Complete mitochondrial genome of the Pasiphila chloerata (Lepidoptera: Geometridae) and its phylogenetic implications.

In this study, the complete mitochondrial genome of Pasiphila chloerata (Mabille) was sequenced and its phylogenetic implications were investigated. The P. chloerata mitogenome is a circular, double-stranded molecule, with 15,602 bp in length. The typical 37 mitochondrial genes (13 protein-coding genes (PCGs), 22 tRNAs, and 2 rRNAs) and an A + T-rich region are included. Gene content and arrangement are highly conserved and typical of Lepidoptera. Phylogenetic analyses based on the combined 37 mitochondrial genes consistently recovered the Larentiinae and Ennominae involved are reciprocally monophyletic with the highest supports. The P. chloerata was clustered with other two members of the Larentiinae, reinforcing that of previous morphological studies.

The first mitochondrial genome from the Sterrhinae (Lepidoptera: Geometridae) and its phylogenetic implications.

In this study, the complete mitochondrial genome of a geometrid species, Idaea simplicior (Prout), was sequenced. The I. simplicior mitogenome is a circular, double-stranded molecule, with 15,950 bp in size. The typical 37 mitochondrial genes (13 PCGs, 22 tRNAs, and 2 rRNAs) and an A + T-rich region are included. Gene content and arrangement are highly conserved and typical of Lepidoptera. Interestingly, the I. simplicior mitogenome is rich in microsatellite sequences of (TA)12-18 with a scattered distribution in six intergenic regions. Phylogenetic analyses based on the combined 37 mitochondrial genes show that the Larentiinae and Ennominae are monophyletic. The Sterrhinae, which is represented by the only I. simplicior sequenced in this study, shows a closer relationship with the Larentiinae than Ennominae, which confirms previous morphological studies.

T-2 toxin induces degenerative articular changes in rodents: link to Kaschin-Beck disease.

Osteoarthritis (OA) is a degenerative joint disease that is characterized by joint pain and a progressive loss of articular cartilage. Kaschin-Beck Disease is a form of endemic OA in China whose etiology is unclear, but epidemiological data indicate a possible link to trichothecenes mycotoxin exposure. In vitro, T-2 toxin, a trichothecenes mycotoxin, has been demonstrated to inhibit aggrecan synthesis and promote aggrecanase and pro-inflammatory cytokine production in cultured chondrocytes. To assess the effects of T-2 toxin on articular cartilage in vivo, Wistar rats were fed a diet containing T-2 toxin (100 ng/kg chow) for six and ten months. Following six months of T-2 toxin exposure, histopathological changes in femorotibial cartilage were characterized by chondrocyte degeneration/necrosis and loss, chondrocyte clones, and loss of proteoglycan staining of articular cartilage, sometimes involving the entire thickness of the cartilage in the tibial plateaus and femoral condyles. By ten months, in addition to these changes, there was evidence of cartilage fibration in some rats. In conclusion, T-2 toxin exposure in rats induced degenerative lesions in articular cartilage similar to spontaneous OA, lending support to an etiologic role of mycotoxins in Kaschin-Beck Disease. T-2 toxin-induced degenerative joint disease may be a useful model of metabolic polyarticular OA.

[Effect of triptorelin and an extended-interval dosing regimen in the treatment of patients with endometriosis and adenomyoma].

OBJECTIVE: To study the role of triptorelin in the treatment of patients with endometriosis, adenomyoma and fibromyoma and the effect of an extended-interval dosing regimen. METHODS: Seventy patients suffering from endometriosis, adenomyoma and fibromyoma were divided into two groups: extended-interval dosing (group E) and conventional dosing (group C). There were treated with injection of triptorelin 3.75 mg intramuscularly either every 6 weeks of totally four dose regimen (group E) or every 4 weeks of six dose regimen (group C). Comparison was made in improvement of symptoms, size of uterus and volume of tumor, as well as in serum levels of 17beta-estradiol, luteinizing hormone, and follicle-stimulating hormone. RESULTS: In each group, symptoms and tumor growth significantly improved after treatment (P < 0.05). For the patients of both groups E and C, the levels of gonadotropins and gonadal steroids were obviously reduced throughout the treatment period and up to 8 - 10 weeks after the injection of the last dose (P < 0.05). The hormonal profile of group E was similar to group C (P > 0.05). CONCLUSIONS: Gonadotropin-releasing hormone agonist is efficacious in the treatment of endometriosis and adenomyoma through reducing the serum levels of follicle-stimulating hormone, luteinizing hormone and 17beta-estradiol. The curative effect is satisfactory in most patients receiving an extended interval dosing regimen. To reduce the cost of treatment, the extended-interval dosing regimen of triptorelin should be adopted in well-equipped hospitals.