430 research outputs found

    New Directions and New Problems for Arms Transfers Policy

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    The climate for the transfer of American arms to other countries has changed in the year since Ronald Reagan became President. In the fin-a months of President Carter\u27s term there was a commitment to constraint. But it was undermined by events during the last two years of Mr. Carter\u27s Presidency. Just as substantial obstacles prevented President Carter from restraining the sale of arms as much as he would have liked, so roo wilI President Reagan confront many obstacles in his plan to increase arms transfers

    Set & Drift: Conflicting Trends for Arms Transfer Restraint

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    President Carter stated that the United States could not be both the world\u27s champion of peace and the world\u27s leading supplier of the weapons of war

    The Grizzly, October 25, 2012

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    UCARE Directs Week of Local Service • UC Gears up for Homecoming • Report on Grads\u27 Successes • Grizzly Gala: Food, Drinks and Music • Teach for America • Homecoming Nominations • Headphone Disco • Opinion: Ursinus Sports Teams Need More Support; Varsity Teams and Athletes Overvalued at Ursinus • Ursinus Finalizes New Athletics Logo • Senior Spotlight: Kristin Hanratty, UC Volleyball • Homecoming Special for Class of \u2713https://digitalcommons.ursinus.edu/grizzlynews/1867/thumbnail.jp

    The Grizzly, October 11, 2012

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    Students Debate Alcohol Rules • UC Conservatives Feel Outnumbered • UC Celebrates LGBT History • Art, Music Festival • Literary Society Welcomes Student Writers • No Bells Ever Resided in Bomberger Bell Tower • R.D. Brooks Karns is a 2nd Lt. in the National Guard • UCTV Returns to Campus After 3-Year Absence • Opinion: We Must Inform Ourselves on Syria; Romney, a Stronger Candidate After Debate • UC Athletics Struggle Throughout Week • Senior Spotlight: Leah Shaw, Soccer • Sports Spotlight: Bryan Ellis, Footballhttps://digitalcommons.ursinus.edu/grizzlynews/1866/thumbnail.jp

    The Grizzly, November 15, 2012

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    Website Sparks Campus Controversy • New Sculptures Share Connections with CIE Text • Underclassmen to Register on New Electronic System • Sandy Victims Still Need Aid • UCDC Fall Preview • Dr. Romano\u27s Book • Radio City Christmas Spectacular • Commuters at UC • Opinion: Disputed Website Shows Ursinus\u27 True Colors; It\u27s Becoming More Popular to Follow Celebrities\u27 Lives • Rough Time to be a Philadelphia Fan • Women\u27s Basketball Looks to Youth for Victories • Men\u27s Basketball Looks to Reboundhttps://digitalcommons.ursinus.edu/grizzlynews/1870/thumbnail.jp

    Failure of Supervised Chloroquine and Primaquine Regimen for the Treatment of Plasmodium vivax in the Peruvian Amazon

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    The widespread use of primaquine (PQ) and chloroquine (CQ), together, may be responsible for the relatively few, isolated cases of chloroquine-resistant P. vivax (CQRPV) that have been reported from South America. We report here a case of P. vivax from the Amazon Basin of Peru that recurred against normally therapeutic blood levels of CQ. Four out of 540 patients treated with combination CQ and PQ had a symptomatic recurrence of P. vivax parasitemia within 35 days of treatment initiation, possibly indicating CQ failure. Whole blood total CQ level for one of these four subjects was 95 ng/ml on the day of recurrence. Based on published criteria that delineate CQRPV as a P. vivax parasitemia, either recrudescence or relapse, that appears against CQ blood levels >100 ng/mL, we document the occurrence of a P. vivax strain in Peru that had unusually high tolerance to the synergistic combination therapy of CQ + PQ that normally works quite well

    Neutrophil Signaling During Myocardial Infarction Wound Repair

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    Neutrophils are key effector cells of the innate immune system, serving as a first line of defense in the response to injury and playing essential roles in the wound healing process. Following myocardial infarction (MI), neutrophils infiltrate into the infarct region to propagate inflammation and begin the initial phase of cardiac wound repair. Pro-inflammatory neutrophils release proteases to degrade extracellular matrix (ECM), a necessary step for the removal of necrotic myocytes as a prelude for scar formation. Neutrophils transition their phenotype over time to regulate MI inflammation resolution and stabilize scar formation. Neutrophils contribute to the evolution from inflammation to resolution and scar formation by serving anti-inflammatory and repair functions. As anti-inflammatory cells, neutrophils contribute ECM proteins during scar formation, in particular fibronectin, galectin-3, and vimentin. The diverse and polarizing functions that contribute to MI wound repair make this innate immune cell a viable target to improve MI outcomes. Thus, understanding the signaling involved in neutrophil physiology in the context of MI may help to identify novel therapeutic targets

    Redefining the Expression and Function of the Inhibitor of Differentiation 1 in Mammary Gland Development

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    The accumulation of poorly differentiated cells is a hallmark of breast neoplasia and progression. Thus an understanding of the factors controlling mammary differentiation is critical to a proper understanding of breast tumourigenesis. The Inhibitor of Differentiation 1 (Id1) protein has well documented roles in the control of mammary epithelial differentiation and proliferation in vitro and breast cancer progression in vivo. However, it has not been determined whether Id1 expression is sufficient for the inhibition of mammary epithelial differentiation or the promotion of neoplastic transformation in vivo. We now show that Id1 is not commonly expressed by the luminal mammary epithelia, as previously reported. Generation and analysis of a transgenic mouse model of Id1 overexpression in the mammary gland reveals that Id1 is insufficient for neoplastic progression in virgin animals or to prevent terminal differentiation of the luminal epithelia during pregnancy and lactation. Together, these data demonstrate that there is no luminal cell-autonomous role for Id1 in mammary epithelial cell fate determination, ductal morphogenesis and terminal differentiation
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