Tuftsin Promotes an Anti-Inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 Tcell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS

Improved Linear Key Recovery Attacks on PRESENT

PRESENT is an ultra-lightweight block cipher designed by Bogdanov et al., and has been widely studied since its proposal. It supports 80-bit and 128-bit keys, which are referred as PRESENT-80 and PRESENT-128, respectively. Up to now, linear cryptanalysis is the most effective method on attacking this cipher, especially when accelerated with the pruned Walsh transform. Combing pruned Walsh transform with multiple linear attacks, one can recover the right key for 28-round PRESENT-80 and -128. Later, this method is further improved with affine pruned Walsh transform by adding more zeros in the Walsh spectrum through rejecting some data. This leads to the 29-round attack on PRESENT-128 with full codebook. In this paper, we follow the affine pruned Walsh transform accelerated linear method, and propose 29-round attacks on both PRESENT-80 and PRESENT-128 without using full codebook. Both attacks rely on a statistical model depicting distributions of the experimental correlation when some data are artificially rejected in its computation. Besides, detailed analysis of complexity reduction for each linear hull used in attacking PRESENT is also provided and supported by an automatic tool. Our 29-round attack on PRESENT-80 mainly benefits from this tool. According to our knowledge, both attacks are the best ones on PRESENT so far

Tuftsin Promotes an Anti-Inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 Tcell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS

Implementering i skolen, top down eller bottom up? En kvalitativ studie av hvilke grep og tanker rektor har om implementeringsprosesser

Tema for oppgaven er implementering i skolen. Hovedutfordringen i skolen er å minske avstanden mellom reformideene og praksisen i klasserommet, og rektor som skolens øverste leder har her en nøkkelrolle i kraft av sin posisjon. Problemstilling for oppgaven er: Hva kjennetegner rektorers tenkning om- og idealer for "god implementering"- og hvordan utfører de implementering i praksis? Oppgaven er en kvalitativ studie hvor det empiriske materialet baserer seg på intervju med åtte rektorer i Tromsø kommune. Hovedteoriene bottom up og top down er oppgavens teoretiske referanseramme, samt Røviks (2014)implementeringsdoktriner. Intensjonen med studiet er om mulig å finne noen felles oppfatninger om gode måter å implementere på, eller er det snakk om mer eller mindre "private" implementeringsdoktriner. Funnene gir ikke grunnlag for noen entydig konklusjon om en felles strategi for å møte implementeringsutfordringene i skolen. Men data viser likevel noen sammenfallende forestillinger om iverksetting, hvor det er en miks av elementer fra de ulike doktrinene

Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis-1

<p><b>Copyright information:</b></p><p>Taken from "Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis"</p><p>http://www.biomedcentral.com/1471-2172/8/10</p><p>BMC Immunology 2007;8():10-10.</p><p>Published online 16 Jul 2007</p><p>PMCID:PMC1937009.</p><p></p>t MIFd7 compared to wt PBS; recovery was complete (p = 0.0005). wt PBS n = 18; wt MIF d7 n = 11. (B) Luxol Fast Blue staining shows very little demyelination at day 23 in wt MIFd7 mice. The dashed line and the asterisk demarcate the ventral column of the spinal cord. The intensity of luxol fast blue staining within the ventral column was quantified using the NIH Image freeware and was normalized to day 0 staining. Background staining was subtracted. (C) Immunohistochemistry for reactive macrophages/microglia using antibody against F4/80. (D) Immunohistochemistry for CD3+ T cells

Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis-2

<p><b>Copyright information:</b></p><p>Taken from "Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis"</p><p>http://www.biomedcentral.com/1471-2172/8/10</p><p>BMC Immunology 2007;8():10-10.</p><p>Published online 16 Jul 2007</p><p>PMCID:PMC1937009.</p><p></p> n = 13. (B) Luxol fast blue histological stain reveals levels of myelination. The dashed line and the asterisk demarcate the ventral column of the spinal cord. The intensity of luxol fast blue staining within the ventral column was quantified using the NIH Image freeware and was normalized to day 0 staining. Background staining was subtracted. (C) Reactive macrophages/microglia are visible in the coronal sections of experimental mice at different timepoints. (D) Infiltrating T cells were detected by immunohistochemistry using an anti-CD3 antibody

Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis-7

<p><b>Copyright information:</b></p><p>Taken from "Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis"</p><p>http://www.biomedcentral.com/1471-2172/8/10</p><p>BMC Immunology 2007;8():10-10.</p><p>Published online 16 Jul 2007</p><p>PMCID:PMC1937009.</p><p></p> Daily scores were averaged. PBS n = 18; MIF d-1 n = 12. Wilcoxon test showed no statistically significant differences in onset, severity or recovery, but the progression of the disease is more delayed. (B) Frozen spinal cord sections were stained with Luxol Fast Blue to show areas of myelination. The dashed line and the asterisk demarcate the ventral column of the spinal cord. The intensity of luxol fast blue staining within the ventral column was quantified using the NIH Image freeware and was normalized to day 0 staining. Background staining was subtracted. (C) Immunohistochemistry for activated macrophage/microglial cells using F4/80 in frozen spinal cord sections. (D) Immunohistochemistry for infiltrating T cells using an anti-CD3 antibody