ABSTRACT
Seasonality of the nematode Gnathostoma turgidum in Virginia opossums (Didelphis virginiana) in the wild has been reported; however, the mechanisms involved in deworming are unknown. We monitored the parasitologic and biologic changes in four Virginia opossums naturally infected with G. turgidum by coproparasitologic examination and abdominal ultrasonography. Eggs became detectable in the feces of opossums in May, peaked in July and August, and suddenly decreased in October. Adults of G. turgidum were expelled in the feces mainly in September. Ultrasonography of the liver showed slight damage during May. Lesions in the stomach appeared in April and persisted until September. The abnormalities of the liver and stomach were resolved in November. These data suggest that G. turgidum is likely expelled as a result of host immunologic mechanisms, although termination of a natural life span cannot be definitively excluded.
Subject(s)
Didelphis/parasitology , Gnathostoma/physiology , Gnathostomiasis/veterinary , Animals , Feces/parasitology , Female , Gnathostomiasis/epidemiology , Gnathostomiasis/immunology , Gnathostomiasis/parasitology , Male , Mexico/epidemiology , SeasonsABSTRACT
This study investigated whether white spot syndrome virus and Infectious hypodermal and hematopoietic necrosis virus, can survive in wild invertebrates and vertebrates in the environment surrounding shrimp farms along the Pacific coast of Mexico. The evidences imply that both viruses have a potential of persisting in crabs, blue, white and brown shrimps. The most prevalent virus, IHHNV was present in 19.5% (344/1736) followed by WSSV in 3.6% (65/1736). Coinfection of WSSV and IHHNV was also detected in crabs, blue and white shrimps. This is the first prevalence report of WSSV and IHHNV associated with wildlife species in Mexico.
Subject(s)
Aquatic Organisms/virology , Densovirinae/isolation & purification , White spot syndrome virus 1/isolation & purification , Animals , Disease Susceptibility , MexicoABSTRACT
We studied the sites of prolactin inhibition upon FSH-iniduced ovarian steroidogenesis and the ability of prolactin (Prl) to inhibit the synthesis of estradiol and cAMP accumulation under the stimulation of FSH or cAMP-dependent activators. The participation of other signal pathways such as PKC and Gi proteins on the inhibitory actions of Prl was also investigated using calfostine C and pertusis toxin as inhibitors. Results showed a dose-dependent prolactin decrease in FSH-induced estradiol and cAMP production prior and after the generation of the cyclic nucleotide by a mechanisn involving the catalytic subunit of adeniyl cyclase and/or through activation of PKC or by the interaction with pertusin toxin-sensitive G proteins. Our results suggest a mechanism by which G protein-coupled receptors are linked with those coupled with tyrosine kinase through the involvement of a Gi protein mediated mechanism.
Subject(s)
Estradiol/biosynthesis , Granulosa Cells/metabolism , Prolactin/pharmacology , Adenylyl Cyclases/metabolism , Analysis of Variance , Animals , Catalysis , Cells, Cultured , Cyclic AMP/metabolism , Enzyme Activation , Female , Follicle Stimulating Hormone/pharmacology , GTP-Binding Proteins , Granulosa Cells/drug effects , Naphthalenes/pharmacology , Pertussis Toxin/pharmacology , Protein Kinase C/metabolism , Protein-Tyrosine Kinases/metabolism , Rats , Rats, Wistar , Receptors, FSH/metabolism , Signal Transduction , Stimulation, ChemicalABSTRACT
En este estudio se investigaron los sitios probables de la acción inhibitoria de prolactina (Prl) sobre la esteroidogénesis ovárica inducida por la hormona folículo estimulante (FSH). Para esta finalidad se estudió la capacidad de cultivos primarios de células de la granulosa de la rata de sintetizar estradiol y AMPc bajo la estimulación con FSH o de activadores de la vía dependiente de AMPc en presencia de Prl humana. La participación de otros sistemas de transducción de señal como los dependientes de PKC y proteínas Gi en los mecanismos de acción inhibitoria de la Prl fue también investigada utilizando inhibidores de estos sistemas como la calfostina C y la toxina pertusis. Los resultados demostraron la habilidad de la Prl de alterar la esteroidogénesis previa y posterior a la generación de AMPc, muy probablemente por mecanismos que involucran la activación de la subunidad catalítica de la adenilato ciclasa, así como a través de interactuar con sistemas de transducción de señal dependientes de PKC y proteínas sensibles a la toxina pertusis. Nuestros resultados sugieren un mecanismo de interacción entre receptores acoplados a proteínas G con aquéllos acoplados a cinasas de tirosinas mediado muy probablemente por vías de señalización dependientes de proteínas Gi.
We studied the sites of prolactin inhibition upon FSH induced ovarian steroidogenesis and the ability of prolactin (Prl) to inhibit the synthesis of estradiol and cAMP accumulation under the stimulation of FSH or cAMP dependent activators. The participation of other signal pathways such as PKC and Gi proteins on the inhibitory actions of Prl was also investigated using calfostine C andpertusis toxin as inhibitors. Results showed a dose dependent prolactin decrease in FSH-induced estradiol and cAMP production prior and after the generation of the cyclic nucleotide by a mechanism involving the catalytic subunit of adenyl cyclase and/or through activation of PKC or by the interaction with pertusin toxin sensitive G proteins. Our results suggest a mechanism by which G protein coupled receptors are linked with those coupled with tyrosine kinase through the involvement of a Gi protein mediated mechanism.
