First report of fibropapillomatosis in an olive ridley turtle Lepidochelys olivacea from the southeastern Pacific.

An adult olive ridley turtle Lepidochelys olivacea with lesions suggestive of fibropapillomatosis was rescued on the coast of San Antonio, central Chile. Histopathologic analysis showed an exophytic and pedunculated mass formed by epidermal papillary projections supported by fibrovascular cores, epidermal hyperplasia and marked orthokeratotic hyperkeratosis. ChHV5 unique long genes UL27, UL28 and UL30 were amplified from tumor lesions and sequenced for phylogeny. Phylogenetic reconstruction showed the Chilean sequences clustering with the Eastern Pacific group. This is the first case of fibropapillomatosis in an olive ridley turtle diagnosed in Chile and in the southeastern Pacific region. Our results suggest a regional grouping of ChHV5 variants independent of the marine turtle's species.

Fibropapillomatosis in a Green Sea Turtle ( Chelonia mydas) from the Southeastern Pacific.

Fibropapillomatosis is a neoplastic disease that afflicts sea turtles. Although it is disseminated worldwide, cases of the disease have not been reported in the southeastern Pacific region. We describe a case of fibropapillomatosis in a green sea turtle ( Chelonia mydas) during its rehabilitation at the Machalilla National Park Rehabilitation Center, Ecuador. Viral presence was confirmed by PCR, targeting fragments of the chelonid alphaherpesvirus 5 (ChHV5) unique long (UL) genes, UL27, UL28, and UL30. The amplicons were sequenced and included in a global phylogenetic analysis of the virus with other reported sequences from GenBank. Results showed that the available viral sequences segregated into five phylogeographic groups: western Atlantic and eastern Caribbean, central Pacific, western Pacific, Atlantic, and eastern Pacific groups. The concatenated ChHV5 sequences from Ecuador clustered with the eastern Pacific sequences.

Chemotherapy inhibits skeletal muscle ubiquitin-proteasome-dependent proteolysis.

Chemotherapy has cachectic effects, but it is unknown whether cytostatic agents alter skeletal muscle proteolysis. We hypothesized that chemotherapy-induced alterations in protein synthesis should result in the increased incidence of abnormal proteins, which in turn should stimulate ubiquitin-proteasome-dependent proteolysis. The effects of the nitrosourea cystemustine were investigated in skeletal muscles from both healthy and colon 26 adenocarcinoma-bearing mice, an appropriate model for testing the impact of cytostatic agents. Muscle wasting was seen in both groups of mice 4 days after a single cystemustine injection, and the drug further increased the loss of muscle proteins already apparent in tumor-bearing animals. Cystemustine cured the tumor-bearing mice with 100% efficacy. Surprisingly, within 11 days of treatment, rates of muscle proteolysis progressively decreased below basal levels observed in healthy control mice and contributed to the cessation of muscle wasting. Proteasome-dependent proteolysis was inhibited by mechanisms that include reduced mRNA levels for 20S and 26S proteasome subunits, decreased protein levels of 20S proteasome subunits and the S14 non-ATPase subunit of the 26S proteasome, and impaired chymotrypsin- and trypsin-like activities of the enzyme. A combination of cisplatin and ifosfamide, two drugs that are widely used in the treatment of cancer patients, also depressed the expression of proteasomal subunits in muscles from rats bearing the MatB adenocarcinoma below basal levels. Thus, a down-regulation of ubiquitin-proteasome-dependent proteolysis is observed with various cytostatic agents and contributes to reverse the chemotherapy-induced muscle wasting.