Prevalence of the pathogenic crustacean virus Callinectes sapidus reovirus 1 near flow-through blue crab aquaculture in Chesapeake Bay, USA.

Understanding the ecology of diseases is important to understanding variability in abundance, and therefore management, of marine animals exploited commercially. The blue crab Callinectes sapidus fills a crucial benthic-pelagic niche in Atlantic estuarine ecosystems and supports large commercial fisheries in both North and South America. In the USA, pre-molt blue crabs are typically held in short-term shedding (ecdysis) facilities to produce soft-shell crabs of increased value. However, mortality rates in these facilities are high and commonly associated with the pathogenic C. sapidus reovirus 1 (CsRV1). To assess whether crab mortalities in these facilities might increase CsRV1 prevalence in wild crab populations, tissue sampled from crabs collected over 2 summers either near to or far from shedding facilities using flow-through water systems were tested by reverse transcription quantitative PCR (RT-qPCR) for the presence of CsRV1 RNA. In support of our hypothesis, PCR data identified the probability of detecting CsRV1 in wild crabs sampled close to shedding facilities to be 78% higher than in crabs sampled from far sites. PCR detections were also 61-72% more probable in male crabs and 21% more likely in male and female crabs over the minimum landing size. As the prevalence at which CsRV1 was detected varied within seasons, among locations and between years, blue crab migration and/or population fluctuations appear to also be involved.

Delimiting species within the Lysmata vittata (Stimpson, 1860) (Decapoda: Lysmatidae) species complex in a world full of invaders.

Historically, Lysmata vittata has been reported with a near global non-polar distribution. Early studies reported a wide morphological variation in this species, which served as a basis for further synonymization of at least four species. Herein, we investigated the species diversity within L. vittata complex and tested whether L. rauli and L. durbanensis are valid species instead of junior synonyms of L. vittata. Our integrated morphological and molecular data strongly supports the validity of at least six taxonomic entities within the broader L. vittata complex, including L. rauli and L. durbanensis and three undescribed species. Multivariate analyses highlighted prominent morphological differences in accessory branch structure of dorsolateral antennular flagellum, number of carpal and meral segments of the second pereopod, and color pattern which segregated shrimps into distinct morpho-groups. Phylogenetic analyses supported morphological groupings and recovered five widely divergent lineages, which corresponded to the morphological groupings: L. vittata sensu stricto; L. rauli sensu stricto; L. sp. CHINA; L. sp. AUS1; and L. sp. AUS2. Therefore, we formally resurrect L. rauli to valid species status and posit it is native to the subtropical and tropical Indo West-Pacific. Although data were limited, we also formally resurrect L. durbanensis to valid species status from southern Africa. Our results imply L. vittata and L. rauli are exotic species in the western Atlantic, New Zealand, and the Mediterranean. This study provides a solid framework to continue untangling the historic L. vittata species complex, which is likely to include additional species to the ones included in the present study.

Vaccination with inhibin-α provides effective immunotherapy against testicular stromal cell tumors.

BACKGROUND: Testicular cancer is the most common male neoplasm occurring in men between the ages of 20 and 34. Although germ-line testicular tumors respond favorably to current standard of care, testicular stromal cell (TSC) tumors derived from Sertoli cells or Leydig cells often fail to respond to chemotherapy or radiation therapy and have a 5-year overall survival significantly lower than the more common and more treatable germ line testicular tumors. METHODS: To improve outcomes for TSC cancer, we have developed a therapeutic vaccine targeting inhibin-α, a protein produced by normal Sertoli and Leydig cells of the testes and expressed in the majority of TSC tumors. RESULTS: We found that vaccination against recombinant mouse inhibin-α provides protection and therapy against transplantable I-10 mouse TSC tumors in male BALB/c mice. Similarly, we found that vaccination with the immunodominant p215-234 peptide of inhibin-α (Inα 215-234) inhibits the growth of autochthonous TSC tumors occurring in male SJL.AMH-SV40Tag transgenic mice. The tumor immunity and enhanced overall survival induced by inhibin-α vaccination may be passively transferred into naive male BALB/c recipients with either CD4+ T cells, B220+ B cells, or sera from inhibin-α primed mice. CONCLUSIONS: Considering the lack of any alternative effective treatment for chemo- and radiation-resistant TSC tumors, our results provide for the first time a rational basis for immune-mediated control of these aggressive and lethal variants of testicular cancer.

Regulation of Murine Ovarian Epithelial Carcinoma by Vaccination against the Cytoplasmic Domain of Anti-Müllerian Hormone Receptor II.

Anti-Müllerian hormone receptor, type II (AMHR2), is a differentiation protein expressed in 90% of primary epithelial ovarian carcinomas (EOCs), the most deadly gynecologic malignancy. We propose that AMHR2 may serve as a useful target for vaccination against EOC. To this end, we generated the recombinant 399-amino acid cytoplasmic domain of mouse AMHR2 (AMHR2-CD) and tested its efficacy as a vaccine target in inhibiting growth of the ID8 transplantable EOC cell line in C57BL/6 mice and in preventing growth of autochthonous EOCs that occur spontaneously in transgenic mice. We found that AMHR2-CD immunization of C57BL/6 females induced a prominent antigen-specific proinflammatory CD4+ T cell response that resulted in a mild transient autoimmune oophoritis that resolved rapidly with no detectable lingering adverse effects on ovarian function. AMHR2-CD vaccination significantly inhibited ID8 tumor growth when administered either prophylactically or therapeutically, and protection against EOC growth was passively transferred into naive recipients with AMHR2-CD-primed CD4+ T cells but not with primed B cells. In addition, prophylactic AMHR2-CD vaccination of TgMISIIR-TAg transgenic mice significantly inhibited growth of autochthonous EOCs and provided a 41.7% increase in mean overall survival. We conclude that AMHR2-CD vaccination provides effective immunotherapy of EOC with relatively benign autoimmune complications.

A re-assessment of the effects of treatment with a non-steroidal anti-inflammatory (ibuprofen) on promoting axon regeneration via RhoA inhibition after spinal cord injury.

This study was undertaken as part of the NIH "Facilities of Research Excellence-Spinal Cord Injury" project to support independent replication of published studies. Here, we repeat key parts of a study reporting that rats treated with ibuprofen via subcutaneous minipump exhibited greater recovery of motor function and enhanced axonal growth after spinal cord injury. We carried out 3 separate experiments in which young adult female Sprague-Dawley rats received dorsal over-hemisections at T6-T7, and then were implanted with osmotic minipumps for subcutaneous delivery of ibuprofen or saline. Motor function was assessed with the BBB Locomotor Rating Scale, footprint analysis, and with a grid walk task. Combined group sizes for functional analyses were n=34 rats treated with ibuprofen and n=39 controls. Bladder function was assessed by measuring the amount of urine retained in the bladder twice per day. Four weeks post-injury, CST axons were traced by injecting BDA into the sensorimotor cortex; 5HT axons were assessed by immunostaining. Analysis of data from all rats revealed no significant differences between groups. Analysis of data excluding rats with lesions that were larger than intended indicated improved locomotor function in ibuprofen-treated rats at early post-lesion intervals in one of the individual experiments. Rats that received Ibuprofen did not demonstrate statistically significant improvements in bladder function. Quantitative analyses of CST and 5HT axon distribution also did not reveal differences between ibuprofen-treated and control rats. Taken together, our results only partially replicate the findings that treatment with ibuprofen improves motor function after SCI but fail to replicate findings regarding enhanced axon growth.