at 72hpf is similar in WT and mutants. (K, L) <i>cntnap2 in situ</i> expression pattern at 36hpf shows less expression in mutant embryos, more noticeably in the telencephalon (arrows). (M) quantitative RT-PCR at 72hpf confirms decreased expression of <i>cntnap2</i> in mutants, which is rescued by injection with full-length <i>foxP2</i> mRNA (* <i>p</i><0.05). Y-axis indicates fold-change.</p

<i>foxP2</i> mutant has normal morphology and CNS patterning.

<p>Whole-mount embryos, brightfield images, scale bar  = 50 μm. Lateral views, rostral to the left (A-F); dorsal views, rostral to the top (G, H). (A, B) Gross head morphology is unchanged in mutants at 72hpf. Arrow in (B) shows line used to measure brain size, from the midbrain-hindbrain boundary to the edge of the head by dissecting the midpoint of the lens. (C-D) mRNA expression of <i>foxP2</i> transcript is unchanged in intensity and pattern in <i>foxP2</i> mutants. (E-H) <i>in situ</i> expression patterns and intensity of <i>zic2a</i> and <i>dlx2</i> is unchanged in mutants compared to wild-type embryos.</p

<i>foxP2</i> does not affect axon pathfinding.

<p>Confocal z-stack images of whole-mount embryos, scale bars 50 μm, show no difference between wild-type and <i>foxP2</i> mutant (−/−) embryos for axon pathfinding using a variety of axonal labels. (A–D) anti-SV2 immunohistochemistry at 24hpf, lateral views of the brain, rostral to the left (A, B) and 72hpf, dorsal views of the spinal cord, rostral to the top (C, D). (E, F) anti-acetylated tubulin immunohistochemistry at 72hpf, ventral views of the optic chiasm. (G-L) GFP immunohistochemistry at 72hpf in Tg(<i>foxP2-enhancerA.2:egfp-caax</i>) embryos that labels <i>foxP2</i> neurons show no pathfinding errors in anterior commissure (ac), longitudinal commissures (lc), tract of the commissure of the posterior tuberculum (TCPTc), or reticulospinal axons (rs). (M-R) GFP immunohistochemistry at 72hpf in Tg(<i>otpb.A:egfp-caax</i>) embryos for visualization of dopaminergic and neuroendocrine projections (M, N, with insets shown in O, P) in the brain, and dopaminergic axon tracts in spinal cord (Q, R).</p