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This paper analysed Sickle cell anaemia literature on Nigeria listed in PubMed to understand the research performance of medical researchers on sickle cell anaemia literature on Nigeria. Data covering the period of 2006-2016 were collected from the PubMed, a citation database developed by the National Centre for Biotechnology Information (NCBI).The search strategy used was ((sickle cell anaemia) OR (sickle cell anemia)) AND Nigeria AND (('2006/01/01'[PDat]: '2016/12/31'[PDat])), bearing in mind variance in spelling (anaemia and anemia), which retrieved 326 sickle cell literature on Nigeria between 2006 and 2016. Article productivity increased between 2006 and 2010. However, there was a drastic drop in article publication between 2010 and 2011 as well as between 2013 and 2015. The degree of collaboration ranged between 0.85 and 1. University of Nigeria Teaching Hospital, Enugu, Nigeria, had the highest number of contributing authors. Authors published more in journals located in Nigeria, with Nigeria Journal of Clinical Practice being the most prolific publication outlet for authors publishing sickle cell anaemia literature on Nigeria. Keywords Bibliometric Analysis, Sickle Cell Anaemia, Nigeria, PubMed, Introduction Sickle cell anaemia, recognized as a major public health problem by the World Health Organization (WHO) (WHO, 2006) is a genetic blood disorder characterized by abnormal red blood cells [...]

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1467-8551.2007.00553.x Byline: Andreas Al-Laham ([double dagger]), Terry L. Amburgey (*), Kimberly Bates ([dagger]) Abstract: Few studies have moved beyond the dyadic level of an ongoing alliance and examined factors contributing to the success of entering a series of alliances. In this paper we expect biotechnology firms over time to learn from their alliance experience and to develop general alliance capabilities. Specifically, we expect the speed with which they enter into new research alliances, e.g. their alliance formation rate, to be affected by capabilities built up in prior alliances as well as by characteristics of their partners. We use longitudinal event history data for the complete population of US biotechnology firms for 1973-1999 to test four hypotheses about factors affecting the rate of new alliance formation. Our analysis suggests that the speed of entering research alliances is affected by prior experience of the focal firm, but not by partner characteristics. Our findings provide evidence that biotech firms learn how to learn more effectively from multiple research alliances; however, this effect is generalized and not tied to specific characteristics of the alliance partner. Author Affiliation: ([double dagger])TU Kaiserslautern, Lehrstuhl fur Internationales Management, D-67653 Kaiserslautern, Postfach 3049, Germany (*)Joseph L. Rotman School of Management, University of Toronto, Toronto, Ontario, Canada ([dagger])Trent University, Gzowski College, 1600 West Bank Drive, Peterborough, Ontario, K9J 7B8 Canada Article note: Corresponding author email: kimberlybates@trentu.ca

Biotechnology is a rapidly expanding field of science that has led to the formation of a large number of companies that together form a significant sector within the Australian economy. Even though there has been considerable growth in the Australian biotechnology sector as a whole, a large percentage of Australian biotechnology firms are small and medium sized enterprises (SMEs) that suffer from a lack of funding and expertise. The development and management of effective strategic alliances are critical to the success and development of biotechnology firms as they provide opportunities to share resources and expertise, access funding and develop new ideas. However, developing and managing strategic alliances is fraught with difficulties which are compounded by size and resource asymmetries and the nature of the biotechnology market. In this paper, we identify the difficulties faced by biotechnology firms and examine the importance of knowledge management related to alliance formation and development with special reference to the Australian context. We examine the knowledge and expertise that are required to be effective in developing strategic alliances in the biotechnology sector and provide a framework for managing knowledge related to strategic alliances. We suggest that critical systems approaches, in particular creative holism, are needed to manage the various forms of knowledge associated with strategic alliances. Keywords knowledge management; creative holism; biotechnology; strategic alliances; systems approaches, INTRODUCTION Although there has been rapid growth in the Australian biotechnology sector in recent years many biotechnology firms face difficulties in developing as viable entities. The development of strategic alliances [...]

A critical component for successful entrance of baccalaureate graduates into academic and industrial scientific positions is the acquisition of relevant hands-on laboratory experience and problem solving skills. We designed a senior-level inquiry-based course that simulates an operational research laboratory with the goals of applying diverse laboratory techniques combined with a learning environment promoting independent thinking, organizational skills, data management and team work skills. Students formulated research proposals that were reviewed by faculty two months prior to the beginning of the semester. Approved projects represented broad-based research directions so that, in subsequent laboratory meetings, students were exposed to problems and techniques ancillary to their individual projects. In the formal course, students held bi-weekly lab meetings with instructors acting primarily as facilitators. Students pooled their knowledge and talents to solve current problems, even though their research topics were unrelated. Upon completion of the project, students submitted formal reports in the format of a scientific paper and orally presented their research to the College of Science and Technology. The research proposal, lab notebook, final paper and presentation were critiqued by the biotechnology faculty and included as a major component of their research experience portfolio. This project was supported by NSF CCLI grant #DUE0410712.

Byline: Peilei Fan, Kazuo N. Watanabe This paper uses India's biotech industry as a case to study the catching up of late-industrialising economies. Several conclusions can be drawn. First, innovation capability is critical for domestic companies' success. Second, certain institutional factors have encouraged indigenous technology development of domestic companies in India, such as the price control imposed by the government, technology transfer from Indian public and international research institutions, and funding from the government and the international charity organisations. Third, domestic companies have utilised manufacturing capability to quickly turn the technology into products and reinvest the profit into R&D.

Metastasis is the main cause of death for patients with breast cancer. Many studies have characterized the genomic landscape of breast cancer during its early stages. However, there is evidence that genomic alterations are acquired during the evolution of cancers from their early to late stages, and that the genomic landscape of early cancers is not representative of that of lethal cancers.sup.1-7. Here we investigated the landscape of somatic alterations in 617 metastatic breast cancers. Nine driver genes (TP53, ESR1, GATA3, KMT2C, NCOR1, AKT1, NF1, RIC8A and RB1) were more frequently mutated in metastatic breast cancers that expressed hormone receptors (oestrogen and/or progesterone receptors; HR.sup.+) but did not have high levels of HER2 (HER2.sup.-; n = 381), when compared to early breast cancers from The Cancer Genome Atlas. In addition, 18 amplicons were more frequently observed in HR.sup.+/HER2.sup.- metastatic breast cancers. These cancers showed an increase in mutational signatures S2, S3, S10, S13 and S17. Among the gene alterations that were enriched in HR.sup.+/HER2.sup.- metastatic breast cancers, mutations in TP53, RB1 and NF1, together with S10, S13 and S17, were associated with poor outcome. Metastatic triple-negative breast cancers showed an increase in the frequency of somatic biallelic loss-of-function mutations in genes related to homologous recombination DNA repair, compared to early triple-negative breast cancers (7% versus 2%). Finally, metastatic breast cancers showed an increase in mutational burden and clonal diversity compared to early breast cancers. Thus, the genomic landscape of metastatic breast cancer is enriched in clinically relevant genomic alterations and is more complex than that of early breast cancer. The identification of genomic alterations associated with poor outcome will allow earlier and better selection of patients who require the use of treatments that are still in clinical trials. The genetic complexity observed in advanced breast cancer suggests that such treatments should be introduced as early as possible in the disease course. Patient data from six clinical trials are used to compare the genomic landscapes of breast cancer metastases with those of primary tumours, revealing an increase in mutational burden and clonal diversity., Author(s): François Bertucci [sup.1] , Charlotte K. Y. Ng [sup.2] [sup.3] [sup.24] , Anne Patsouris [sup.4] [sup.5] , Nathalie Droin [sup.6] [sup.7] [sup.8] , Salvatore Piscuoglio [sup.2] [sup.3] , Nadine [...]

Germinal centres are important sites for antibody diversification and affinity maturation, and are also a common origin of B cell malignancies. Despite being made up of motile cells, germinal centres are tightly confined within B cell follicles. The cues that promote this confinement are incompletely understood. P2RY8 is a G[alpha].sub.13-coupled receptor that mediates the inhibition of migration and regulates the growth of B cells in lymphoid tissues.sup.1,2. P2RY8 is frequently mutated in germinal-centre B cell-like diffuse large B cell lymphoma (GCB-DLBCL) and Burkitt lymphoma.sup.1,3-6, and the ligand for this receptor has not yet been identified. Here we perform a search for P2RY8 ligands and find P2RY8 bioactivity in bile and in culture supernatants of several mouse and human cell lines. Using a seven-step biochemical fractionation procedure and a drop-out mass spectrometry approach, we show that a previously undescribed biomolecule, S-geranylgeranyl-l-glutathione (GGG), is a potent P2RY8 ligand that is detectable in lymphoid tissues at the nanomolar level. GGG inhibited the chemokine-mediated migration of human germinal-centre B cells and T follicular helper cells, and antagonized the induction of phosphorylated AKT in germinal-centre B cells. We also found that the enzyme gamma-glutamyltransferase-5 (GGT5), which was highly expressed by follicular dendritic cells, metabolized GGG to a form that did not activate the receptor. Overexpression of GGT5 disrupted the ability of P2RY8 to promote B cell confinement to germinal centres, which indicates that GGT5 establishes a GGG gradient in lymphoid tissues. This work defines GGG as an intercellular signalling molecule that is involved in organizing and controlling germinal-centre responses. As the P2RY8 locus is modified in several other types of cancer in addition to GCB-DLBCL and Burkitt lymphoma, we speculate that GGG might have organizing and growth-regulatory roles in multiple human tissues. S-geranylgeranyl-l-glutathione (GGG) is identified as a cell signalling molecule that interacts with the receptor P2RY8 to mediate migration inhibition and growth regulation of germinal-centre B cells., Author(s): Erick Lu [sup.1] , Finn D. Wolfreys [sup.1] , Jagan R. Muppidi [sup.1] [sup.2] , Ying Xu [sup.1] , Jason G. Cyster [sup.1] Author Affiliations: (1) Howard Hughes Medical [...]

Neutrophil (PMN) infiltration of the intestinal mucosa is a hallmark of tissue injury associated with inflammatory bowel diseases (IBDs). The pathological effects of PMNs are largely attributed to the release of soluble mediators and reactive oxygen species (ROS). We identified what we believe is a new, ROS-independent mechanism whereby activated tissue-infiltrating PMNs release microparticles armed with proinflammatory microRNAs (miR-23a and miR-155). Using IBD clinical samples, and in vitro and in vivo injury models, we show that PMN-derived miR-23a and miR-155 promote accumulation of double-strand breaks (DSBs) by inducing lamin B1-dependent replication fork collapse and inhibition of homologous recombination (HR) by targeting HR-regulator RAD51. DSB accumulation in injured epithelium led to impaired colonic healing and genomic instability. Targeted inhibition of miR-23a and miR-155 in cultured intestinal epithelial cells and in acutely injured mucosa decreased the detrimental effects of PMNs and enhanced tissue healing responses, suggesting that this approach can be used in therapies aimed at resolution of inflammation, in wound healing, and potentially to prevent neoplasia., Introduction Epithelial injury resulting from an exacerbated inflammatory response is a common pathological feature of gastrointestinal disorders, including inflammatory bowel diseases (IBDs) (1, 2). Another important feature of IBD is [...]

Mutations that attenuate homologous recombination (HR)-mediated repair promote tumorigenesis and sensitize cells to chemotherapeutics that cause replication fork collapse, a phenotype known as 'BRCAness'.sup.1. BRCAness tumours arise from loss-of-function mutations in 22 genes.sup.1. Of these genes, all but one (CDK12) function directly in the HR repair pathway.sup.1. CDK12 phosphorylates serine 2 of the RNA polymerase II C-terminal domain heptapeptide repeat.sup.2-7, a modification that regulates transcription elongation, splicing, and cleavage and polyadenylation.sup.8,9. Genome-wide expression studies suggest that depletion of CDK12 abrogates the expression of several HR genes relatively specifically, thereby blunting HR repair.sup.3-7,10,11. This observation suggests that the mutational status of CDK12 may predict sensitivity to targeted treatments against BRCAness, such as PARP1 inhibitors, and that CDK12 inhibitors may induce sensitization of HR-competent tumours to these treatments.sup.6,7,10,11. Despite growing clinical interest, the mechanism by which CDK12 regulates HR genes remains unknown. Here we show that CDK12 globally suppresses intronic polyadenylation events in mouse embryonic stem cells, enabling the production of full-length gene products. Many HR genes harbour more intronic polyadenylation sites than other expressed genes, and these sites are particularly sensitive to loss of CDK12. The cumulative effect of these sites accounts for the enhanced sensitivity of HR gene expression to CDK12 loss, and we find that this mechanism is conserved in human tumours that contain loss-of-function CDK12 mutations. This work clarifies the function of CDK12 and underscores its potential both as a chemotherapeutic target and as a tumour biomarker.The kinase CDK12 suppresses usage of intronic polyadenylation sites and thereby promotes the expression of genes involved in homologous recombination DNA repair., Author(s): Sara J. Dubbury [sup.1] [sup.2] , Paul L. Boutz [sup.1] [sup.3] , Phillip A. Sharp [sup.1] [sup.2] Author Affiliations:(1) Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, [...]