Adapting conservation breeding techniques using a data-driven approach to restore the 'Alalā (Hawaiian crow, Corvus hawaiiensis).

For some critically endangered species, conservation breeding is a vital steppingstone toward re-establishing wild populations. The 'Alalā (Hawaiian crow, Corvus hawaiiensis), currently extinct in the wild, exists today only in a conservation breeding program, which, for many years, utilized successful hands-on husbandry approaches such as separating and resocializing pairs, providing partially manmade nests, artificially incubating eggs, and puppet rearing nestlings. Yet, a top priority of any conservation breeding program is to retain natural behaviors essential to postrelease survival and reproduction, to achieve successful reintroduction and restoration to the wild.

Animal Welfare in Conservation Breeding: Applications and Challenges.

Animal welfare and conservation breeding have overlapping and compatible goals that are occasionally divergent. Efforts to improve enclosures, provide enriching experiences, and address behavioral and physical needs further the causes of animal welfare in all zoo settings. However, by mitigating stress, increasing behavioral competence, and enhancing reproduction, health, and survival, conservation breeding programs must also focus on preparing animals for release into the wild.

Come on baby, let's do the twist: the kinematics of killing in loggerhead shrikes.

Shrikes use their beaks for procuring, dispatching and processing their arthropod and vertebrate prey. However, it is not clear how the raptor-like bill of this predatory songbird functions to kill vertebrate prey that may weigh more than the shrike itself. In this paper, using high-speed videography, we observed that upon seizing prey with their beaks, shrikes performed rapid (6-17 Hz; 49-71 rad s) axial head-rolling movements.

Lack of interaction between ErbB2 and insulin receptor substrate signaling in breast cancer.

Background: ErbB2 Receptor Tyrosine Kinase 2 (ErbB2, HER2/Neu) is amplified in breast cancer and associated with poor prognosis. Growing evidence suggests interplay between ErbB2 and insulin-like growth factor (IGF) signaling. For example, ErbB2 inhibitors can block IGF-induced signaling while, conversely, IGF1R inhibitors can inhibit ErbB2 action.

Role of IGF1R in Breast Cancer Subtypes, Stemness, and Lineage Differentiation.

Insulin-like growth factor (IGF) signaling is fundamental for growth and survival. A large body of evidence (laboratory, epidemiological, and clinical) implicates the exploitation of this pathway in cancer. Up to 50% of breast tumors express the activated form of the type 1 insulin-like growth factor receptor (IGF1R).

Expression of Six1 in luminal breast cancers predicts poor prognosis and promotes increases in tumor initiating cells by activation of extracellular signal-regulated kinase and transforming growth factor-beta signaling pathways.

Introduction: Mammary-specific overexpression of Six1 in mice induces tumors that resemble human breast cancer, some having undergone epithelial to mesenchymal transition (EMT) and exhibiting stem/progenitor cell features. Six1 overexpression in human breast cancer cells promotes EMT and metastatic dissemination. We hypothesized that Six1 plays a role in the tumor initiating cell (TIC) population specifically in certain subtypes of breast cancer, and that by understanding its mechanism of action, we could potentially develop new means to target TICs.

Contribution of xanthine oxidoreductase to mammary epithelial and breast cancer cell differentiation in part modulates inhibitor of differentiation-1.

Loss of xanthine oxidoreductase (XOR) has been linked to aggressive breast cancer in vivo and to breast cancer cell aggressiveness in vitro. In the present study, we hypothesized that the contribution of XOR to the development of the normal mammary gland may underlie its capacity to modulate breast cancer. We contrasted in vitro and in vivo developmental systems by differentiation marker and microarray analyses.

Homeoprotein Six1 increases TGF-beta type I receptor and converts TGF-beta signaling from suppressive to supportive for tumor growth.

The Six1 homeodomain protein is a developmental transcription factor that has been implicated in tumor onset and progression. Our recent work shows that Six1 overexpression in human breast cancer cell lines is sufficient to induce epithelial-to-mesenchymal transition (EMT) and metastasis. Importantly, Six1-induced EMT and metastasis are dependent on TGF-β signaling.

Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression.

From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis.

Ribozyme cleavage reveals connections between mRNA release from the site of transcription and pre-mRNA processing.

We report a functional connection between splicing and transcript release from the DNA. A Pol II CTD mutant inhibited not only splicing but also RNA release from the site of transcription. A ribozyme situated downstream of the gene restored accurate splicing inhibited by the CTD mutant or a mutant poly(A) site, suggesting that cleavage liberates RNA from a niche that is inaccessible to splicing factors.