Elevated expression of neuropeptide signaling genes in the eyestalk ganglia and Y-organ of Gecarcinus lateralis individuals that are refractory to molt induction.

Molting is induced in decapod crustaceans via multiple leg autotomy (MLA) or eyestalk ablation (ESA). MLA removes five or more walking legs, which are regenerated and become functional appendages at ecdysis. ESA eliminates the primary source of molt-inhibiting hormone (MIH) and crustacean hyperglycemic hormone (CHH), which suppress the production of molting hormones (ecdysteroids) from the molting gland or Y-organ (YO). Both MLA and ESA are effective methods for molt induction in Gecarcinus lateralis. However, some G. lateralis individuals are refractory to MLA, as they fail to complete ecdysis by 12weeks post-MLA; these animals are in the "blocked" condition. Quantitative polymerase chain reaction was used to quantify mRNA levels of neuropeptide and mechanistic target of rapamycin (mTOR) signaling genes in YO, eyestalk ganglia (ESG), thoracic ganglion (TG), and brain of intact and blocked animals. Six of the seven neuropeptide signaling genes, three of four mTOR signaling genes, and Gl-elongation factor 2 (EF2) mRNA levels were significantly higher in the ESG of blocked animals. Gl-MIH and Gl-CHH mRNA levels were higher in the TG and brain of blocked animals and levels increased in both control and blocked animals in response to ESA. By contrast, mRNA levels of Gl-EF2 and five of the 10 MIH signaling pathway genes in the YO were two to four orders of magnitude higher in blocked animals compared to controls. These data suggest that increased MIH and CHH synthesis in the ESG contributes to the prevention of molt induction by MLA in blocked animals. The up-regulation of MIH signaling genes in the YO of blocked animals suggests that the YO is more sensitive to MIH produced in the ESG, as well as MIH produced in brain and TG of ESA animals. Both the up-regulation of MIH signaling genes in the YO and of Gl-MIH and Gl-CHH in the ESG, TG, and brain appear to contribute to some G. lateralis individuals being refractory to MLA and ESA.

The growing spine: how spinal deformities influence normal spine and thoracic cage growth.

PURPOSE: This article aims to provide an overview of how spinal deformities can alter normal spine and thoracic cage growth. METHODS: Some of the data presented in this article are gathered from studies performed in 1980 and 1990, and their applicability to populations of different ethnicity, geography or developmental stage has not yet been elucidated. In the present article, older concepts have been integrated with newer scientific data available to give the reader the basis for a better understanding of both normal and abnormal spine and thoracic cage growth. RESULTS: A thorough analysis of different parameters, such as weight, standing and sitting height, body mass index, thoracic perimeter, arm span, T1-S1 spinal segment length, and respiratory function, help the surgeon to choose the best treatment modality. Respiratory problems can develop after a precocious vertebral arthrodesis or as a consequence of pre-existing severe vertebral deformities and can vary in patterns and timing, according to the existing degree of deformity. The varying extent of an experimental arthrodesis also affects differently both growth and thoracopulmonary function. CONCLUSIONS: Growth is a succession of acceleration and deceleration phases and a perfect knowledge of normal growth parameters is mandatory to understand the pathologic modifications induced on a growing spine by an early onset spinal deformity. The challenges associated with the growing spine for the surgeon include preservation of the thoracic spine, thoracic cage, and lung growth without reducing spinal motion.