Lymphocytic choriomeningitis (LCM) is a rodent-borne viral infectious disease that presents as aseptic meningitis, encephalitis or meningoencephalitis. Its causative agent is the lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae. The name was coined by Charles Armstrong in 1934. The Gale Encyclopedia of Medicine defines lymphocytic choriomeningitis (LCM) as "a viral infection of the membranes surrounding the brain and spinal cord and of the cerebrospinal fluid". The name is based on the tendency of an individual to have abnormally high levels of lymphocytes during infection. Choriomeningitis is "cerebral meningitis in which there is marked cellular infiltration of the meninges, often with a lymphocytic infiltration of the choroid plexuses". There are several strains of LCM virus, among which the most widely used are LCMV Armstrong and LCMV Clone 13. Armstrong is the original virus strain which was isolated from the brain by Charles Armstrong in 1934. It triggers a ...
Isolates of lymphocytic choriomeningitis virus (LCMV) that elicit a cytotoxic T-lymphocyte response (CTL+) have been compared with isolates that suppress the CTL response (CTL-) in an effort to map this phenotype. A single amino acid change in the glycoprotein of the LCMV Armstrong (ARM) strain is consistently associated with the CTL- trait and the ability of the virus to persist (P+). The CTL+ P- parental strain spontaneously gives rise to CTL- P+ variants within lymphoid tissues of mice persistently infected from birth. To map the structural basis of the phenotype, the complete RNA sequence of LCMV ARM 53b (CTL+) was compared with that of its variant ARM clone 13 (CTL-). Differences in 5 of 10,600 nucleotides were found. Three changes are noted in the large L RNA segment, and two are noted in the small S RNA segment. Only two of the changes distinguishing CTL+ from CTL- isolates affect amino acid coding: lysine to glutamine at amino acid 1079 of the polymerase protein, and phenylalanine to ...
Goldsmith, Cynthia S.; Ksiazek, Thomas G.; Rollin, Pierre E.; Comer, James A.; Nicholson, William L.; Peret, Teresa C.T.; Erdman, Dean D.; Bellini, William J.; Harcourt, Brian H.; Rota, Paul A.; Bhatnagar, Julu; Bowen, Michael D.; Erickson, Bobbie R.; McMullan, Laura K.; Nichol, Stuart T.; Shieh, Wun-Ju; Paddock, Christopher D.; Zaki, Sherif R ...
We determined the prevalence of infection with lymphocytic choriomeningitis virus (LCMV) among small mammals in northern Italy and analyzed long-term dynamics of LCMV in a rodent population in the province of Trento. LCMV is circulating among the most widespread and common wild rodent species in this area (Apodemus flavicollis, Myodes glareolus, and Microtus arvalis); overall prevalence is 6.8%. During 2000-2006, intensive monitoring of LCMV in a population of yellow-necked mice (A. flavicollis) showed a positive correlation between prevalence of infection and rodent density. At the individual level, weight and sex appeared to correlate with antibody prevalence, which suggests that horizontal transmission of LCMV occurs principally among heavier, older males and occurs during fighting. Isolation and genetic characterization of this virus will be the crucial next steps for a better understanding of its ecology.
Persistent infection of C3H/St mice with certain strains of lymphocytic choriomeningitis virus (LCMV) causes a growth hormone (GH) deficiency syndrome (GHDS) manifested as growth retardation and hypoglycemia. Infected mice show high levels of viral replication in the GH-producing cells in the anterior pituitary leading to decreased synthesis of GH mRNA and protein despite the absence of detectable virus-induced cell structural damage. Virus clones isolated from the GHDS-negative LCMV WE strain can cause the disease, while others cannot. The genetic basis of this phenotypic difference is a nucleotide substitution resulting in a single amino acid difference in the viral glycoprotein. Reassortant studies indicate that the single amino acid substitution (Ser-153 to Phe) is sufficient to allow infection of the GH-producing cells and cause GHDS. These results show that a single change in the genome can affect viral pathogenicity by altering the tropism of the virus.
Lymphocytic choriomeningitis virus RNA-directed RNA polymerase L (L) datasheet and description hight quality product and Backed by our Guarantee
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TY - JOUR. T1 - Effect of Chronic Viral Infection on Epitope Selection, Cytokine Production, and Surface Phenotype of CD8 T Cells and the Role of IFN-γ Receptor in Immune Regulation. AU - Tewari, Kavita. AU - Sacha, Jonah. AU - Gao, Xiaoyan. AU - Suresh, M.. PY - 2004/2/1. Y1 - 2004/2/1. N2 - Regulation of CD8 T cell responses in chronic viral infections is not well understood. In this study, we have compared the CD8 T cell responses to immunodominant and subdominant epitopes during an acute and a chronic lymphocytic choriomeningitis virus (LCMV) infection in mice. The epitope hierarchy of the primary CD8 T cell response was similar in acute and chronic LCMV infections. However, strikingly, the epitope hierarchy of the primary CD8 T cell response was conserved in the T cell memory only in an acute but not in a chronic LCMV infection. Interestingly, in an acute infection, increasing the viral dose caused significant changes in the epitope hierarchy of the LCMV-specific memory CD8 T cell pool, ...
THE interaction of lymphocytic choriomeningitis (LCM) virus with mouse tissues has been discussed recently1-5. The fulminating disease, which occurs in adult mice after intracerebral inoculation with LCM virus, can be ameliorated by several treatments known to impair the immune response of the host, such as X-rays6, amethopterin7, thymectomy8 and anti-lymphocyte serum9. The pathology of the disease10 supports the current view that an immune reaction by the host against the virus or a virus product, located in or on infected cells, plays an essential part in its pathogenesis. A similar mechanism may be important in the chronic autoimmune-like disease in virus carrier mice2,5. Further elucidation of this disease mechanism depends on understanding the nature of the immune response and its target. A question of considerable interest is what the consequences might be for virus infected cells in the event of an immune response against the virus or a virus product. Here we report preliminary experiments
To establish if a correlation exists between the expansion of GP33-specific cells observed by flow cytometry and GP33-specific cytotoxicity, direct CTL assays were carried out using spleen cells from the mice described above. CTL activity mediated by antigen-specific CD8+ cells is usually difficult to measure at day 3 after infection since LCMV induces, at this early time point, strong NK cell activity that lyses both antigen-pulsed and unpulsed target cells. To circumvent this problem, direct CTL assays were carried out by adding a twofold excess of unlabeled NK-sensitive target cells (YAC-1 cells) to assay wells as cold-target competitors. Inclusion of cold YAC-1 cells abrogated lysis of chromium-labeled MC57 target cells by NK cells from the spleens of mice that had been injected 48 h previously with poly-IC (data not shown). No inhibition of antigen-specific CTLs was observed when YAC-1 cells were included as cold-target competitors in a direct CTL assay using spleen cells from mice that had ...
During chronic stimulation, CD8+ T cells acquire an exhausted phenotype characterized by expression of inhibitory receptors, down-modulation of effector function, and metabolic impairments. T cell exhaustion protects from excessive immunopathology but limits clearance of virus-infected or tumor cells. We transcriptionally profiled antigen-specific T cells from mice infected with lymphocytic choriomeningitis virus strains that cause acute or chronic disease. T cell exhaustion during chronic infection was driven by high amounts of T cell receptor (TCR)-induced transcription factors IRF4, BATF, and NFATc1. These regulators promoted expression of inhibitory receptors, including PD-1, and mediated impaired cellular metabolism. Furthermore, they repressed the expression of TCF1, a transcription factor required for memory T cell differentiation. Reducing IRF4 expression restored the functional and metabolic properties of antigen-specific T cells and promoted memory-like T cell development. These ...
Three clusters of organ transplant-associated lymphocytic choriomeningitis virus (LCMV) transmissions have been identified in the United States; 9 of 10 recipients died. In February 2011, we identified a fourth cluster of organ transplant-associated LCMV infections. Diabetic ketoacidosis developed in the organ donor in December 2010; she died with generalized brain edema after a short hospitalization. Both kidneys, liver, and lung were transplanted to 4 recipients; in all 4, severe posttransplant illness developed; 2 recipients died. Through multiple diagnostic methods, we identified LCMV infection in all persons, including in at least 1 sample from the donor and 4 recipients by reverse transcription PCR, and sequences of a 396-bp fragment of the large segment of the virus from all 5 persons were identical. In this cluster, all recipients developed severe illness, but 2 survived. LCMV infection should be considered as a possible cause of severe posttransplant illness ...
Lymphocytic choriomeningitis: Lymphocytic choriomeningitis, inflammation of the meninges (membranes covering the central nervous system) and choroid plexus (an area of the brain that regulates the
(a) Schematic view of acute and chronic LCMV infections including virus and cytotoxic T lymphocyte (CTL) dynamics. (b) Representation of the CTL-induced immunop
Katrina Armstrong, MD, MSCE, a world-renowned investigator in the areas of medical decision-making, quality of care and cancer prevention and outcomes, has been selected as the MGHs next physician-in-chief of the MGH Department of Medicine. Armstrong will succeed internationally regarded physician-scientist Dennis Ausiello, MD, who has led the department since 1996.. Armstrong, who currently serves as chief of the Division of General Medicine and professor of Medicine and Obstetrics and Gynecology at the Perelman School of Medicine at the University of Pennsylvania, will start in the new position April 15. "We are at a time of unparalleled opportunity to advance science, education and clinical care to benefit our patients and our communities," says Armstrong. "MGH is an extraordinary institution with a long tradition of leadership in internal medicine, and I am honored to become part of that tradition.". Armstrong is a graduate of Yale University and Johns Hopkins University School of Medicine ...
Armstrong was promoted to the rank of Lieutenant with seniority of 13 November, 1892.[1] He married Ethel M. Heath on 23 February, 1893 at Kensington.[2] He was appointed in command of the destroyer Lynx on 3 August, 1897.[3] On 15 October, 1897, Armstrong was tried at a Court Martial for negligently stranding Lynx while following Thrasher in dense fog off the Cornish coast. He was acquitted.[4][5][6][7] In September, 1902, Armstrong was credited with the "cleaver capture" of a pair of pirate dhows at Bussorah.[8] He was promoted to the rank of Commander dated 1 January, 1903.[9] After commanding Lively in the 1903 manoeuvres, Armstrong undertook a war course and a senior officers gunnery course and was then appointed to the second class protected cruiser Challenger on 3 May, 1904. Upon paying her off on 20 July, 1906, he was appointed to Hyacinth, to assume command, temporarily for one month from 20 December, 1906.[10] Armstrong was promoted to the rank of Captain on 31 December, 1908.[11] On ...
Armstrong was promoted to the rank of Lieutenant with seniority of 13 November, 1892.[1] He married Ethel M. Heath on 23 February, 1893 at Kensington.[2] He was appointed in command of the destroyer Lynx on 3 August, 1897.[3] On 15 October, 1897, Armstrong was tried at a Court Martial for negligently stranding Lynx and was acquitted.[4] In September, 1902, Armstrong was credited with the "cleaver capture" of a pair of pirate dhows at Bussorah.[5] He was promoted to the rank of Commander dated 1 January, 1903.[6] After commanding Lively in the 1903 manoeuvres, Armstrong undertook a war course and a senior officers gunnery course and was then appointed to the second class protected cruiser Challenger on 3 May, 1904. Upon paying her off on 20 July, 1906, he was appointed to Hyacinth, to assume command, temporarily for one month from 20 December, 1906.[7] Armstrong was promoted to the rank of Captain on 31 December, 1908.[8] On 12 February, 1910, he was appointed in command of the repair ship ...
tags: hamster, PetSmart, lawsuit, lymphocytic choriomeningitis virus, LCMV, zoonosis Portrait of a murderer: A Siberian dwarf hamster, Phodopus sungorus. Orphaned image. I just learned that a lawsuit was recently filed in Massachusetts Superior Court on behalf of a man who died one month after receiving a transplanted liver that was later determined to be infected…. ...
Microbial infection) Acts as a receptor for Japanese encephalitis virus (PubMed:24623090). Acts as a receptor for ebolavirus (PubMed:16051304). Acts as a receptor for SARS coronavirus/SARS-CoV (PubMed:16051304). Acts as a receptor for lassa virus and Lymphocytic choriomeningitis virus glycoprotein (PubMed:22156524, PubMed:22673088 ...
TY - JOUR. T1 - Viral immune evasion due to persistence of activated T cells without effector function. AU - Zajac, Allan J.. AU - Blattman, Joseph N.. AU - Murali-Krishna, Kaja. AU - Sourdive, David J.D.. AU - Suresh, M.. AU - Altman, John D.. AU - Ahmed, Rafi. PY - 1998/12/1. Y1 - 1998/12/1. N2 - We examined the regulation of virus-specific CD8 T cell responses during chronic lymphocytic choriomeningitis virus (LCMV) infection of mice. Our study shows that within the same persistently infected host, different mechanisms can operate to silence antiviral T cell responses; CD8 T cells specific to one dominant viral epitope were deleted, whereas CD8 T cells responding to another dominant epitope persisted indefinitely. These virus- specific CD8 T cells expressed activation markers (CD69(hi), CD44(hi), CD62L(lo)) and proliferated in vivo but were unable to elaborate any antiviral effector functions. This unresponsive phenotype was more pronounced under conditions of CD4 T cell deficiency, ...
Lymphocytic Choriomeningitis (LCM) Lymphocytic choriomeningitis, or LCM, is a rodent-borne viral infectious disease caused by lymphocytic choriomeningitis virus (LCMV), a member of the family Arenaviridae that was initially isolated in 1933. The primary host of LCMV is the common house mouse, Mus musculus. Infection in house mouse populations may vary by geographic location, though it is estimated that 5% of house mice throughout the United States carry LCMV and are able to transmit virus for the duration of their lives without showing any sign of illness. Other types of rodents, such as hamsters, are not the natural reservoirs but can become infected with LCMV from wild mice at the breeder, in the pet store, or home environment. Humans are more likely to contract LCMV from house mice, but infections from pet rodents have also been reported.. LCMV infections have been reported in Europe, the Americas, Australia, and Japan, and may occur wherever infected rodent hosts of the virus are found. The ...
TY - JOUR. T1 - 4-1BB signaling synergizes with programmed death ligand 1 blockade to augment CD8 T cell responses during chronic viral infection. AU - Vezys, Vaiva. AU - Penaloza-Macmaster, Pablo. AU - Barber, Daniel L.. AU - Ha, Sang Jun. AU - Konieczny, Bogumila. AU - Freeman, Gordon J.. AU - Mittler, Robert S.. AU - Ahmed, Rafi. PY - 2011/8/15. Y1 - 2011/8/15. N2 - Previous studies have identified the inhibitory role that the programmed death 1 (PD-1) pathway plays during chronic infection. Blockade of this pathway results in rescue of viral-specific CD8 T cells, as well as reduction of viral loads in mice chronically infected with lymphocytic choriomeningitis virus (LCMV). We tested the effect of combining PD ligand 1 (PD-L1) blockade with an agonistic regimen that induces 4-1BB costimulation during chronic LCMV infection. There is a boosting effect in the rescue of LCMV-specific CD8 T cell responses after dual treatment with PD-L1 blockade and 4-1BB agonistic Abs when the amount and timing ...
Persistent viral infections can interfere with FcγR-mediated antibody effector functions by excessive immune complex (IC) formation, resulting in resistance to therapeutic FcγR-dependent antibodies. We and others have previously demonstrated that mice persistently infected with lymphocytic choriomeningitis virus (LCMV) are resistant to a wide range of depleting antibodies due to excessive IC formation. Here, we dissect the mechanisms by which two depleting antibodies overcome the obstacle of endogenous ICs and achieve efficient target cell depletion in persistently infected mice. Efficient antibody-mediated depletion during persistent LCMV infection required increased levels of antibody bound to target cells or use of afucosylated antibodies with increased affinity for FcγRs. Antibodies targeting the highly expressed CD90 antigen or overexpressed human CD20 efficiently depleted their target cells in naïve and persistently infected mice, whereas antibodies directed against less abundant ...
Jan. 2001-present SCIENTIFIC PUBLICATIONS: 1 Beck,M.L., S.H. Butch, W.R. Armstrong, and H.A. Oberman. An Auto-antibody with U- Specificity in a Patient with Myasthenia Gravis. Transfusion, 12:280:1972. 2. VanKirk,I.E., A.B. Simon, and W.R. Armstrong. Candida Myocarditis Causing Complete Heart Block. JAMA 25, Feb74, p.931-33. 3. Amistrong,W.R. and E.W. Catalano. The PAS Stain in Acute Leukemia - Increased Sensitivity with Diastase. Am.J.Clin.Path. 72:652, 1979. 4. Godder,K, Pati,AR, Abhyankar,SH, Lamb,LS, Armstrong,W and Henslee-Downey, J: De-novo Chronic Graft versus Host Disease Presenting as Hemolytic Anemia Following Partially Mismatched Related Donor Bone Marrow Transplant. Bone Marrow Transplant 19:813-817, 1997. 5. Thurer,Robert L, Luban,N., AuBuchonjP, et al: Universal WBC Reduction. Letters to the Editor, Transfusion 40:751-2, June 2000. PRESENTATIONS: 1 Armstrong,W.R. Fibrous Histiocytic Neoplasms. Department of Postgraduate Medicine, University of Michigan, 4/73. M.R. Abell, MD, ...
Transfer of photosynthetic NADP+/NADPH recycling activity to a porous metal oxide for highly specific, electrochemically-driven organic synthesis. B. Siritanaratkul, C. F. Megarity, T. G. Roberts, T. O. M. Samuels, M. Winkler, J. H. Warner, T. Happe and F. A. Armstrong, Chem. Sci, 8, 4579-4586 (2017). Importance of the Active Site Canopy Residues in an O2-tolerant [NiFe]-hydrogenase. E. J. Brooke, R. M. Evans, S. T. A. Islam, G. M. Roberts, S. A. M. Wehlin, S. B. Carr, S. E. V. Phillips and F. A. Armstrong. Biochemistry 56, 132-142 (2017).. Electrochemical investigations of the mechanism of assembly of the active-Site H-cluster of [FeFe]-Hydrogenases. C. F. Megarity, J. Esselborn, S. V. Hexter, F. Wittkamp, U.-P. Apfel, T. Happe and F. A. Armstrong. J. Amer. Chem. Soc. 138, 15227-15233 (2016).. Catalysis of solar hydrogen production by iron atoms on the surface of Fe-doped silicon carbide. Z. Wang and F. A. Armstrong. Catalysis Science and Technology, 6, 7038 - 7041 (2016).. Guiding Principles ...
AUSTIN, Texas (AP) - Lance Armstrong is facing more doping allegations just a few months after he thought he had finally put them to rest. Although federal investigators in February closed a two-year investigation without bringing criminal charges, the U.S. Anti-Doping Agency has filed new doping charges that could strip the seven-time Tour de France winner of his victories in cyclings premier race. Armstrong insists he is innocent. I have never doped, and, unlike many of my accusers, I have competed as an endurance athlete for 25 years with no spike in performance, passed more than 500 drug tests and never failed one, Armstrong said in a statement. Any fair consideration of these allegations has and will continue to vindicate me. The move by USADA immediately bans him from competing in triathlons, which he turned to after he retired from cycling last year. Armstrong has been dogged by doping allegations since his first Tour victory in 1999, but had hoped his fight to be viewed as a clean
Dendritic cells (DC) play a key role in the initiation of T cell-mediated immune responses and may therefore be successfully used in antiviral and antitumor vaccination strategies. Because both strength and duration of an immune response determines the outcome of a vaccination protocol, we evaluated the life span of DC-induced antiviral CTL memory against systemic and peripheral challenge infections with lymphocytic choriomeningitis virus (LCMV). We found that expansion and activation of CTL by DC was transient. Protection against systemic LCMV infection after DC immunization was relatively long-lived (,60 days), whereas complete protection against peripheral infection via intracerebral infection or infection into the footpad with LCMV, where rapid recruitment of effector T cells to the site of infection and elimination of viral pathogen plays a major role, was short-lived (,30 days). Protective immunity was most efficiently restored by administration of antigenic peptides via DC, rather than in ...
Dendritic cells (DCs) comprise the major antigen-presenting cells (APCs) of the host, uniquely programmed to stimulate immunologically naïve T lymphocytes. Viruses that can target and disorder the...
Persistierende virale Infektionen wie z.B. Hepatitis C und HIV stellen wegen des Trägertums durch Tiere oder Menschen ein Virus-Reservoir dar, welches eine zunehmende Gesundheitsbedrohung bedeutet. Besonders im Bereich der Impfung, aber ebenso hinsichtlich Therapie der Infektion selbst und ihrer Langzeitkomplikationen, sind die Erfolge bescheiden oder unzureichend. Geläufige Konzepte und ...
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Infections induce complex host responses linked to antiviral defense, inflammation, and tissue damage and repair. We hypothesized that the liver, as a central metabolic hub, may orchestrate systemic metabolic changes during infection. We infected mice with chronic lymphocytic choriomeningitis virus …
Adoptive immunization of syngeneic, immunosuppressed recipients infected with lymphocytic choriomeningitis (LCM) virus causes fatal neurologic disease within 2 to 4 days of cell transfer, providing that donors are sampled when the in vitro 51Cr release assay shows maximal specific activity of sensitized thymus-derived lymphocytes (T cells). Prior treatment of immune spleen cells with AKR anti-θ ascitic fluid and complement causes total abrogation of this in vivo activity. Fatal neurologic disease is induced only when donor and recipient share at least one set of H-2 antigenic specificities. Parent → F1 and F1 → parent combinations are as effective as syngeneic systems, but mice given allogeneic immune cells survive as long as controls. Differences at the M-locus in H-2 compatible mice do not inhibit effector activity. Homing of transferred lymphocytes to spleen is similar in syngeneic or allogeneic recipients, but only syngeneic immune cells cross the blood-cerebrospinal fluid (CSF) barrier ...
In a mouse colony in which lymphocytic choriomeningitis is endemic infection takes place either in utero or shortly after birth. Virus is discharged from infected mice with the nasal secretions and urine. In some mice the infection lasts for several months, and such carriers can transmit the disease to healthy mice by contact. The portal of entry appears to be the nasal mucosa rather than the gastrointestinal tract. Mice infected by contact show no definite symptoms while those infected in utero often do. The disease has persisted in the colony for at least 15 months without change in its character. Mouse stocks differ in their susceptibility to contact infection and the findings given in the paper could be reproduced only with a very susceptible stock. Wild mice (Mus musculus) can be infected by contact, although less easily than our white mice.. The source of the infection in the colony has not been determined. The fact that the serum of the caretaker neutralizes the virus indicates that he ...
We use simple mathematical models to examine the dynamics of primary and secondary cytotoxic T-lymphocyte (CTL) responses to viral infections. In particular, we are interested in conditions required to resolve the infection and to protect the host upon secondary challenge. While protection against reinfection is only effective in a restricted set of circumstances, we find that resolution of the primary infection requires persistence of CTL precursors (CTLp), as well as a fast rate of activation of the CTLp. Since these are commonly the defining characteristics of CTL memory, we propose that CTL memory may have evolved in order to clear the virus during primary challenge. W e show experimental data from lymphocytic choriomeningitis virus infection in mice, supporting our theory on CTL memory. We adapt our models to HIV and find that immune impairment during the primary phase of the infection may result in the failure to establish CTL memory which in turn leads to viral persistence. Based on our ...
PENSACOLA, Fla. - Top-ranked Armstrong Atlantic State advanced in penalty kicks, 6-5, past No. 19 Columbus State University on Friday afternooon, capturing the NCAA Division II Womens Soccer Southeast Region title and setting up a showdown with nationally-ranked No. 2 West Florida in the NCAA Quarterfinals on Sunday. The two teams played to a scoreless draw prior to PKs.. It was the first PK shootout win for Armstrong (19-1-2) in program history and keeps the Pirates drive towards a return trip to the Final Four alive. Columbus State (18-3-2) sees its season end on PKs in the NCAA Tournament for a third time in its history.. A tight defensive struggle between both teams generated just five shots between the two teams in the first half. The game opened up a little bit in the second half as each goalkeeper, Mary Mancin for Columbus State and Morgan Luckie for Armstrong, was called upon to make saves to preserve the shutout.. As time ran down in regulation, Columbus States Jackie Ellis had a ...
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Dr. David Armstrong, MD is a Colorectal Surgery Specialist in Alpharetta, GA. Dr. Armstrong has more experience with Colorectal Surgery and Transplant Surgery than other specialists in his area. He is affiliated with medical facilities such as Emory Decatur Hospital and Emory University Hospital Midtown. He is accepting new patients and has indicated that he accepts telehealth appointments. Be sure to call ahead with Dr. Armstrong to book an appointment.
Armstrong State University is now Georgia Southern University. For information about Fall 2018 and beyond, visit GeorgiaSouthern.edu. Current Armstrong students (spring and summer 2018) can continue to access information through Armstrong.edu. For details about the consolidation, visit consolidation.georgiasouthern.edu ...
In a series of emails to media organistions and cycling officials disgraced former Tour de France winner Floyd Landis yesterday admitted to systematic doping and implicated a number of other riders too including arguably cyclings biggest ever star, Lance Armstrong.. Amongst those emailed were the Wall Street Journal, it has been able to confirm to its satisfaction that the emails were genuinely from Landis - the newspaper has taken nearly three weeks to go public on the mails. That Landis doped is not a surprise, that he has finally admitted it is something of a bombshell given the loud and long campaign he waged, and which was waged by many on his behalf in the US media, to proclaim his innocence.. That particuar bombshell pales in to insignificance compared to what Landis has to say about his fellow American and erstwhile team mate, Lance Armstrong. However Armstrong, who has so far seemed to laugh off the accusations in allusions to them on his Twitter page, is not the only American rider ...
Armstrong State University is now Georgia Southern University. For information about Fall 2018 and beyond, visit GeorgiaSouthern.edu. Current Armstrong students (spring and summer 2018) can continue to access information through Armstrong.edu. For details about the consolidation, visit consolidation.georgiasouthern.edu ...
Acute viral infections induce immune deficiencies, as shown by unresponsiveness to mitogens and unrelated antigens. T lymphocytes isolated from mice acutely infected with lymphocytic choriomeningitis virus (LCMV) were found in this study to undergo activation-induced apoptosis upon signalling through the T-cell receptor (TcR)-CD3 complex. Kinetic studies demonstrated that this sensitivity to apoptosis directly correlated with the induction of immune deficiency, as measured by impaired proliferation in response to anti-CD3 antibody or to concanavalin A. Cell cycling in interleukin-2 (IL-2) alone stimulated proliferation of LCMV-induced T cells without inducing apoptosis, but preculturing of T cells from acutely infected mice in IL-2 accelerated apoptosis upon subsequent TcR-CD3 cross-linking. T lymphocytes isolated from mice after the acute infection were less responsive to IL-2, but those T cells, presumably memory T cells, responding to IL-2 were primed in each case to die a rapid apoptotic death upon
MHC class II presentation of antigenic peptides derived from soluble proteins is usually preceded by antigenic uptake via (nonreceptor-mediated) endocytosis by professional APCs, followed by processing in endosomal compartments. Although in vitro alternative pathways for MHC class II loading have been described for certain intracellularly synthesized proteins, the importance of these pathways has not been assessed in vivo. We have shown previously that endogenously produced membrane-associated glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV), a noncytopathic virus, can be presented in vitro on MHC class II molecules in the absence of the invariant chain (Ii), whereas the cytosolic LCMV nucleoprotein (LCMV-NP) failed to be presented under the same conditions. Taking advantage of this system, we analyzed presentation of LCMV-GP and LCMV-NP in vivo in Ii-deficient mice and followed the induced Th cell and B cell responses. At early time points after LCMV infection of li-deficient mice, we
Mice, Antigens, Cell, Cells, T Cells, Virus, Hepatitis, Hepatitis C, Iodine, Acids, Cytotoxic T Lymphocytes, Fatty Acids, Immunity, Infections, Liposomes, Lymphocytes, Lymphocytic Choriomeningitis, Lymphocytic Choriomeningitis Virus, Memory, Peptides
It has been difficult to correlate the quality of CD8 T cell responses with protection against viral infections. To investigate the relationship between efficacy and magnitude of T cell responses, we quantify the rate at which individual CD8 effector and memory T cells kill target cells in the mouse spleen. Using mathematical modeling, we analyze recent data on the loss of target cells pulsed with three different peptides from the mouse lymphocytic choriomeningitis virus (LCMV) in mouse spleens with varying numbers of epitope-specific CD8 T cells. We find that the killing of targets follows the law of mass-action, i.e., the death rate of individual target cells remains proportional to the frequency (or the total number) of specific CD8 T cells in the spleen despite the fact that effector cell densities and effector to target ratios vary about a 1000-fold. The killing rate of LCMV-specific CD8 T cells is largely independent of T cell specificity and differentiation stage. Our results thus allow one to
Invariant natural killer T (iNKT) cells promote immune responses to various pathogens, but exactly how iNKT cells control antiviral responses is unclear. Here, we showed that iNKT cells induced tissue-specific antiviral effects in mice infected by lymphocytic choriomeningitis virus (LCMV). Indeed, iNKT cells inhibited viral replication in the pancreas and liver but not in the spleen. In the pancreas, iNKT cells expressed the OX40 molecule and promoted type I interferon (IFN) production by plasmacytoid dendritic cells (pDCs) through OX40-OX40 ligand interaction. Subsequently, this iNKT cell-pDC cooperation attenuated the antiviral adaptive immune response in the pancreas but not in the spleen. The dampening of pancreatic anti-LCMV CD8(+) T cell response prevented tissue damage in transgenic mice expressing LCMV protein in islet beta cells. Thus, this study identifies pDCs as an essential partner of iNKT cells for mounting an efficient, nondeleterious antiviral response in peripheral tissue.
The central nervous system (CNS) is considered as largely isolated from the immune system - a status referred to as "immune privilege". But CNS-tissue is constantly surveyed by immune cells and can under certain circumstances, such as viral infections, become a target of inflammatory responses. Cytotoxic T cells (CTLs) combat viruses in peripheral organs as well as the CNS and can contribute to inflammation-induced tissue damage. This concept drives the viral déjà vu mouse model, where defined sequences of lymphocytic choriomeningitis virus (LCMV) infections cause severe CNS inflammation. The CTL response targets viral epitopes of persistently infected neurons that are shared by the used viruses. To better understand the requirements and consequences for CTL:neuron interactions in vivo, different epitope mutants of the immunodominant LCMV epitopes NP396-404 and GP33-41 with different affinities to MHC class I were tested for their contribution in déjà vu disease. While the CTL response ...
Erythropoietin (EPO), also known as "E," "Po," "Edgar" or "Edgar Allen Poe," among other names. EPO is used by athletes to increase the number of red blood cells in their circulatory system which are available to carry oxygen. … Even after the EPO urine test was developed and implemented in sport in late 2000 EPO was difficult to detect and the Respondents [Armstrong, a team director, team captain and team doctors] implemented a number of means to avoid detection of EPO use, including: micro-dosing (i.e., using smaller amounts of EPO to reduce the clearance time of the drug), intravenous injections (i.e., injecting the drug directly into the vein rather than subcutaneously to reduce clearance time), saline, plasma or glycerol infusions (described below) and various effort to avoid testing by drug testers at times that EPO might still be detectable in the riders urine. … Multiple riders with firsthand knowledge will testify that between 1998 and 2005 Armstrong personally used EPO and on ...
The Contact CT Gauge from Armstrong Optical offers thickness measurements of upto 100mm with a standard diameter range of 300mm. Used for quick, accurate measurement of glass components this system incorporates 2 Heidenhain linear gauges mounted in opposition to each other. These are linked to a digital display which shows the difference between the 2 probes thus giving a direct reading of center thickness. The top gauge has a range of 25mm, resolution of 0.1?m and is movable to give access for thicker lenses. The bottom gauge has a range of 12mm, resolution of 0.1?m and is generally fixed. Both gauges have probe lifters attached so that the probes may be retracted allowing easy access for positioning of the lens prior to measurement. The table, mounted between the 2 gauges, is constructed of TUFSET plastic on an aluminium backing plate, offering robust construction along with a non-marking surface. The whole is mounted onto a granite base offering stability with low maintenance (corrosion ...
Though not a president, Lance Armstrong was the king of cycling for almost a decade, and he also beats Clinton for longest time for hiding the truth. This fall from race is a huge story for plenty of reasons. By choice, Armstrong was a serial liar, and its incredible how he not only fooled the world, his family, sponsors, cancer patients, donors, and big business employers, but how long he did it, and, what an amazing acting job! Not a man of much apparent outward emotion, he vehemently denied on many occasions, ever doping to win bike races. When questioned by USADA (the US Anti-Doping Agency) in 2005, while videotaped, he denied all doping allegations. Take a look at his acting skills as guest on the biggest prime time U.S. shows. As a matter of fact, it was only in the last several days, with Oprah Winfrey, that he has finally admitted that, well, he took us all for a ride. So, since 1998 around when there first was talk about illegal performance enhancing drugs while riding in the Tour de ...
I honestly dont even know what to say about them," Armstrong said of his injury troubles in December, according to the Globe and Mail. "I tried to wrap my head around them while I was sitting out. The first couple weeks that I was down this time again, I was like, What the hecks going on? "But theres no real answer to it." So, Armstrong is tough. Hes also physical and a decent penalty killer, which makes him a potentially decent third- or fourth-liner if he can stay healthy. Despite the contract he signed with Toronto in 2010, hes not a legitimate top-six winger, though he did have 40-point seasons for bad teams (2005-06 Penguins, 2007-08 Thrashers). Armstrongs also regarded as a nice guy and a good teammate, which will help him hook on with another team. "Thanks to the leaf nation for the support over the last couple seasons. Although I had tough luck thanks for everything," he tweeted on Saturday. Free agency begins on Sunday afternoon. The Leafs project to have about $15 million in ...