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phytohemagglutinin/blutung

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ArtikelKlinische VersuchePatente
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Hemorrhagic disease, caused by various serotypes of two closely related orbivirus serogroups, the epizootic hemorrhagic disease viruses (EHDV) and the bluetongue viruses (BTV), is a major cause of morbidity and mortality in white-tailed deer (WTD) in the United States. Despite the importance of

Concanavalin A in vivo: induction of hemorrhagic skin lesions (Arthus-like reactions) in mice.

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Concanavalin A injected into the skin of mice induced the formation of hemorrhagic Arthus-like lesions. No lesions resulted if concanavalin A was adsorbed with insoluble (a2)- macroglobulin or if mice were first treated with nitrogen mustard. The ability of concanavalin A, phytohemagglutinin, or

[Immunological investigation of late cerebral vasospasm in subarachnoid hemorrhage. (Part 1)].

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Although the occurrence of so-called late cerebral vasospasm after subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysm is well-known, its etiology still remains obscure. This time, the authors investigated the etiology by immunological research. Following results were obtained, Out of 13
Proliferative response to mitogens concanavalin A, phytohemagglutinin and pokeweed mitogen, and other chosen indicators of the activity of the immune system were assayed in peripheral blood mononuclear cells isolated from blood of patients with subarachnoid haemorrhage from ruptured aneurysm.

[The pathogenetic role of peripheral T-lymphocytes activation-induced cell death in hemorrhagic fever with renal syndrome].

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OBJECTIVE To study the activation-induced cell death (AICD) in peripheral blood T-lymphocytes (PBL-T) from patients of hemorrhagic fever with renal syndrome (HFRS) and the effect of AICD on the pathogenesis of HFRS. METHODS The PBL-T of patients with HFRS were isolated by negative selection with

Cellular and humoral bases of hemorrhage-induced depression of lymphocyte function.

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Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, the effect of hemorrhage on phytohemagglutinin-induced lymphocyte proliferation was investigated. Lymphocytes obtained from rats 2 h after blood

Effects of hemorrhagic serum on interleukin-2 generation and utilization.

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Exposure of normal peripheral blood mononuclear cells (PBMCs) to serum obtained from hemorrhaged animals produces marked depression of mitogen-induced cellular proliferation. In order to examine the mechanism which underlies its suppressive action, the effects of hemorrhagic serum on the production

The effects of hemorrhage and trauma on interleukin 2 production.

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Sepsis remains the major cause of postresuscitation death after hemorrhage and trauma. The high incidence of infection in this setting has been attributed to host defense abnormalities, including dysfunction in cell-mediated immunity. To elucidate the interaction between injury and host defense

In vitro depression of the mitogenic response of lymphocytes from turkeys infected with hemorrhagic enteritis virus.

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A depression in the mitogenic response of lymphocytes was demonstrated in turkeys inoculated with hemorrhagic enteritis virus. Blood samples were collected (in heparin) once a week, beginning 1 week after the turkeys were inoculated. The whole blood assay was used to study lymphoblastogenesis.

Skin reaction in Callithrix jacchus penicillata to phytohemagglutinin.

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Sixty marmosets (Callithrix jacchus penicillata) were intradermally tested with phytohemagglutinin. It was possible to classify this population into three groups on the basis of the reactions: 1. negatives, 2. those which showed just local hemorrhage, and finally 3. a group which developed a wheal
One week after infection with a virulent strain of hemorrhagic enteritis virus (HEV), turkeys were vaccinated for Newcastle disease. The effect of a virulent strain of HEV on turkeys' immune response to Newcastle disease vaccine and the mitogenic response of their whole blood peripheral lymphocytes

The effects of hemorrhage on mitogen-induced lymphocyte proliferation.

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Bacterial infection often occurs after trauma and hemorrhage and is believed to be a reflection of a compromised host defense system. In the present study, the effect of temporary loss of blood on lymphocyte proliferative capacity was investigated. Hemorrhage was induced in unanesthetized rats with

Depressed cell-mediated immunity in iron-deficiency anemia due to chronic loss of blood.

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Twelve women with iron-deficiency anemia due to chronic loss of blood, but free from any other pathology that might alter the immune response, were studied. The patients were tested for cell immunity both in vitro, by B and T lymphocyte quantitation and by blastic transformation of the lymphocytes
It was previously shown that hypertonic saline (HTS) enhances in vivo and in vitro cellular immune function of normal mice and reverses in vitro prostaglandin E2 (PGE2)-induced immunosuppression of normal peripheral blood mononuclear cells. Hemorrhage induces immunosuppression despite adequate

Monocyte chemotaxis and chemotactic cytokine release after exposure to hydroxyethyl starch.

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Hydroxyethyl starch (HES) is commonly used in leukapheresis and infused as an alternative to blood components for the treatment of hypotension due to hemorrhage and trauma. Its prolonged intravascular persistence and retention in tissue raise concerns about possible effects on humoral and
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