Stephens College is a women's college located in Columbia, Missouri. It is the second oldest female educational establishment that is still a women's college in the United States. It was founded on August 24, 1833, as the Columbia Female Academy. In 1856, David H. Hickman helped secure the college's charter under the name The Columbia Female Baptist Academy. In the late 19th century it was renamed Stephens Female College after James L. Stephens endowed the college with $20,000. The campus includes a National Historic District: Stephens College South Campus Historic District. Wikipedia.
News Article | December 5, 2016
JERUSALEM--(BUSINESS WIRE)--Teva Pharmaceutical Industries Ltd. (NYSE and TASE: TEVA) today announced that Dipankar Bhattacharjee has been appointed President and Chief Executive Officer, Global Generic Medicines Group, effective today. Mr. Bhattacharjee, who has served as President and CEO of Teva Generics Europe since April 2013, succeeds Sigurdur (Siggi) Olafsson, who will step down from his role and remain active with the Company until officially retiring at the end of the first quarter of 2017 to ensure an orderly transition. Mr. Bhattacharjee will be based in the U.S. As President and CEO of Teva Generics Europe, Mr. Bhattacharjee has a proven track record of improving revenues and profitability, significantly increasing operating profit margins in the European generics business. Under his leadership, Teva’s European business demonstrated consistent improvement in sales and profits, establishing Teva as one of the premier generics companies in Europe. He has focused on improving and enhancing the European generics operations, leading a full European integration of Actavis Generics and overseeing successful new product launches. “Dipankar has been an integral part of Teva's management team since he joined the Company in 2009, and we are fortunate to have someone with his experience to lead our generics business at this important time,” said Erez Vigodman, Teva’s President and Chief Executive Officer. “Teva will benefit from Dipankar’s extensive experience in generics and specialty medicines, his financial and operational expertise and his deep understanding and appreciation for Teva’s culture of innovation and our outstanding people. As we continue to focus on integrating and realizing the value of the Actavis Generics transaction, which is progressing according to plan, Dipankar and his team will focus on generating organic growth through new launches and replenishing the pipeline through our industry-leading R&D, and drive efficiencies across the generics organization. I have been incredibly impressed by Dipankar’s work in Europe, and I am confident that his capabilities, proven track record and experience make him the right person for this global leadership role.” “I am honored to lead the Global Generic Medicines Group, a business with a robust R&D pipeline, a talented team of employees, well-established relationships with business partners and customers and significant prospects for organic growth,” said Mr. Bhattacharjee. “With the integration of Actavis proceeding on schedule and the complementary U.S. distribution capabilities provided by our recent acquisition of Anda, we have a matchless opportunity to add value in the U.S. healthcare system, and in the fast-changing global generics marketplace. I look forward to working with the rest of the management team to strengthen our generics business and help position Teva to achieve its full potential.” “I am proud of the incredible progress we have made since I joined Teva to lead the newly formed Global Generic Medicines Group,” said Mr. Olafsson. “I firmly believe that Teva is the best positioned generics company in the industry in terms of market presence, manufacturing capabilities and R&D pipeline. I am grateful for the support from the talented team at Teva and am fully committed to ensuring a smooth transition into 2017.” Mr. Vigodman continued, “On behalf of the Board and management team, I would like to thank Siggi for all of his valuable contributions to Teva over the years. He has been instrumental to the Company’s growth, and we wish him the very best in the future.” Dipankar Bhattacharjee was appointed President and CEO, Generics Europe in April 2013. Mr. Bhattacharjee joined Teva as General Manager, Teva UK Limited in 2009. Prior to joining Teva, he served 15 years at Bausch + Lomb in various senior roles, including Vice President Commercial in both Europe and Asia-Pacific regions and Corporate Vice President and President, Asia Pacific Region. He began his career at Nestle S.A. and Bank of America. Mr. Bhattacharjee received his BA degree in economics from St. Stephens College, University of Delhi, and his Masters degree in Management Studies from Jamnalal Bajaj Institute of Management Studies, University of Mumbai. In conjunction with today’s announcement, Teva is reaffirming its full-year 2016 outlook. Revenues for full year 2016 are expected to be $21.6-$21.9 billion and revenues for the fourth quarter of year 2016 are expected to be $6.2-$6.5 billion. Non-GAAP EPS for 2016 is expected to be $5.10-$5.20, based on a weighted average number of shares of 1,020 million; non-GAAP EPS is expected to be $1.34-$1.44, based on a weighted average number of shares of 1,077 million. Cash flow from operating activities for 2016 is expected to be $4.8-$5.0 billion; cash flow from operating activities for the fourth quarter of 2016 is expected to be $1.0-$1.2 billion. Teva now expects to provide its 2017 guidance in January 2017. Teva Pharmaceutical Industries Ltd. (NYSE and TASE: TEVA) is a leading global pharmaceutical company that delivers high-quality, patient-centric healthcare solutions used by millions of patients every day. Headquartered in Israel, Teva is the world’s largest generic medicines producer, leveraging its portfolio of more than 1,000 molecules to produce a wide range of generic products in nearly every therapeutic area. In specialty medicines, Teva has a world-leading position in innovative treatments for disorders of the central nervous system, including pain, as well as a strong portfolio of respiratory products. Teva integrates its generics and specialty capabilities in its global research and development division to create new ways of addressing unmet patient needs by combining drug development capabilities with devices, services and technologies. Teva's net revenues in 2015 amounted to $19.7 billion. For more information, visit www.tevapharm.com. Teva's Safe Harbor Statement under the U. S. Private Securities Litigation Reform Act of 1995: This press release contains forward-looking statements, which are based on management’s current beliefs and expectations and involve a number of known and unknown risks and uncertainties that could cause our future results, performance or achievements to differ significantly from the results, performance or achievements expressed or implied by such forward-looking statements. Important factors that could cause or contribute to such differences include risks relating to: our ability to develop and commercialize additional pharmaceutical products; competition for our specialty products, especially Copaxone® (which faces competition from orally-administered alternatives and existing and potential generic versions); our ability to integrate Allergan plc’s worldwide generic pharmaceuticals business (“Actavis Generics”) and to realize the anticipated benefits of the acquisition (and the timing of realizing such benefits); the fact that following the consummation of the Actavis Generics acquisition, we are dependent to a much larger extent than previously on our generic pharmaceutical business; potential restrictions on our ability to engage in additional transactions or incur additional indebtedness as a result of the substantial amount of debt incurred to finance the Actavis Generics acquisition; the fact that for a period of time following the Actavis Generics acquisition, we will have significantly less cash on hand than previously, which could adversely affect our ability to grow; the possibility of material fines, penalties and other sanctions and other adverse consequences arising out of our ongoing FCPA investigations and related matters; our ability to achieve expected results from investments in our pipeline of specialty and other products; our ability to identify and successfully bid for suitable acquisition targets or licensing opportunities, or to consummate and integrate acquisitions; the extent to which any manufacturing or quality control problems damage our reputation for quality production and require costly remediation; increased government scrutiny in both the U.S. and Europe of our patent settlement agreements; our exposure to currency fluctuations and restrictions as well as credit risks; the effectiveness of our patents, confidentiality agreements and other measures to protect the intellectual property rights of our specialty medicines; the effects of reforms in healthcare regulation and pharmaceutical pricing, reimbursement and coverage; competition for our generic products, both from other pharmaceutical companies and as a result of increased governmental pricing pressures; governmental investigations into sales and marketing practices, particularly for our specialty pharmaceutical products; adverse effects of political or economic instability, major hostilities or acts of terrorism on our significant worldwide operations; interruptions in our supply chain or problems with internal or third-party information technology systems that adversely affect our complex manufacturing processes; significant disruptions of our information technology systems or breaches of our data security; competition for our specialty pharmaceutical businesses from companies with greater resources and capabilities; the impact of continuing consolidation of our distributors and customers; decreased opportunities to obtain U.S. market exclusivity for significant new generic products; potential liability in the U.S., Europe and other markets for sales of generic products prior to a final resolution of outstanding patent litigation; our potential exposure to product liability claims that are not covered by insurance; any failure to recruit or retain key personnel, or to attract additional executive and managerial talent; any failures to comply with complex Medicare and Medicaid reporting and payment obligations; significant impairment charges relating to intangible assets, goodwill and property, plant and equipment; the effects of increased leverage and our resulting reliance on access to the capital markets; potentially significant increases in tax liabilities; the effect on our overall effective tax rate of the termination or expiration of governmental programs or tax benefits, or of a change in our business; variations in patent laws that may adversely affect our ability to manufacture our products in the most efficient manner; environmental risks; and other factors that are discussed in our Annual Report on Form 20-F for the year ended December 31, 2015 and in our other filings with the U.S. Securities and Exchange Commission (the "SEC"). Forward-looking statements speak only as of the date on which they are made and we assume no obligation to update or revise any forward-looking statements or other information contained herein, whether as a result of new information, future events or otherwise. You are advised, however, to consult any additional disclosures we make in our reports to the SEC on Form 6-K. Also note that we provide a cautionary discussion of risks and uncertainties under “Risk Factors” in our Annual Report on Form 20-F for the year ended December 31, 2015. These are factors that we believe could cause our actual results to differ materially from expected results. Other factors besides those listed could also adversely affect us. This discussion is provided as permitted by the Private Securities Litigation Reform Act of 1995.
Ge Y.,Stephens College |
O'Shea D.F.,Stephens College
Chemical Society Reviews | Year: 2016
Azadipyrromethenes were first described over 70 years ago as blue pigments, but now are rapidly emerging as a compound class with highly desirable near infrared photophysical properties. Since the turn of the century several routes to azadipyrromethenes have been developed and numerous post-synthesis derivatizations have allowed for their exploitation in both biological and material sciences. The relative ease of access to specifically designed derivatives is now allowing their use in multiple technological formats from real-time fluorescence imaging, to solar energy materials, to optoelectronic devices and many more. In this review we have highlighted the synthetic component of this story as it is the ability to generate the designer azadipyrromethene that opens the door to exciting applications. © 2016The Royal Society of Chemistry.
Henshall D.C.,Stephens College
Current Opinion in Neurology | Year: 2014
Purpose of review: This review provides a synthesis of recent profiling studies investigating microRNA (miRNA) changes in experimental and human epilepsy, and outlines mechanistic, therapeutic and diagnostic potentials of this research area for clinical practice. Recent findings: A series of studies in experimental and human epilepsy have undertaken large-scale expression profiling of miRNAs, key regulatory molecules in cells controlling protein levels. Levels of over 100 different miRNAs were found to either increase or decrease in the hippocampus, of which more than 20 were identified in more than one study, including higher levels of miR-23a, miR-34a, miR-132 and miR-146a. Altered levels of enzymes involved in miRNA biogenesis and function, including Dicer and Argonaute 2, have also been found in epileptic brain tissue. Functional studies using oligonucleotide-based inhibitors support roles for miRNAs in the control of cell death, synaptic structure, inflammation and the immune response. Finally, data show brain injuries that precipitate epilepsy generate unique miRNA profiles in biofluids. Summary: miRNA represents a potentially important mechanism controlling protein levels in epilepsy. As such, miRNAs might be targeted to prevent or disrupt epilepsy as well as serve as diagnostic biomarkers of epileptogenesis.
Roy L.,Indian Association for The Cultivation of Science |
Mittal S.,Stephens College |
Paul A.,Indian Association for The Cultivation of Science
Angewandte Chemie - International Edition | Year: 2012
Chemical hydrogen storage: Theoretical investigations showed that the dehydrogenation of chemisorbed hydrogen atoms on boron nitride nanotubes (BNNT) could be triggered by appropriate reagents through simultaneous proton and hydride transfer (see picture). The computed free-energy of the activation barrier for the reduction of formaldehyde to methanol by chemisorbed hydrogen atoms on a zigzag BNNT was predicted to be 12.7kcal mol -1 in THF. Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Mitrugno A.,Stephens College |
Williams D.,Beaumont Hospital |
Kerrigan S.W.,Stephens College |
Moran N.,Stephens College
Blood | Year: 2014
Platelets play a role in cancer by acting as a dynamic reservoir of effectors that facilitate tumor vascularization, growth, and metastasis. However, little information is available about the mechanism of tumor cell-induced platelet secretion (TCIPS) or the molecular machinery by which effector molecules are released from platelets. Here we demonstrate that tumor cells directly induce platelet secretion. Preincubation of platelets with human colon cancer (Caco-2), prostate cancer (PC3M-luc), or breast cancer cells (MDA-MB-231;MCF-7) resulted in a marked dose-dependent secretion of dense granules. Importantly, TCIPS preceded aggregation which always displayed a characteristic lag time. We investigated the role of platelet receptors and downstream molecules in TCIPS. The most potent modulators of TCIPS were the pharmacologic antagonists of Syk kinase, phospholipase C and protein kinase C, all downstream mediators of the immunoreceptor tyrosine-based activation motif (ITAM) cascade in platelets. Supporting this, we demonstrated a central role for the immune Fcγ receptor IIa (FcγRIIa) in mediating platelet-tumor cell cross-talk. In conclusion, we demonstrate that cancer cells can promote platelet dense-granule secretion, which is required to augment platelet aggregation. In addition, we show a novel essential role for FcγRIIa in prostate cancer cell-induced platelet activation opening the opportunity to develop novel antimetastatic therapies. © 2014 by The American Society of Hematology.
Allen S.,Stephens College |
Moran N.,Stephens College
Seminars in Thrombosis and Hemostasis | Year: 2015
The diversity of integrins and their complex role in many diseases suggests great potential for this superfamily as drug targets. The initial successes of anti-integrin therapeutics in the treatment of thrombotic disorders suggested that similar anti-integrin agents could be developed for the treatment of inflammatory disorders. While initially a promising strategy, inhibition of the integrins proved to be elusive despite the discovery of highly potent inhibitors. This is due to several reasons, including redundancy among the integrins and the importance of integrins in key physiological systems. Further exploration of the selective role for distinct leukocytic integrins indicated that homing of inflammatory cells to select disease sites depends on a highly regulated expression of discrete integrins and their ligands in limited locations. Selective control of integrin function is also regulated by local chemokines permitting exquisite homing of populations of inflammatory cells to disease sites. A more complete understanding of the regulation of integrin activation in disease states will permit the development of more effective and specific anti-integrin therapeutic agents. Copyright © 2015 by Thieme Medical Publishers, Inc.
Unkelbach C.,TU Dortmund |
O'Shea D.F.,Stephens College |
Strohmann C.,TU Dortmund
Angewandte Chemie - International Edition | Year: 2014
The metalation of benzene by Schlosser's base (nBuLi/tBuOK) occurs smoothly in THF at low temperatures to afford a discrete mixed-metal Li 2K4 cluster that contains phenyl anions and tert-butoxide. The aggregate itself exhibits superbasic behavior by metalating toluene. The delocalized benzyl anion obtained this way πbonds to potassium counterions, thereby creating a 2D coordination polymer. A discrete mixed-metal Li 2K4 cluster that contains phenyl anions and tert-butoxide is formed smoothly by the metalation of benzene by Schlosser's base (nBuLi/tBuOK) in THF at low temperatures (see picture). The aggregate itself exhibits superbasic behavior by metalating toluene. The delocalized benzyl anion obtained this way πbonds to potassium counterions, thereby creating a 2D coordination polymer. © 2014 WILEY-VCH Verlag GmbH.
Killian L.M.,Stephens College |
Docherty J.R.,Stephens College
European Journal of Pharmacology | Year: 2014
Stimulants are banned in competition by the World Anti-Doping Agency, except for a small number of therapeutic agents subject to monitoring, including bupropion. We have examined the potency of bupropion in comparison with two agents banned in competition, adrafinil and modafinil, and with cocaine and desipramine as blockers of the noradrenaline re-uptake transporter in peripheral tissues of the rat. For studies in vivo, the pressor response to noradrenaline in the anaesthetized rat was studied. Cocaine, desipramine and bupropion at doses of 0.1, 0.3 and 1 mg/kg, respectively, significantly increased the pressor response to noradrenaline. Overall, cocaine and desipramine were approximately 2-5 times more potent than bupropion in vivo in the rat. Adrafinil and modafinil (both 3 mg/kg) did not significantly affect the pressor response. Bupropion was chosen for further study. In 1 Hz paced rat right ventricular strips, bupropion (30 μM) significantly increased the potency of noradrenaline at increasing the force of contraction. In rat vas deferens, bupropion and cocaine produced concentration-dependent increases in the contractile response to nerve stimulation, and cocaine was 11 times more potent than bupropion. Since bupropion is used clinically in doses of up to 300 mg, it is likely that bupropion has actions at the noradrenaline transporter, and thus cardiovascular stimulant actions, in clinical doses. This may explain findings of increased exercise performance with bupropion. © 2014 Elsevier B.V.
Kinahan C.E.,Stephens College |
Mazloom S.,Cleveland Clinic |
Fernandez A.P.,Cleveland Clinic
British Journal of Dermatology | Year: 2015
Background Smoking is a well-established risk factor for developing psoriasis and is associated with development of more severe disease. Smoking cessation does not appear to result in clinical improvement of psoriasis. Whether smoking in patients with psoriasis impacts response to systemic therapy is unknown. Objectives To determine whether smokers with psoriasis with or without psoriatic arthritis respond to systemic agents as well as nonsmokers do. Methods We performed a retrospective review of patients with moderate-to-severe psoriasis with or without psoriatic arthritis seen at our institution, who were either active smokers or nonsmokers, and calculated changes in Physician's Global Assessment (PGA) scores after 3-16 months of systemic treatment. We also calculated the average number of systemic treatments tried per patient. Results Sixty-six patients (46 nonsmokers, 20 smokers) met our inclusion criteria. Changes in PGA scores between baseline and 3-16 months after initiation of systemic treatment did not significantly differ between smokers and nonsmokers, nor did the average number of systemic treatments tried per patient. We detected a borderline significant trend in the percentage of patients who had significant outcomes after treatment, with a higher percentage of patients smoking < 10 cigarettes daily achieving target PGA scores compared with those smoking > 10 cigarettes daily. Limitations of our study include its retrospective nature and the relatively small number of patients meeting our inclusion criteria. Conclusions In our retrospectively studied cohort, smoking did not affect response to systemic treatment in patients with psoriasis. A prospective study examining the complex relationship between smoking, psoriasis and response to systemic therapy is warranted to explore this association better. © 2014 British Association of Dermatologists.
Sridharan R.,Stephens College |
Karp J.M.,Harvard University |
Zhao W.,University of California at Irvine
Biochemical Society Transactions | Year: 2014
For the last decade, stem cell therapies have demonstrated enormous potential for solving some of the most tragic illnesses, diseases and tissue defects worldwide. Currently, more than 1300 clinical trials use stem cell therapy to solve a spectrum of cardiovascular, neurodegenerative and autoimmune diseases (http://www.clinicaltrials.gov, Jan 2014, search term: stem cell therapy; only currently recruiting and completed studies are included in the search). However, the efficacy of stem cell transplantation in patients has not been well established, and recent clinical trials have produced mixed results. We attribute this lack of efficacy in part to an incomplete understanding of the fate of stem cells following transplantation and the lack of control over cell fate, especially cell-homing and therapeutic functions. In the present review, we present two of our recently developed technologies that aim to address the above-mentioned bottlenecks in stem cell therapy specifically in the areas of MSCs (mesenchymal stem cells): (i) aptamer-based cell-surface sensors to study cellular microenvironments, and (ii) mRNA engineering technology to enhance the homing and immunomodulatory efficacy of transplanted stem cells. The first engineering strategy aims to elucidate the basic cellular signalling that occurs in the microenvironment of transplanted stem cells in real time. The second technique involves a simple mRNA transfection that improves the homing and anti-inflammatory capability of MSCs. Although we have specifically applied these engineering techniques to MSCs, these strategies can be incorporated for almost any cell type to determine and control the fate of transplanted stem cells. © 2014 Biochemical Society.