Integrating Ontogenetic Shift, Growth and Mortality to Determine a Species' Ecological Role from Isotopic Signatures

<div><p>Understanding species linkages and energy transfer is a basic goal underlying any attempt at ecosystem analysis. Although the first food-web studies were based on gut contents of captured specimens, the assessment of stable isotopes, mainly <i>δ¹³C</i> and <i>δ¹⁵N</i>, has become a standard methodology for wide-range analyses in the last 30 years. Stable isotopes provide information on the trophic level of species, food-web length, and origin of organic matter ingested by consumers. In this study, we analyzed the ontogenetic variability of <i>δ¹³C</i> and <i>δ¹⁵N</i> obtained from samples of three Neotropical fish species: silver sardine (<i>Lycengraulis grossidens</i>, <i>n</i>=46), white lambari (<i>Cyanocharax alburnus</i>, <i>n</i>= 26), and the red-tail lambari (<i>Astyanax fasciatus</i>, <i>n</i>=23) in Pinguela Lagoon, southern Brazil. We developed a new metric, called the Weighted Isotopic Signature (<i>φ¹⁵N</i> or <i>φ¹³C</i>, ‰), that incorporates ontogenetic variability, body growth, and natural mortality into a single number.</p></div

<i>Astyanax fasciatus</i> in Pinguela Lagoon, southern Brazil: (a) survival curve; (b) weight growth curve; (c) <i>δ</i>^<i>15</i><i>N</i>-to-age response; (d) weighted impact of <i>δ</i>^<i>15</i><i>N</i> according to age.

<p><i>Astyanax fasciatus</i> in Pinguela Lagoon, southern Brazil: (a) survival curve; (b) weight growth curve; (c) <i>δ</i>^<i>15</i><i>N</i>-to-age response; (d) weighted impact of <i>δ</i>^<i>15</i><i>N</i> according to age.</p

Ontogenetic variability of isotope signatures of carbon (<i>δ</i>^<i>13</i><i>C</i>) and nitrogen (<i>δ</i>^<i>15</i><i>N</i>) for <i>Cyanocharax alburnus</i>, <i>Lycengraulis grossidens</i> and <i>Astyanax fasciatus</i> in Pinguela Lagoon, southern Brazil.

<p>Ontogenetic variability of isotope signatures of carbon (<i>δ</i>^<i>13</i><i>C</i>) and nitrogen (<i>δ</i>^<i>15</i><i>N</i>) for <i>Cyanocharax alburnus</i>, <i>Lycengraulis grossidens</i> and <i>Astyanax fasciatus</i> in Pinguela Lagoon, southern Brazil.</p

Growth, mortality and isotopic parameters (‰) for <i>Astyanax fasciatus</i> and <i>Lycengraulis grossidens</i> in Pinguela Lagoon, southern Brazil.

<p>Growth, mortality and isotopic parameters (‰) for <i>Astyanax fasciatus</i> and <i>Lycengraulis grossidens</i> in Pinguela Lagoon, southern Brazil.</p

Occurrence of limnic molluscs and crustaceous on clusters of the golden mussel Limnoperna fortunei (Dunker, 1857), formed on “sarandi” at Guaíba Lake (rs, Brazil)

In order to verify the occurrence of invetebrates associated with macro clusters of Limnoperna fortunei (Dunker, 1857) formed on branches of “sarandi” (Chephalanthus glabratus (Spreng.) K. Schum), quantitative samplings (N=28) were conducted for two years (2002 to 2004) at Veludo Beach on Guaíba Lake (municipality of Porto Alegre, RS, Brazil). From the results, the gastropod Heleobia piscium (Orbigny, 1835) was identified as a constant (78.57%) species, while Potamolithus jacuyensis Pilsbry 1899 (35.71%) and the crustaceous Hyalella curvispina Shoemaker 1942 (26%) were indicated as accessory species. The other taxa were accidental (<25%): Ampullariidae (young individuals), Heleobia davisi (Silva & Thomé, 1985), Chilina parva (Martens, 1868) and Corbicula fluminea (Müller, 1774). Currently, the interspecific relationships among these taxa are poorly known

Ocorrência de moluscos límnicos e crustáceo em macroaglomerados do mexilhão dourado, Limnoperna fortunei (Dunker, 1857) sobre sarandi no lago Guaíba (RS, Brasil)

Objetivando avaliar a ocorrência de invertebrados associados aos macroaglomerados de Limnoperna fortunei (Dunker, 1857) sobre galhos de sarandi (Chephhalanthus glabratus (Spreng.) K. Schum) foram realizadas coletas qualitativas (N=28) no período de 2002 a 2004, na Praia do Veludo, lago Guaíba (Porto Alegre, RS). Destacaram-se os gastrópodes Heleobia piscium (Orbigny, 1835) (78,57%), como espécie constante nas amostras; Potamolithus jacuhyensis Pilsbry, 1899 (35,71%), como espécie acessória e o crustáceo Hyalella curvispina Shoemaker, 1942 (26%), como espécie acessória. Os demais táxons foram acidentais (<25%): Ampullariidae (indivíduos jovens); Heleobia davisi (Silva & Thomé, 1985); Chilina parva (Martens, 1868) e Corbicula fluminea (Müller, 1774). As relações interespecíficas destes táxons são até o momento pouco conhecidas

The Adaptor Protein Myd88 Is a Key Signaling Molecule in the Pathogenesis of Irinotecan-Induced Intestinal Mucositis.

Intestinal mucositis is a common side effect of irinotecan-based anticancer regimens. Mucositis causes cell damage, bacterial/endotoxin translocation and production of cytokines including IL-1 and IL-18. These molecules and toll-like receptors (TLRs) activate a common signaling pathway that involves the Myeloid Differentiation adaptor protein, MyD88, whose role in intestinal mucositis is unknown. Then, we evaluated the involvement of TLRs and MyD88 in the pathogenesis of irinotecan-induced intestinal mucositis. MyD88-, TLR2- or TLR9-knockout mice and C57BL/6 (WT) mice were given either saline or irinotecan (75 mg/kg, i.p. for 4 days). On day 7, animal survival, diarrhea and bacteremia were assessed, and following euthanasia, samples of the ileum were obtained for morphometric analysis, myeloperoxidase (MPO) assay and measurement of pro-inflammatory markers. Irinotecan reduced the animal survival (50%) and induced a pronounced diarrhea, increased bacteremia, neutrophil accumulation in the intestinal tissue, intestinal damage and more than twofold increased expression of MyD88 (200%), TLR9 (400%), TRAF6 (236%), IL-1β (405%), IL-18 (365%), COX-2 (2,777%) and NF-κB (245%) in the WT animals when compared with saline-injected group (P<0.05). Genetic deletion of MyD88, TLR2 or TLR9 effectively controlled the signs of intestinal injury when compared with irinotecan-administered WT controls (P<0.05). In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL-18 versus irinotecan-injected WT controls. Additionally, the expression of MyD88 was reduced in the TLR2-/- or TLR9-/- mice. This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis

Intestinal mucositis is dependent on MyD88 and NF-κB expression.

<p>The mice (n = 6–9) were injected for 4 days with saline (3 mL/kg, open bars) or irinotecan (75 mg/kg, i.p., black bars) and were killed on the seventh day after the first dose. Ileal samples were collected and processed for MyD88 and NF-κB expression. Irinotecan injection increased MyD88 (<b>A</b>) and NF-κB (<b>B, C and D</b>) expression as detected by qPCR (<b>A and C</b>), immunohistochemistry (<b>B</b>) or western blot (<b>D</b>) versus the saline-treated WT mice. The basal expression of MyD88 was found in the irinotecan-injected MyD88-/-, TLR2-/- or TLR9-/- mice when compared to their respective saline-injected knockout controls (<b>A</b>). Deletion of the MyD88 gene also prevented the expression of NF-κB (<b>B, C and D</b>). The values are expressed as the means ± SEM.</p

IL–1β levels and IL–18 expression are markedly decreased in the MyD88^-/- and TLR2^-/- mice.

<p>The mice (n = 6–9) were injected for 4 days with saline (3 mL/kg) or irinotecan (75 mg/kg, i.p.) and were killed on the seventh day after the first dose. Ileal samples were collected and processed for IL–1β levels (ELISA) and qPCR for IL–18. The irinotecan injection in the WT mice increased the IL–1β levels (<b>A, C</b> and <b>E</b>) and IL–18 expression (<b>B, D and F</b>) compared with the normal WT control animals. The MyD88-/- or TLR2-/- mice that received irinotecan showed a significant reduction in these inflammatory markers compared to the irinotecan-injected WT animals (<b>A-D</b>). The irinotecan-treated TLR9-/- animals showed reduced levels of IL–1β, but increased expression of IL–18 (<b>E and F</b>). The values are expressed as the means ± SEM.</p