On the productivity of the diminutive suffixation in Greek child language*

This paper addresses the issue of the productivity of derivational structures, namely diminutives, in the acquisition of Greek as a first language. In order to determine the productivity of diminutive patterns, the rate at which ‘new’ diminutives appear in the speech of a Greek child on a monthly basis (‘rate of additions’) is compared to the respective frequency rates of the diminutive patterns in the same data. The present approach shows how productivity may be determined in the absence of truly innovative uses

How mothers experience personal growth after a perinatal loss

In the UK, babies are considered stillborn when they are born dead after the 24th week of gestation. Death within the first four weeks of life is defined as a neonatal death. Both stillbirths and neonatal deaths comprise perinatal deaths. This type of bereavement constitutes a traumatic loss and although there is a plethora of research focusing on the resulting parental psychopathology, research on adaptive grief resolution and posttraumatic growth is scarce. Qualitative methodologies exploring perinatal bereavement and posttraumatic growth from a perspective of counselling psychology are absent in the literature although repeatedly invited by theorists. To date, only one quantitative study has explored the phenomenon of posttraumatic growth on bereaved parents after a perinatal loss (Büchi, et al., 2007). Moreover, the available qualitative literature on bereaved mothers after a perinatal loss is conducted by disciplines other than psychology and has largely focused on birth, hospital practices, burial ceremonies and the initial grief reactions. Thus, this project aims to address psychology’s relative neglect of the topic by exploring qualitatively “How mothers experience personal growth after a perinatal loss”. The research methodology employed was Interpretative Phenomenological Analysis (IPA). Eight semi-structured interviews with women who had lost their firstborn baby perinatally were conducted. The analysis revealed four super-ordinate themes; the first and the second mainly present the traumatic quality of this type of bereavement and the multiple losses involved. The third super-ordinate theme presents all the coping mechanisms that were activated by participants in order to work through their loss; while the fourth presents the positive changes that came as a consequence of the experience and their efforts to psychologically survive that loss. The research findings suggest that following this traumatic loss mothers, struggling with distress and anguish, can also experience positive transformations. The possible role of counselling psychologists and psychotherapists in this journey of personal positive transformation of bereaved mothers is explored

BAX (BCL2-associated X protein)

Review on BAX (BCL2-associated X protein), with data on DNA, on the protein encoded, and where the gene is implicated

BCL2L12 (BCL2-like 12 (proline-rich))

Review on BCL2L12 (BCL2-like 12 (proline-rich)), with data on DNA, on the protein encoded, and where the gene is implicated

Pancreatic cancer cells resistance to gemcitabine: the role of MUC4 mucin

BACKGROUND: A major obstacle to the successful management of pancreatic cancer is to acquire resistance to the existing chemotherapeutic agents. Resistance to gemcitabine, the standard first-line chemotherapeutic agent for advanced and metastatic pancreatic cancer, is mainly attributed to an altered apoptotic threshold in the pancreatic cancer. The MUC4 transmembrane glycoprotein is aberrantly overexpressed in the pancreatic cancer and recently, has been shown to increase pancreatic tumour cell growth by the inhibition of apoptosis. METHODS: Effect of MUC4 on pancreatic cancer cells resistance to gemcitabine was studied in MUC4-expressing and MUC4-knocked down pancreatic cancer cell lines after treatment with gemcitabine by Annexin-V staining, DNA fragmentation assay, assessment of mitochondrial cytochrome c release, immunoblotting and co-immunoprecipitation techniques. RESULTS: Annexin-V staining and DNA fragmentation experiment demonstrated that MUC4 protects CD18/HPAF pancreatic cancer cells from gemcitabine-induced apoptosis. In concert with these results, MUC4 also attenuated mitochondrial cytochrome c release and the activation of caspase-9. Further, our results showed that MUC4 exerts anti-apoptotic function through HER2/extracellular signal-regulated kinase-dependent phosphorylation and inactivation of the pro-apoptotic protein Bad. CONCLUSION: Our results elucidate the function of MUC4 in imparting resistance to pancreatic cancer cells against gemcitabine through the activation of anti-apoptotic pathways and, thereby, promoting cell survival

Heat Stress Enhances the Accumulation of Polyadenylated Mitochondrial Transcripts in Arabidopsis thaliana

Background: Polyadenylation of RNA has a decisive influence on RNA stability. Depending on the organisms or subcellular compartment, it either enhances transcript stability or targets RNAs for degradation. In plant mitochondria, polyadenylation promotes RNA degradation, and polyadenylated mitochondrial transcripts are therefore widely considered to be rare and unstable. We followed up a surprising observation that a large number of mitochondrial transcripts are detectable in microarray experiments that used poly(A)-specific RNA probes, and that these transcript levels are significantly enhanced after heat treatment. Methodology/Principal Findings: As the Columbia genome contains a complete set of mitochondrial genes, we had to identify polymorphisms to differentiate between nuclear and mitochondrial copies of a mitochondrial transcript. We found that the affected transcripts were uncapped transcripts of mitochondrial origin, which were polyadenylated at multiple sites within their 39region. Heat-induced enhancement of these transcripts was quickly restored during a short recovery period. Conclusions/Significance: Our results show that polyadenylated transcripts of mitochondrial origin are more stable than previously suggested, and that their steady-state levels can even be significantly enhanced under certain conditions. As many microarrays contain mitochondrial probes, due to the frequent transfer of mitochondrial genes into the genome

CCR9-CCL25 interactions promote cisplatin resistance in breast cancer cell through Akt activation in a PI3K-dependent and FAK-independent fashion

<p>Abstract</p> <p>Background</p> <p>Chemotherapy heavily relies on apoptosis to kill breast cancer (BrCa) cells. Many breast tumors respond to chemotherapy, but cells that survive this initial response gain resistance to subsequent treatments. This leads to aggressive cell variants with an enhanced ability to migrate, invade and survive at secondary sites. Metastasis and chemoresistance are responsible for most cancer-related deaths; hence, therapies designed to minimize both are greatly needed. We have recently shown that CCR9-CCL25 interactions promote BrCa cell migration and invasion, while others have shown that this axis play important role in T cell survival. In this study we have shown potential role of CCR9-CCL25 axis in breast cancer cell survival and therapeutic efficacy of cisplatin.</p> <p>Methods</p> <p>Bromodeoxyuridine (BrdU) incorporation, Vybrant apoptosis and TUNEL assays were performed to ascertain the role of CCR9-CCL25 axis in cisplatin-induced apoptosis of BrCa cells. Fast Activated Cell-based ELISA (FACE) assay was used to quantify <it>In situ </it>activation of PI3K^p85, Akt^Ser473, GSK-3β^Ser9and FKHR^Thr24in breast cancer cells with or without cisplatin treatment in presence or absence of CCL25.</p> <p>Results</p> <p>CCR9-CCL25 axis provides survival advantage to BrCa cells and inhibits cisplatin-induced apoptosis in a PI3K-dependent and focal adhesion kinase (FAK)-independent fashion. Furthermore, CCR9-CCL25 axis activates cell-survival signals through Akt and subsequent glycogen synthase kinase-3 beta (GSK-3β) and forkhead in human rhabdomyosarcoma (FKHR) inactivation. These results show that CCR9-CCL25 axis play important role in BrCa cell survival and low chemotherapeutic efficacy of cisplatin primarily through PI3K/Akt dependent fashion.</p