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At least 541 records · Page 30Linked to original sources
PubMed1983

Kinin formation in hereditary angioedema plasma: evidence against kinin derivation from C2 and in support of "spontaneous" formation of bradykinin.

Hereditary angioedema (HAE) is due to a functional deficiency of the inhibitor of the activated first component of complement (C1 INH). This abnormality is thought to be responsible for the generation of a kininlike peptide in HAE plasma that is derived from the second component of complement (C2). Specifically, a combination of C2 cleavage by C1s and C2 fragment cleavage by plasmin has been reported to generate a kinin that is distinguishable from bradykinin. We have attempted to generate this peptide by activating the classical complement pathway by incubation of plasma with immune complexes and then adding plasmin or by incubating purified C1s with C4 and C2 and then adding either plasmin or trypsin. We performed a total of 13 experiments, and in no case was a kininlike molecule generated as assessed by contraction of the estrus rat uterus. However, incubation of EDTA-treated HAE plasma at 37 degrees C for time intervals up to 1 hr progressively generated a smooth muscle-contracting activity. This activity was resistant to tryptic digestion but was destroyed after incubation with carboxypeptidase B, an inhibition profile consistent with that of bradykinin. We therefore propose that bradykinin alone, or in combination with other factors heretofore unrecognized, might be responsible for the swelling that is characteristic of hereditary angioedema.

Angioedema↗
PubMed1988

Myelin formation in rat dorsal root ganglion cultured in a serum-free medium: influence of various culture media on myelin formation.

Survival and myelination in dorsal root ganglion culture were observed using 6 kinds of modified commercial serum-free media: MEM, neMEM, alpha-MEM, DMEM, F12 medium and DF medium (see Materials and Methods). The results showed that the survival rates of dorsal root ganglia cultured in alpha-MEM and DF medium are the highest and that the rates of myelinated ganglia are the highest when alpha-MEM is used as culture medium, as compared with other serum-free media.

Animals↗
PubMed2004

Dimer formation of receptor activator of nuclear factor kappaB induces incomplete osteoclast formation.

Receptor activator of nuclear factor kappaB-ligand (RANKL) transduces a differentiation signal appropriate to osteoclasts likely through induction a receptor homotrimer; however, biological importance of RANK-trimerizarion is unknown. To address the signaling mechanism of the RANK receptor, we analyzed the effect of two different types of homodimer inducers RANK-TM-FKBP36v and hEpoR-RANK-TM on osteoclastogenesis. Dimerizing component FKBP36v or extracellular portion of human erythropoietin receptor (hEpoR) was fused to RANK lacking the extracellular domain, and the dimerization of this fusion protein was induced by addition of the chemical inducer of dimerization AP20187 or erythropoietin, respectively. Such treatment resulted in induction of TRAP-activity, a marker of osteoclast in a dose dependent manner, with an efficiency equivalent to that of induction by RANKL. However, dimerized-RANK-induced osteoclasts showed relatively low levels of multinucleation, pit forming activity, and expression of calcitonin receptor and cathepsin K, compared with osteoclasts which were induced in the presence of RANKL. As expression of nuclear factor of activated T cells 1 (NFATc1) was also reduced in dimerized-RANK-induced osteoclasts, RANK oligomerization by RANKL is a critical event to generate fully matured osteoclasts through upregulation of NFATc1.

Animals↗
PubMed1987

High-molecular-weight crystallin aggregate formation resulting from non-enzymic carbamylation of lens crystallins: relevance to cataract formation.

Incubation of mixed bovine lens crystallins with 100 mM potassium cyanate causes almost all the protein to form large aggregates. These aggregates are not dispersed by powerful chaotropic agents and are held together by disulphide bonds. Experiments with beta L-crystallin show that carbamylation of this one protein class can bring about the aggregation of other unmodified crystallins. The carbamylated crystallin served as a nucleus for aggregation of other crystallins. These changes are related to the chemical modification of crystallins and the ensuing conformational changes in cataractogenesis.

Animals↗
PubMed1998

Is plaque formation in the common carotid artery representative for plaque formation and luminal stenosis in other atherosclerotic peripheral arteries? A post mortem study.

The atherosclerotic carotid artery is easily accessible for non-invasive duplex investigation. The aim of the present post mortem study was to examine whether plaque accumulation and luminal stenosis in the common carotid artery is representative for atherosclerotic plaque accumulation and luminal stenosis in other peripheral arteries. A total of 3765 cross-sections were obtained at regular intervals from 240 arteries (24 individuals). Five types of peripheral arteries were investigated: common carotid, femoral, common iliac, external iliac and renal arteries. In each cross-section, the lumen area, vessel area, plaque area and maximal plaque thickness was measured. For each location, the percentage luminal stenosis and relative plaque area was calculated. Relative plaque area was defined as the percentage of the vessel area which was occupied by plaque. Weak correlations (r=0.41-0.59) were observed between percentage relative plaque area or maximal plaque thickness in the common carotid artery and percentage relative plaque area in other peripheral arteries. Neither plaque accumulation nor luminal stenosis in the common carotid artery correlated with the percentage luminal stenosis in other peripheral arteries (P > 0.05). We conclude that plaque area in the common carotid artery is weakly correlated with plaque area and not correlated with luminal stenosis in other peripheral arteries.

Aged↗
PubMed1995

Effect of T-cell deficiency on the formation of periapical lesions in mice: histological comparison between periapical lesion formation in BALB/c and BALB/c nu/nu mice.

The role of T-cells in the development of periapical lesions was investigated immunohistochemically using 16 normal (BALB/c) mice and 16 nude (BALB/c nu/nu) mice (congenitally T-cell-deficient mice). The pulp chambers of maxillar first molars of all mice were opened, and the infiltrated immunocytes (anti-Thy1.2, -Lyt-1, -Lyt-2, -L3T4, -I-Ad, -IgG, and -IgM positive cells) were determined immunohistochemically at 2, 4, 6, and 8 wk after operation. Periapical lesions appeared at 2 wk in both mouse groups. Numerous anti-I-Ad positive-stained cells appeared at 2 wk, anti-I-Ad, -Thy1.2 (-Lyt-1, -L3T4), -IgG positive-stained cells appeared between 4 and 8 wk, and periapical lesions with bone resorption rapidly increased until 4 wk in normal mice. On the other hand in nude mice, only anti-I-Ad and -IgG positive cells were present from 4 to 6 wk, and the progress of periapical lesions with inflammatory cells stopped at 6 wk. Furthermore, numerous fibroblasts were found instead of inflammatory cells at 8 wk. These findings suggest that the progression of periapical lesions with bone resorption required helper T-cells and numerous immunoglobulin-producing cells.

Animals↗