scholarly journals Proteomic Analysis of Urine from California Sea Lions (Zalophus californianus): a Resource for Urinary Biomarker Discovery

2018 ◽  
Author(s):  
Benjamin A. Neely ◽  
Katherine C. Prager ◽  
Alison M. Bland ◽  
Christine Fontaine ◽  
Frances M. Gulland ◽  
...  

AbstractUrinary markers for the assessment of kidney diseases in wild animals are limited, in part, due to the lack of urinary proteome data, especially for marine mammals. One of the most prevalent kidney diseases in marine mammals is caused byLeptospira interrogans, which is the second most common etiology linked to stranding of California sea lions (Zalophus californianus). Urine proteins from eleven sea lions with leptospirosis kidney disease and eight sea lions without leptospirosis or kidney disease were analyzed using shotgun proteomics. In total, 2694 protein groups were identified and 316 were differentially abundant between groups. Major urine proteins in sea lions were similar to major urine proteins in dogs and humans except for the preponderance of resistin, lysozyme C, and PDZ domain containing 1, which appear to be over-represented. Previously reported urine protein markers of kidney injury in humans and animals were also identified. Notably, neutrophil gelatinase-associated lipocalin, osteopontin, and epidermal fatty acid binding protein were elevated over 20-fold in the leptospirosis-infected sea lions. Consistent with leptospirosis infection in rodents, urinary proteins associated with the renin-angiotensin system were depressed, including neprilysin. This study represents a foundation from which to explore the clinical use of urinary protein markers in California sea lions.AbbreviationsRASrenin-angiotensin systemleptoleptospirosisSCrserum creatinineBUNblood urea nitrogen

2021 ◽  
Vol 8 ◽  
Author(s):  
Jerko Hrabar ◽  
Hrvoje Smodlaka ◽  
Somayeh Rasouli-Dogaheh ◽  
Mirela Petrić ◽  
Željka Trumbić ◽  
...  

In marine mammals, nematode-inflicted pathological lesions combined with other pathogens and factors (i.e., pollution, climate change, domoic acid poisoning events, and seasonal El Nino starvation events) negatively impact pinnipeds’ health and may cause mortality. Five California sea lions (Zalophus californianus)—a female pup, three male yearlings, and an adult female—suffered mortalities during rehabilitation at the Marine Mammal Care Center Los Angeles (San Pedro, CA). According to the necropsy reports, animals developed multisystemic parasitism as a leading cause of death, combined with malnutrition and hypoglycemia. In order to reveal host–parasite dynamics that may play a role in pinniped health and recovery, we examined the type and level of histopathological stomach lesions in California sea lions caused by anisakid nematodes. All isolated anisakids were morphologically and molecularly identified, and their phylogenetic relationships were reconstructed using the sequence of the mitochondrial COII gene. Co-parasitation of different Anisakidae spp. within the same host or lesions presented the opportunity to evaluate the existence of recombinant haplotypes and their eventual pathological pressure exerted onto host. The lesions were presented as chronic granulomatous gastritis, with moderate edema and hyperemia of the tunica submucosa and lamina propria, followed by mild, focal fibrosis of the gastric wall. Ulcerative changes with mixed leukocytic infiltrate showed to be localized, shallow, and non-perforative and with no apparent bacterial coinfection, mostly accompanied by healing granulation tissue. Isolated anisakids are grouped into three distinctively separated monophyletic clades corresponding to genera Anisakis, Contracaecum, and Pseudoterranova. Most abundant were representatives of Contracaecum ogmorhini sensu lato (55.36%), followed by Anisakis pegreffii (23.21%), Pseudoterranova azarasi (17.86%), Pseudoterranova decipiens sensu lato (1.79%), and Anisakis simplex (1.79%). Phylogenetic trees revealed no differentiation at intra-species level. Our analysis of divergence revealed Contracaecum separated from other lineages in the Jurassic period at the 176.2 Mya and Anisakis diverging from Pseudoterranova in Cenozoic period at 85.9 Mya.


2015 ◽  
Vol 370 (1673) ◽  
pp. 20140228 ◽  
Author(s):  
Helen M. Browning ◽  
Frances M. D. Gulland ◽  
John A. Hammond ◽  
Kathleen M. Colegrove ◽  
Ailsa J. Hall

Naturally occurring cancers in non-laboratory species have great potential in helping to decipher the often complex causes of neoplasia. Wild animal models could add substantially to our understanding of carcinogenesis, particularly of genetic and environmental interactions, but they are currently underutilized. Studying neoplasia in wild animals is difficult and especially challenging in marine mammals owing to their inaccessibility, lack of exposure history, and ethical, logistical and legal limits on experimentation. Despite this, California sea lions ( Zalophus californianus ) offer an opportunity to investigate risk factors for neoplasia development that have implications for terrestrial mammals and humans who share much of their environment and diet. A relatively accessible California sea lion population on the west coast of the USA has a high prevalence of urogenital carcinoma and is regularly sampled during veterinary care in wildlife rehabilitation centres. Collaborative studies have revealed that genotype, persistent organic pollutants and a herpesvirus are all associated with this cancer. This paper reviews research to date on the epidemiology and pathogenesis of urogenital carcinoma in this species, and presents the California sea lion as an important and currently underexploited wild animal model of carcinogenesis.


Author(s):  
Dominique M. Bovée ◽  
Lodi C. W. Roksnoer ◽  
Cornelis van Kooten ◽  
Joris I. Rotmans ◽  
Liffert Vogt ◽  
...  

Abstract Background Acidosis-induced kidney injury is mediated by the intrarenal renin-angiotensin system, for which urinary renin is a potential marker. Therefore, we hypothesized that sodium bicarbonate supplementation reduces urinary renin excretion in patients with chronic kidney disease (CKD) and metabolic acidosis. Methods Patients with CKD stage G4 and plasma bicarbonate 15–24 mmol/l were randomized to receive sodium bicarbonate (3 × 1000 mg/day, ~ 0.5 mEq/kg), sodium chloride (2 × 1,00 mg/day), or no treatment for 4 weeks (n = 15/arm). The effects on urinary renin excretion (primary outcome), other plasma and urine parameters of the renin-angiotensin system, endothelin-1, and proteinuria were analyzed. Results Forty-five patients were included (62 ± 15 years, eGFR 21 ± 5 ml/min/1.73m2, plasma bicarbonate 21.7 ± 3.3 mmol/l). Sodium bicarbonate supplementation increased plasma bicarbonate (20.8 to 23.8 mmol/l) and reduced urinary ammonium excretion (15 to 8 mmol/day, both P < 0.05). Furthermore, a trend towards lower plasma aldosterone (291 to 204 ng/L, P = 0.07) and potassium (5.1 to 4.8 mmol/l, P = 0.06) was observed in patients receiving sodium bicarbonate. Sodium bicarbonate did not significantly change the urinary excretion of renin, angiotensinogen, aldosterone, endothelin-1, albumin, or α1-microglobulin. Sodium chloride supplementation reduced plasma renin (166 to 122 ng/L), and increased the urinary excretions of angiotensinogen, albumin, and α1-microglobulin (all P < 0.05). Conclusions Despite correction of acidosis and reduction in urinary ammonium excretion, sodium bicarbonate supplementation did not improve urinary markers of the renin-angiotensin system, endothelin-1, or proteinuria. Possible explanations include bicarbonate dose, short treatment time, or the inability of urinary renin to reflect intrarenal renin-angiotensin system activity. Graphic abstract


2016 ◽  
Vol 90 (3) ◽  
pp. 696-704 ◽  
Author(s):  
Matthew R. Weir ◽  
George L. Bakris ◽  
Coleman Gross ◽  
Martha R. Mayo ◽  
Dahlia Garza ◽  
...  

2005 ◽  
Vol 5 (1) ◽  
pp. 140-142 ◽  
Author(s):  
F. D. HERNANDEZ-VELAZQUEZ ◽  
C. E. GALINDO-SANCHEZ ◽  
M. I. TAYLOR ◽  
J. DE LA ROSA-VELEZ ◽  
I. M. COTE ◽  
...  

2011 ◽  
Vol 119 (4) ◽  
pp. c348-c354 ◽  
Author(s):  
Anderson Roman Gonçalves ◽  
Arif Khwaja ◽  
Aimune K. Ahmed ◽  
Mohsen El Kossi ◽  
Meguid El Nahas

2001 ◽  
Vol 79 (6) ◽  
pp. 1080-1087 ◽  
Author(s):  
Anthony J Orr ◽  
James T Harvey

The purpose of this study was to quantify the errors associated with using fecal samples to determine the diet of the California sea lion (Zalophus californianus). Fishes and squids of known size and number were fed to five sea lions held in enclosures with seawater-filled pools. Enclosures were washed and pools were drained periodically so that sea lion feces could be collected using a 0.5 mm mesh bag. Fish otoliths and squid beaks were collected from feces and used to estimate number and size of prey eaten. An average of 50.7% (SE = 6.4%) of 430 fishes and 73.5% (SE = 12.0%) of 49 cephalopods fed to sea lions were represented by otoliths and beaks in feces, respectively. Estimated lengths of fish from feces were less than lengths of fish fed to sea lions by an average of 30.1% (SE = 2.8%). Beaks were not digested significantly; estimated lengths of squid were underestimated by an average of only 3.3% (SE = 1.5%) relative to actual lengths. Passage rates of otoliths varied, but more than 70% were recovered within 48 h after the fish was consumed. Passage rates of beaks were generally less than those of otoliths; six beaks (11%) were collected in feces 4 days after the squid were eaten. Correction factors were created to more reliably estimate the number and size of fishes and cephalopods eaten by California sea lions.


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