38 research outputs found

    The Vehicle, Spring 2007

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    Table of Contents She Might Just Take You for GrantedRebecca M. Griffithpage 1 ShwagDarius Juttipage 2 In LoveAmanda Vealepage 9 SubmissiveSarah Ellerpage 10 Wedding SongRebecca M. Griffithpage 11 Why No Ladies and Gentlemen, My Shit Never StinksJacob Fosterpage 13 Death of an English MajorLindsey Durbinpage 14 Summer\u27s PerfumeRebecca M. Griffithpage 15 Gigavolt and ChrisEric Schumacherpage 16 UntitledKris Jonespage 22 Ode to the MuseGreg Harrellpage 23 TenderAmanda Vealepage 24 When the Muses HeaveElizabeth Hoodpage 25 Depression LiftingAmanda Vealepage 26 Red SwordAndrew Deckerpage 27 Warring IdeologyMargaret B. Hamperpage 29 ConfessionGreg Harrellpage 34 A Glass PuzzleBrittany Morganpage 35 Hey MaJacob Fosterpage 36 As July Faded AwayRebecca M. Griffithpage 37 About the LeftoversGina LoBiancopage 38 Me, Myself & ILindsey Durbinpage 39 Iced Parking LotRebecca M. Griffithpage 41 About the Authors Art Submissions Mike\u27s Revelation and MikeSean Walkercovers UntitledChad Navelpage 9 Morning in Tintern AbbeyCarrie Muellerpage 12 WestminsterCarrie Muellerpage 21 A Fighting ChanceOsha Rudduckpage 22 Rooftop SunsetJennifer O\u27Neilpage 25 EIU IVCarrie Muellerpage 28 MandolinOsha Rudduckpage 38 EIU IIICarrie Muellerpage 42https://thekeep.eiu.edu/vehicle/1087/thumbnail.jp

    Case Reports1. A Late Presentation of Loeys-Dietz Syndrome: Beware of TGFβ Receptor Mutations in Benign Joint Hypermobility

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    Background: Thoracic aortic aneurysms (TAA) and dissections are not uncommon causes of sudden death in young adults. Loeys-Dietz syndrome (LDS) is a rare, recently described, autosomal dominant, connective tissue disease characterized by aggressive arterial aneurysms, resulting from mutations in the transforming growth factor beta (TGFβ) receptor genes TGFBR1 and TGFBR2. Mean age at death is 26.1 years, most often due to aortic dissection. We report an unusually late presentation of LDS, diagnosed following elective surgery in a female with a long history of joint hypermobility. Methods: A 51-year-old Caucasian lady complained of chest pain and headache following a dural leak from spinal anaesthesia for an elective ankle arthroscopy. CT scan and echocardiography demonstrated a dilated aortic root and significant aortic regurgitation. MRA demonstrated aortic tortuosity, an infrarenal aortic aneurysm and aneurysms in the left renal and right internal mammary arteries. She underwent aortic root repair and aortic valve replacement. She had a background of long-standing joint pains secondary to hypermobility, easy bruising, unusual fracture susceptibility and mild bronchiectasis. She had one healthy child age 32, after which she suffered a uterine prolapse. Examination revealed mild Marfanoid features. Uvula, skin and ophthalmological examination was normal. Results: Fibrillin-1 testing for Marfan syndrome (MFS) was negative. Detection of a c.1270G > C (p.Gly424Arg) TGFBR2 mutation confirmed the diagnosis of LDS. Losartan was started for vascular protection. Conclusions: LDS is a severe inherited vasculopathy that usually presents in childhood. It is characterized by aortic root dilatation and ascending aneurysms. There is a higher risk of aortic dissection compared with MFS. Clinical features overlap with MFS and Ehlers Danlos syndrome Type IV, but differentiating dysmorphogenic features include ocular hypertelorism, bifid uvula and cleft palate. Echocardiography and MRA or CT scanning from head to pelvis is recommended to establish the extent of vascular involvement. Management involves early surgical intervention, including early valve-sparing aortic root replacement, genetic counselling and close monitoring in pregnancy. Despite being caused by loss of function mutations in either TGFβ receptor, paradoxical activation of TGFβ signalling is seen, suggesting that TGFβ antagonism may confer disease modifying effects similar to those observed in MFS. TGFβ antagonism can be achieved with angiotensin antagonists, such as Losartan, which is able to delay aortic aneurysm development in preclinical models and in patients with MFS. Our case emphasizes the importance of timely recognition of vasculopathy syndromes in patients with hypermobility and the need for early surgical intervention. It also highlights their heterogeneity and the potential for late presentation. Disclosures: The authors have declared no conflicts of interes

    Activated immune cells : 1H-NMR spectroscopy and flow cytometry studies

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    Proton nuclear magnetic resonance (lH-NMR) spectroscopy has been used to study immune cell activation. One-dimensional and two—dimensional 1H-NMR spectra of activated immune cells are dominated by signals arising from elevated levels of isotropically tumbling (ie., NMR-visible) mobile lipid. An increase in the level of mobile lipid compared with that seen in resting cells has been observed in a variety of activated immune cells. The appearance of the mobile lipid is associated with activation and can be induced by a variety of stimuli. However, the origin and function of the neutral lipid resonances in 1H-NMR spectra of activated immune and other cell types has been unresolved. I propose that the mobile lipids arise from phosphatidylcholine (PC) cycling

    In vitro measures of membrane changes reveal differences between red blood cells stored in saline-adenine-glucose-mannitol and AS-1 additive solutions: a paired study

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    BACKGROUND: Saline-Adenine-Glucose-Mannitol (SAGM) and a variant solution, AS-1 have been used for over 30 years to preserve red blood cells (RBCs). Reputedly these RBC components have similar quality, although no paired study has been reported. To determine whether differences exist, a paired study of SAGM-RBCs and AS-1-RBCs was conducted to identify membrane changes, including microparticle (MP) quantitation and in vitro RBC-endothelial cell (EC) interaction. STUDY DESIGN AND METHODS: Two whole blood packs were pooled-and-split and RBCs prepared (n=6 pairs). One pack was suspended in SAGM and one in AS-1. Samples were collected during 42 days of refrigerated storage. RBC shape/size, glycophorin A (GPA)(+) and phosphatidylserine (PS)(+) MPs were measured by flow cytometry. RBC adhesion to ECs was determined by an in vitro flow perfusion assay. Routine parameters (pH, hemolysis) were also measured. RESULTS: Compared to SAGM-RBCs, AS-1-RBCs had lower hemolysis (p<0.04), lower GPA(+) MPs (p<0.03) and lower PS(+) MPs (p<0.03) from day 14 onwards. AS-1-RBCs had higher (p<0.02) side scatter from day 28 onwards, compared to SAGM-RBCs. SAGM-RBCs were more adherent to ECs at day 28 of storage compared to AS-1 RBCs (p=0.04), but reversed at day 42 (p=0.02). No significant differences in forward scatter or pH were found. CONCLUSION: SAGM-RBCs lose more membrane during storage. SAGM-RBCs had increased adherence to ECs at day 28 of storage, while AS-1-RBCs were more adherent at day 42. The effect of these differences on the function and survival of SAGM-RBCs and AS-1-RBCs following transfusion remains to be determined
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