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L'Università degli Studi di Ferrara (The University of Ferrara)

L'Università degli Studi di Ferrara è una fra le più antiche università europee, fondata nel 1391 dal marchese Alberto V d'Este su concessione del Papa Bonifacio IX.
The University of Ferrara (Italian: Università degli Studi di Ferrara) is the main university of the city of Ferrara in the Emilia-Romagna region of northern Italy. In the years prior to the First World War the University of Ferrara, with more than 500 students, was the best attended of the free universities in Italy. Today there are approximately 12,000 students enrolled at the University of Ferrara with nearly 400 degrees granted each year. The teaching staff number 600, including 223 researchers. It is organized into 8 Faculties.

LABORATORIO DI INFORMATICA Network Management 1. Introduzione: Network Management e ITU TMN Claudio Salati Copyright © 2001 by Claudio Salati ALMA MATER STUDIORUM - UNIVERSITA' DI BOLOGNA FACOLTA' DI INGEGNERIA - SEDE DI CESENA
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Lez. 5 * Universita' di Ferrara Facolta' di Scienze Matematiche, Fisiche e Naturali Laurea Specialistica in Informatica Algoritmi Avanzati Complessita' degli algoritmi e dei problemi: sorting e searching straight insertion ricerca binaria mergesort, heapsort radix sort (detto anche distribution sort) Copyright © 2006-2009 by Claudio Salati.
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LABORATORIO DI INFORMATICA Network Management 5. Structure of Management Information (SMIv2) 5.3. NOTIFICATION-TYPE Claudio Salati Copyright © 2001 by Claudio Salati ALMA MATER STUDIORUM - UNIVERSITA' DI BOLOGNA FACOLTA' DI INGEGNERIA - SEDE DI CESENA
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Kay, A.B. N Engl J Med 2001;344:30-37 Immunologic and Cellular Factors Regulating the Expression of Th1 and Th2 Cells Figure 1. Immunologic and Cellular Factors Regulating the Expression of Th1 and Th2 Cells. Whether the immune response is dominated by Th1 or Th2 cells is dependent on interleukin-12 and interleukin-4, respectively, as well as on the avidity of interactions between T cells and antigen-presenting cells and the amount of allergen to which the immune system is exposed (antigen).13,14 In addition, the presence of cytidine-phosphate-guanosine (CpG) repeats derived from bacteria favors the Th1 phenotype, whereas the presence of transcription factors such as GATA-3 favors the Th2 phenotype,15 as does the presence of c-maf and prostaglandin E2 (PGE2). Nitric oxide favors the expression of Th2 cells by being less inhibitory to Th2 cells than Th1 cells, whereas in humans interleukin-10 and transforming growth factor {beta} (TGF-{beta}) generally dampen the responses of both types of cells. Interferon-{gamma} (IFN-{gamma}) inhibits Th2-mediated responses; both interleukin-12 and interleukin-18 release interferon-{gamma} from T cells. Interleukin-4 inhibits the expression of Th1 cells and promotes Th2-mediated responses. Green arrows indicate stimulatory effects, and red arrows inhibitory effects, of the cytokines.
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Shock: Clinical features and pathophysiology Mahesh Nirmalan Critical Care Unit, Manchester Royal Infirmary

Shock: Clinical features and pathophysiology Mahesh Nirmalan Critical Care Unit, Manchester Royal Infirmary

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van der Linden, P.-W. G. et. al. Ann Intern Med 1993;118:161-168 Individual values of mean arterial pressure, catecholamines and angiotensins in insect-sting anaphylaxis 5 minutes after the onset of clinical symptoms, classified according to the severity of reaction
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ADRENAL MEDULLA: key player in response to stress Consists of modified post-ganglionic sympathetic axons that release predominantly epinephrine (instead of norepinephrine)
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Copyright ©2003 CMA Media Inc. or its licensors Ellis, A. K. et al. CMAJ 2003;169:307-312 Fig. 1: Schematic representation of a biphasic anaphylactic reaction
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Pharmacokinetics -- part 1 -- W.M. Tom Department of Pharmacology University of Hong Kong

Pharmacokinetics -- part 1 -- W.M. Tom Department of Pharmacology University of Hong Kong

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Mood Disorders Neurobiological Causes and Pharmacological Intervention

Mood Disorders Neurobiological Causes and Pharmacological Intervention

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Shock: Clinical features and pathophysiology Mahesh Nirmalan Critical Care Unit, Manchester Royal Infirmary

Shock: Clinical features and pathophysiology Mahesh Nirmalan Critical Care Unit, Manchester Royal Infirmary

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Kay, A.B. N Engl J Med 2001;344:30-37 Pathways Leading to Acute and Chronic Allergic Reactions 3. Pathways Leading to Acute and Chronic Allergic Reactions. Acute allergic reactions are due to the antigen-induced release of histamine and lipid mediators from mast cells. In the skin and upper airways, basophils (not shown) may also participate in allergic tissue reactions. Chronic allergic reactions, including the late-phase reaction, may depend on a combination of pathways, including the recruitment of eosinophils, the liberation of mast-cell products by histamine-releasing factors,62 and neurogenic inflammation involving neurotrophins and neuropeptides. MHC denotes major histocompatibility complex.
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Copyright ©2001 BMJ Publishing Group Ltd. Emerg Med J 2001;18:393-395 Figure 3 Anaphylactic reactions: treatment for adults in the community. *Ambulance will be equipped with oxygen, salbutamol, and fluids that may be used as adjunctive therapy. {dagger}If profound shock judged to be immediately life threatening give CPR/ALS if necessary. {ddagger} Half doses of adrenaline (epinephrine) may be safer for patients on amitriptyline, imipramine, or {beta} blocker. [&67;]If adults are treated with an EpiPen, the 300 {micro}g will usually be sufficient. A second dose may be required, but this should be considered ONLY if the patient's condition continues to deteriorate five minutes after the first dose. NB Remember the urgency of hospital transfer.
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Copyright ©1998 American Academy of Pediatrics Lowrie, L. et al. Pediatrics 1998;102:e30 1
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Merz, B. N Engl J Med 2003;348:975-976 Interrupting Allergy Allergy. The binding of IgE to mast cells triggers the release or synthesis of histamine, leukotrienes, and other mediators of anaphylaxis. Anti-IgE antibodies suppress mediator release by forming complexes with free IgE, thus preventing it from binding to mast cells.
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Kay, A.B. N Engl J Med 2001;344:109-113 Proposed Mechanisms of Specific Immunotherapy (Hyposensitization or Desensitization) 4. Proposed Mechanisms of Specific Immunotherapy (Hyposensitization or Desensitization). Specific immunotherapy is associated with down-regulation of the cytokines produced by Th2 cells, up-regulation of cytokines produced by Th1 cells, and the induction of regulatory T cells. These changes in turn lead to the inhibition of allergic inflammation, increases in cytokines that control the production of IgE (interferon-{gamma} and interleukin-12), the production of "blocking" antibodies (IgG), and the release of cytokines involved in allergen-specific hyporesponsiveness (interleukin-10 and transforming growth factor {beta}).
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Shock: A Life Threatening Emergency

Shock: A Life Threatening Emergency

Result of circulatory system failure Inadequate blood flow to some part of the body A MAJOR CAUSE OF DEATH !!!
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Anaphylaxis

Anaphylaxis

Massive allergic reaction Always call 911 Causes of Anaphylactic Shock Medications Foods and food additives Monosodium glutamate, peanuts Plant pollens Bee stings Radiographic dyes
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Chaperone mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels Diego De Stefani Department of Experimental and Diagnostic Medicine Section of General Pathology University of Ferrara

Chaperone mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels Diego De Stefani Department of Experimental and Diagnostic Medicine Section of General Pathology University of Ferrara

Title The following experimental data aim to demonstrate the existence of a protein complex (formed by IP3R, VDAC and GRP75) at the interface between endoplasmic reticulum and mitochondria which mediate efficient calcium transfer from one organelle to the other.
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Preventing Food Allergy Emergencies and Managing Anaphylactic Reactions Prepared by Steve Kinsley, RD Nu Connexions *Further food allergy risk management resources are available at www.nuconnexions.com/Allergy/manage.htm

Preventing Food Allergy Emergencies and Managing Anaphylactic Reactions Prepared by Steve Kinsley, RD Nu Connexions *Further food allergy risk management resources are available at www.nuconnexions.com/Allergy/manage.htm

Objectives of this Presentation: Understand how to prevent food allergy emergencies. Recognize signs of anaphylactic (life threatening) allergic reactions. Understand how to deal with an anaphylactic reaction when it occurs.
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