scholarly journals FGF23 Neutralizing Antibody Partially Improves Bone Mineralization Defect of HMWFGF2 Isoforms in Transgenic Female Mice

2018 ◽  
Vol 33 (7) ◽  
pp. 1347-1361 ◽  
Author(s):  
Liping Xiao ◽  
Collin Homer-Bouthiette ◽  
Marja M Hurley
Keyword(s):  
Bone Mineralization ◽  
Neutralizing Antibody ◽  
Female Mice ◽  
Mineralization Defect

Preproenkephalin (Penk) is Expressed in Differentiated Osteoblasts, and its Deletion in Hyp Mice Partially Rescues Their Bone Mineralization Defect

2010 ◽  
Vol 86 (4) ◽  
pp. 282-293 ◽  
Author(s):  
S. Seitz ◽  
F. Barvencik ◽  
M. Gebauer ◽  
J. Albers ◽  
J. Schulze ◽  
...  
Keyword(s):  
Bone Mineralization ◽  
Mineralization Defect

Presence of antibody in virus-infected brain cells of SSPE ferrets

1983 ◽  
Vol 41 ◽  
pp. 804-805
Author(s):  
Hannah R. Brown ◽  
Tammy L. Donato ◽  
Halldor Thormar
Keyword(s):  
Measles Virus ◽  
Plasma Cells ◽  
Subacute Sclerosing Panencephalitis ◽  
Protein A ◽  
Neutralizing Antibody ◽  
Brain Cells ◽  
Antibody Titers ◽  
A Cell ◽  
The Central Nervous System ◽  
The Brain

Measles virus specific immunoglobulin G (IgG) has been found in the brains of patients with subacute sclerosing panencephalitis (SSPE), a slowly progressing disease of the central nervous system (CNS) in children. IgG/albumin ratios indicate that the antibodies are synthesized within the CNS. Using the ferret as an animal model to study the disease, we have been attempting to localize the Ig's in the brains of animals inoculated with a cell associated strain of SSPE. In an earlier report, preliminary results using Protein A conjugated to horseradish peroxidase (PrAPx) (Dynatech Diagnostics Inc., South Windham, ME.) to detect antibodies revealed the presence of immunoglobulin mainly in antibody-producing plasma cells in inflammatory lesions and not in infected brain cells.In the present experiment we studied the brain of an SSPE ferret with neutralizing antibody titers of 1:1024 in serum and 1:512 in CSF at time of sacrifice 7 months after i.c. inoculation with SSPE measles virus-infected cells. The animal was perfused with saline and portions of the brain and spinal cord were immersed in periodate-lysine-paraformaldehyde (P-L-P) fixative. The ferret was not perfused with fixative because parts of the brain were used for virus isolation.

Central forebrain Fos responses to familiar male odours are attenuated in recently mated female mice

2001 ◽  
Vol 13 (2) ◽  
pp. 389-399 ◽  
Author(s):  
Heather A. Halem ◽  
James A. Cherry ◽  
Michael J. Baum
Keyword(s):  
Female Mice ◽  
Mated Female

A subchronic oral toxicity study on medical herb extract, KIOM CRC#BP10A, in male and female mice

Planta Medica ◽  
2015 ◽  
Vol 81 (16) ◽  
Author(s):  
ES Cho ◽  
YJ Lee ◽  
JS Park ◽  
J Kim ◽  
NS Kim ◽  
...  
Keyword(s):  
Toxicity Study ◽  
Oral Toxicity ◽  
Male And Female ◽  
Female Mice ◽  
Subchronic Oral Toxicity Study ◽  
Herb Extract

Antiparasitic Treatment of Patients with P. falciparum Malaria Reduces the Ability of Patient Serum to Induce Tissue Factor by Decreasing NF-κB Activation

1995 ◽  
Vol 73 (01) ◽  
pp. 039-048 ◽  
Author(s):  
A Bierhaus ◽  
Ch J Hemmer ◽  
N Mackman ◽  
R Kutob ◽  
R Ziegler ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Falciparum Malaria ◽  
De Novo ◽  
Neutralizing Antibody ◽  
Mobility Shift ◽  
Before And After ◽  
Tf Gene ◽  
Electrophoretic Mobility Shift Assays ◽  
Antiparasitic Treatment ◽  
Stimulation Of

SummarySerum from patients with P. falciparum malaria at day 1 (pretherapy) induces tissue factor (TF) in cultured endothelial cells. TF induction depends on de novo transcription as shown in Nuclear Run On assays. Electrophoretic mobility shift assays demonstrated binding of AP-1 and NF- κB/Rel proteins to their recognition sites in the TF promotor. After therapy (day 28), stimulation of TF antigen by patient serum is reduced by 70%. When serum obtained before and after therapy was compared, a decrease of NF-κB activation was evident. Activation of NF-κB-like proteins was in part dependent on TNFα in patient serum, since a TNFα neutralizing antibody reduced induction of TF transcription and translation and induction of NF-κB-like proteins. Induction of TF activity was suppressed by pDTC, an inhibitor of NF-κB activation. When different promotor constructs of the TF gene were tested, induction was dependent upon the presence of the intact NF-κB-like binding site in the TF promotor. A mutant with deleted NF-κB, but intact AP-1 sites was not inducible. Mutation of the AP-1 sites did not prevent induction, but reduced inducibility by pretherapy serum. Therefore, NF-κB/Rel proteins are responsible for induction of TF transcription by pretherapy serum, but AP-1 is needed for highest inducibility. The effect of antiparasitic therapy on the induction of TF by serum from patients with complicated P. falciparum malaria is dependent on a therapy-mediated loss of activation of NF-κB-like proteins in post-treatment patient serum.

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