Jacksonville, IL, United States

Illinois College

Jacksonville, IL, United States

Illinois College is a private, liberal arts college, affiliated with the United Church of Christ and the Presbyterian Church , and located in Jacksonville, Illinois. It was the second college founded in Illinois, but the first to grant a degree . It was founded in 1829 by the Illinois Band, students from Yale University who traveled westward to found new colleges. It briefly served as the state's first medical school from 1843–1848, and became co-educational in 1903. Wikipedia.

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News Article | April 17, 2017
Site: co.newswire.com

A new community event slated for Father’s Day Weekend will provide youth athletes the opportunity for great sports experiences, assist area organizations in raising funds for their causes and offer volunteer opportunities for area residents. The Bob Emig Foundation will host the inaugural Mississippi River Games (MRG) on June 16-18, 2017 in Southwestern Illinois and St. Louis, MO.  MRG is an Olympic-style amateur youth sports festival for the 10 states that border the Mississippi River -- Arkansas, Illinois, Iowa, Kentucky, Louisiana, Minnesota, Mississippi, Missouri, Tennessee and Wisconsin. Athletes will compete to win medals in their respective sport, and one state will be honored as the Bob Emig Foundation Cup winner based on our point system. The proceeds of the MRG will benefit the mission of the Bob Emig Foundation:  Promoting the well-being of youth through sports and education. “We developed these games to provide youth athletes with a unique opportunity to participate in an Olympic-style competition,” says Aaron Emig, founder and president of the Bob Emig Foundation.  “This obviously means bringing athletes, coaches and spectators to our area which has a large impact for our economy.” But they offer more.  “We wanted to also help other youth sports organizations by giving them the opportunity to participate in the operations of the games and raise funds to further their goals and objectives,” according to Emig. Five youth sports organizations will receive a portion of the profits to support their missions.  They are: The event promises some unique sports experiences that will be fun for the youth athletes, coaches and spectators.  “The Mississippi River Games team tennis event offers competitive players a unique opportunity to play a co-ed tournament,” says Dave Lipe, Tennis Sport Commissioner and Head Coach Edwardsville High School Boys and Girls Tennis. “The games offer great summer competition from 10 different states to compete in one central location. Winning basketball states will have bragging rights throughout the year,” says Jared Newson, Basketball Sport Commissioner.  Jared currently plays Professional Basketball in the French D1 League and is founder of the Neway Elite Basketball Academy. “Another feature of the games is our leadership success program that offers a development opportunity for high school and college students who are passionate about serving student-athletes and are good with and like to help people,” says Emig. “We can't teach passion or willingness to help people, but we can teach our proven systems.  Learn more at EmigFoundation.org/Programs/Success. “Without the support of volunteers, the Mississippi River Games would not be a success. We are truly grateful for the time and energy that each volunteer will give to serve youth in our regions.” Group discounts are available for schools, clubs and organizations that register two or more teams. To learn more contact Emig at aaron@emigfoundation.org. The Mississippi River Games leadership team brings together 108 years of youth sports management experience and includes:  Emig (27 years); Newson (7 years); Juergen Huettner, Head Coach, Althoff Catholic High School Girls Soccer and Southwestern Illinois College Women Soccer (27 years); Lipe (34 years); and Sara Dietrich, Head Coach, Althoff Catholic High School Girls Volleyball (13 years). Sponsorship and advertising opportunities are also available. For more information on registering for a sport, volunteering or sponsoring, visit MississippiRiverGames.org or contact mrg@emigfoundation.org. The Bob Emig Foundation, a nonprofit, 501(c)3 tax-exempt organization, was started in 2004. Founder Aaron Emig, Bob’s oldest son, created the foundation to continue his father’s work in helping youth develop well-rounded lives by providing them a healthy sports experience.  Bob loved sports - as a participant, coach and sports writer - and felt these experiences were a contributor to the successful family and professional life he built. We believe in providing equal opportunities for youth to enjoy the many benefits of a sports experience including having fun and developing skills that they can use throughout their lives.  We encourage “going beyond the game” to allow for that learning experience on and off the field in and out of the classroom. We also honor the educators who make a tremendous difference in their lives.

News Article | May 11, 2017
Site: www.eurekalert.org

CHAMPAIGN, Ill. -- Researchers have demonstrated that a small molecule can transport iron in human cells and live animals when proteins that normally do the same job are missing, a condition that often causes severe anemia in patients. Such "molecular prosthetics" might treat a host of incurable diseases caused by protein deficiencies, such as anemias, cystic fibrosis or certain types of heart disease. Researchers at the University of Illinois and collaborators at Harvard Medical School and Northeastern University will publish their work in the May 12 issue of the journal Science. "If you've lost a hand, even a simple prosthetic device is really helpful. In the same way, we found that a small molecule that replicates the main job of a missing protein can be sufficient to restore functionality in cells and animals," said Dr. Martin D. Burke, the leader of the study. Burke is a professor of chemistry at Illinois and the interim associate dean for research at the Carle Illinois College of Medicine. "If you're sick because you have too much protein function, in many cases we can do something about it. But if you're sick because you're missing a protein that does an essential function, we struggle to do anything other than treat the symptoms. It's a huge unmet medical need," said Burke, who also is a medical doctor. Burke's team found that a small molecule called hinokitiol, derived from a species of cypress tree found in Japan, can transport iron across cell membranes that are missing transport proteins. In a healthy system, transport proteins move iron across cell membranes to uptake iron from the gut or make hemoglobin for red blood cells. But when the transport protein is missing, iron can't cross the membrane, causing anemia. The researchers found that three hinokitiol molecules can wrap around an iron atom and transport it directly across the membrane where the missing protein should be. The researchers tested hinokitiol in mice, rats and zebrafish that were missing iron-transport proteins. They found that orally administered hinokitiol restored iron uptake in the guts of mice and rats, and that simply adding it to the tank of anemic zebrafish prompted hemoglobin production. They also found that it restored iron transport in human cells taken from the lining of the gut. Next, Burke's group hopes to find more small molecules that can function as molecular prosthetics for other diseases caused by protein deficiencies, with a particular focus on cystic fibrosis. "These findings suggest that replacing missing proteins with molecular-scale prosthetics may represent a general way to think about treating a wide range of human diseases that have thus far remained out of reach with traditional medicine," Burke said. The National Institutes of Health and the Howard Hughes Medical Institute supported this work. The paper "Restored iron transport by a small molecule promotes absorption and hemoglobinization in animals" is available from scipak@aaas.org.

Daugirdas J.T.,Illinois College
Kidney International | Year: 2013

Dialysis time is increasingly being appreciated as an important measure of dialysis adequacy. Increased dialysis time leads to better control of volume excess, to reduced occurrence of intradialytic hypotension, and to better control of serum phosphorus. Nevertheless, the amount of benefit obtainable by moderate increases in dialysis time in patients following a three-times-per-week schedule has not been well established, and the analysis is confounded by associations between prescribed and/or delivered dialysis time and factors related to patient mortality. © 2012 International Society of Nephrology.

Wang K.,Illinois College
Cell Death and Disease | Year: 2014

Apoptosis is a prominent feature of liver diseases. Causative factors such as alcohol, viruses, toxic bile acids, fatty acids, drugs, and immune response, can induce apoptotic cell death via membrane receptors and intracellular stress. Apoptotic signaling network, including membrane death receptor-mediated cascade, reactive oxygen species (ROS) generation, endoplasmic reticulum (ER) stress, lysosomal permeabilization, and mitochondrial dysfunction, is intermixed each other, but one mechanism may dominate at a particular stage. Mechanisms of hepatic apoptosis are complicated by multiple signaling pathways. The progression of liver disease is affected by the balance between apoptotic and antiapoptotic capabilities. Therapeutic options of liver injury are impacted by the clear understanding toward mechanisms of hepatic apoptosis. © 2014 Macmillan Publishers Limited.

Wang K.,Illinois College
Cell Cycle | Year: 2015

Apoptosis is a primary characteristic in the pathogenesis of liver disease. Hepatic apoptosis is regulated by autophagic activity. However, mechanisms mediating their interaction remain to be determined. Basal level of autophagy ensures the physiological turnover of old and damaged organelles. Autophagy also is an adaptive response under stressful conditions. Autophagy can control cell fate through different cross-talk signals. A complex interplay between hepatic autophagy and apoptosis determines the degree of hepatic apoptosis and the progression of liver disease as demonstrated by pre-clinical models and clinical trials. This review summarizes recent advances on roles of autophagy that plays in pathophysiology of liver. The autophagic pathway can be a novel therapeutic target for liver disease. © 2015 Taylor & Francis Group, LLC.

Chen Z.W.,Illinois College
Cellular and Molecular Immunology | Year: 2013

Vγ2Vδ2 T (also known as Vγ9Vδ2 T) cells exist only in primates, and in humans represent a major γδ T-cell sub-population in the total population of circulating γδ T cells. Results from recent studies suggest that while (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMBPP) phosphoantigen from Mycobacterium tuberculosis (Mtb) and other microbes activates and expands primate Vγ2Vδ2 T cells, the Vγ2Vδ2 T-cell receptor (TCR) recognizes and binds to HMBPP on antigen-presenting cells (APC). In response to HMBPP stimulus, Vγ2Vδ2 TCRs array to form signaling-related nanoclusters or nanodomains during the activation of Vγ2Vδ2 T cells. Primary infections with HMBPP-producing pathogens drive the evolution of multieffector functional responses in Vγ2Vδ2 T cells, although Vγ2Vδ2 T cells display different patterns of responses during the acute and chronic phases of Mtb infection and in other infections. Expanded Vγ2Vδ2 T cells in primary Mtb infection can exhibit a broader TCR repertoire and a greater clonal response than previously assumed, with different distribution patterns of Vγ2Vδ2 T-cell clones in lymphoid and non-lymphoid compartments. Emerging in vivo data suggest that HMBPP activation of Vγ2Vδ2 T cells appears to impact other immune cells during infection. © 2013 CSI and USTC.

Protein disulfide isomerase (PDI) derived from intravascular cells is required for thrombus formation. However, it remains unclear whether platelet PDI contributes to the process. Using platelet-specific PDI-deficient mice, we demonstrate that PDI-null platelets have defects in aggregation and adenosine triphosphate secretion induced by thrombin, collagen, and adenosine diphosphate. Such defects were rescued by wild-type but not mutant PDI, indicating that the isomerase activity of platelet surface PDI is critical for the regulatory effect. PDI-deficient platelets expressed increased levels of intracellular ER protein 57 (ERp57) and ERp72. Platelet PDI regulated αIIbβ3 integrin activation but not P-selectin exposure, Ca(2+) mobilization, β3-talin1 interaction, or platelet spreading on immobilized fibrinogen. Inhibition of ERp57 further diminished αIIbβ3 integrin activation and aggregation of activated PDI-deficient platelets, suggesting distinct roles of PDI and ERp57 in platelet functions. We found that platelet PDI is important for thrombus formation on collagen-coated surfaces under shear. Intravital microscopy demonstrates that platelet PDI is important for platelet accumulation but not initial adhesion and fibrin generation following laser-induced arteriolar injury. Tail bleeding time in platelet-specific PDI-deficient mice were not significantly increased. Our results provide important evidence that platelet PDI is essential for thrombus formation but not for hemostasis in mice.

β2 integrins play a crucial role during neutrophil recruitment into the site of vascular inflammation. However, it remains unknown how ligand-binding activity of the integrin is regulated. Using fluorescence intravital microscopy in mice generated by crossing protein disulfide isomerase (PDI) floxed mice with lysozyme-Cre transgenic mice, we demonstrate that neutrophil PDI is required for neutrophil adhesion and crawling during tumor necrosis factor-α-induced vascular inflammation in vivo. Rescue experiments show that the isomerase activity of extracellular PDI is critical for its regulatory effect on neutrophil recruitment. Studies with blocking anti-PDI antibodies and αLβ2 or αMβ2 null mice suggest that extracellular PDI regulates αMβ2 integrin-mediated adhesive function of neutrophils during vascular inflammation. Consistently, we show that neutrophil surface PDI is important for αMβ2 integrin-mediated adhesion of human neutrophils under shear and static conditions and for binding of soluble fibrinogen to activated αMβ2 integrin. Confocal microscopy and biochemical studies reveal that neutrophil surface PDI interacts with αMβ2 integrin in lipid rafts of stimulated neutrophils and regulates αMβ2 integrin clustering, presumably by changing the redox state of the integrin. Thus, our results provide the first evidence that extracellular PDI could be a novel therapeutic target for preventing and treating inappropriate neutrophil sequestration.

Kenter A.L.,Illinois College
Seminars in Immunology | Year: 2012

Activation induced deaminase (AID) is globally targeted to immunoglobulin loci, preferentially focused to switch (S) regions and variable (V) regions, and prone to attack hotspot motifs. Nevertheless, AID deamination is not exclusive to Ig loci and the rules regulating AID targeting remain unclear. Transcription is critically required for class switch recombination and somatic hypermutation. Here, I consider the unique features associated with S region transcription leading to RNA polymerase II pausing, that in turn promote the introduction of activating chromatin remodeling, histone modifications and recruitment of AID to targeted S regions. These findings allow for a better understanding of the interplay between transcription, AID targeting and mistargeting to Ig and non-Ig loci. © 2012 Elsevier Ltd.

Agency: NSF | Branch: Standard Grant | Program: | Phase: S-STEM:SCHLR SCI TECH ENG&MATH | Award Amount: 604.67K | Year: 2015

There is an established need in the United States to increase the number of American scientists in the workforce. This NSF Scholarships in Science, Technology, Engineering, and Mathematics (S-STEM) project will improve the completion rates for math, computer science, biology, chemistry, physics, engineering and earth science transfer students from Southwestern Illinois College. Approximately, 50 scholars will participate in a two-year project that includes (a) targeted recruitment, (b) intensive mentoring and advising, (c) specialized cohort building activities and (d) exposure to career and transfer opportunities. As a new model for thorough, results-driven student support and mentoring the project will act as a template for future retention projects throughout the institution.

The approach for this project, which is grounded in relevant theory and research, recognizes that multiple factors contribute to low STEM enrollment and completion rates among financially needy students. These factors will be addressed through a curriculum that focuses on self-efficacy in STEM, identification with and opinion of STEM fields, and development of metacognitive skills in STEM subjects as well as structure academic and social supports. The program will be evaluated by an education researcher using a logic model that captures the programs theory of change, outputs and activities, midterm outcomes, and long term outcomes. Formative evaluation will address student progress, use of support services, and satisfaction (journaling). Student attitudes will also be assessed using a standardized instrument (STEM-CIS). Summative evaluation will be performed using a logic model (inputs, outputs, mid-term outcomes, and end outcomes). Internal dissemination of the results of evaluation will be done through the institutions annual newsletter. Results will also be reported at meeting of the National Science Teachers Association and eventually submitted to the Journal of College Science Teaching.

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