Results 241 to 250 of about 119,425 (295)

Asymmetric α‐Alkylation With Activated and Unactivated Electrophiles by a Highly Productive and Recyclable Lewis Acid/Imidazolium Catalyst

Angewandte Chemie International Edition, EarlyView.
An air‐stable, easily prepared, bifunctional Cu(II)/imidazolium complex enables highly enantioselective α‐alkylation of 1,3‐dicarbonyls with outstanding productivity (TON up to 1740). Highlights include broad electrophile scope spanning π‐activated and nonactivated reagents, stereo‐retentive allylation, simple catalyst synthesis, and efficient catalyst
Johanna Haußmann, Alexander Beck, Dominik Hornung, Michael Mistele, Alexander Allgaier, Wolfgang Frey, Joris van Slageren, Johannes Kästner, René Peters   +8 more
wiley   +1 more source

Association of Endothelial Cell Activation with Acute Kidney Injury during Coronary Angiography and the Influence of Recombinant Human C1 Inhibitor-A Secondary Analysis of a Randomized, Placebo-Controlled, Double-Blind Trial. [PDF]

Biomedicines
Moser S, Araschmid L, Panagiotou A, Bonati LH, Breidthardt T, Fahrni G, Kaiser C, Jeger R, Trendelenburg M, Osthoff M.   +9 more
europepmc   +1 more source

Acute Abdominal Pain as the Initial Presentation of an Acquired C1 Inhibitor Deficiency. [PDF]

GE Port J Gastroenterol
Pinto AR, Carolino F.
europepmc   +1 more source

Monocyte C1‐inhibitor synthesis in patients with C1‐inhibitor deficiency

European Journal of Clinical Investigation, 1989
Abstract. Monocytes of seven out of eight patients with type 1 C1‐inhibitor (C1‐inh) deficiency (HAE) produced 40% as much C1‐inh as monocytes from normal donors (controls). In contrast, monocytes from three patients with type 2 and three patients with acquired C1‐inh deficiency produced similar amounts of Cl‐inh as controls. Recombinant γ‐interferon (
D F, Lappin, A R, McPhaden, P L, Yap, P E, Carter, G D, Birnie, J E, Fothergill, K, Whaley   +6 more
openaire   +3 more sources

C1 Inhibitor: Quantification and Purification

, 2013
C1 inhibitor is a multipotent serpin capable of inhibiting the classical and the lectin pathways of complement, the fibrinolytic system, and contact/kinin system of coagulation. Deficiency of C1 inhibitor manifest as hereditary angioedema (HAE), an autosomal dominant hereditary disease.
Varga, Lilian, Dobó, József
openaire   +3 more sources

C1-inhibitor deficiency and angioedema

Molecular Immunology, 2001
C1-inhibitor deficiency can be inherited or acquired; both conditions lead to recurrent angioedema that can be life threatening when the larynx is involved (hereditary angioedema, HAE; acquired angioedema, AAE). The genetic defect is due to the heterozygous deficiency of C1-Inh that is transmitted as an autosomal dominant trait.
A. Carugati, E. Pappalardo, L.C. Zingale, M. Cicardi   +3 more
openaire   +4 more sources

C1 inhibitor: molecular and clinical aspects

Springer Seminars in Immunopathology, 2005
C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases.
M. Cicardi, L. Zingale, A. Zanichelli, E. Pappalardo, CICARDI, BENEDETTA   +4 more
openaire   +3 more sources

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Deficiencies of C1 inhibitor

Best Practice & Research Clinical Gastroenterology, 2005
Hereditary and acquired deficiencies of the C1 inhibitor result in a single prominent symptom, namely angioedema. Angioedema may involve the skin, the gastrointestinal tract or the upper airway. Genetically determined defects in C1INH cause hereditary angioedema.
Fred S, Rosen, Alvin E, Davis
openaire   +2 more sources

Self-administration of C1-inhibitor concentrate in patients with hereditary or acquired angioedema caused by C1-inhibitor deficiency

Journal of Allergy and Clinical Immunology, 2006
BACKGROUND: Administration of C1-inhibitor concentrate is effective for prophylaxis and treatment of severe angioedema attacks caused by C1-inhibitor deficiency.
, C Erik Hack
exaly   +2 more sources

The metabolism of C1 inhibitor and C1q in patients with acquired C1-inhibitor deficiency

Journal of Allergy and Clinical Immunology, 1986
The metabolism of 125I-labeled C1 inhibitor (C1INH) and C1q was studied in five patients with B cell lymphoproliferative disorders, C1INH deficiency, and angioedema. C1INH catabolism was markedly accelerated in these patients. The fractional catabolic rate (FCR) was 0.053 of the plasma pool per hour compared to that of normal subjects (0.025) or ...
J, Melamed, C A, Alper, M, Cicardi, F S, Rosen   +3 more
openaire   +4 more sources