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Scand J Rheumatol. 2000;29(4):222-5.
Suppression of collagen-induced arthritis with histone H1.
Jung N, Kim DS, Kwon HY, Yi YW, Kim D, Kang AD, Cho CH, Hong SS, Lee HS, Bae I.
Therapeutic Gene Group, Samyang Genex Biotech Res. Inst., Taejeon, Korea.
Besides roles in nucleus mediating the condensation of DNA into chromatin, the involvement of histones in autoimmune diseases, hormone regulation, and killing leukemia cells has been reported. In order to investigate the functions of histones on an autoimmune disease, histone H1 was injected into collagen-induced arthritis (CIA) mice. A dramatic suppression of CIA by histone H1 was observed at a dose of 1 mg/kg bodyweight of mouse. In addition, the increased level of anti-inflammatory cytokine IL-10 was detected in cultured splenocytes from the mouse treated with histone H1. These findings suggest that histone H1 suppresses the collagen-induced arthritis, possibly by increasing the level of IL-10 production.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11028842&dopt=Abstract
J Endovasc Ther. 2002 Oct;9(5):665-75.
Aneurysm wall stress and tendency to rupture are features of physical wall properties: an experimental study.
Flora HS, Talei-Faz B, Ansdell L, Chaloner EJ, Sweeny A, Grass A, Adiseshiah M.
Vascular/Endovascular Unit, University College, London Hospitals NHS Trust, London, England, UK.
PURPOSE: To use bench top techniques to examine the biophysical phenomena affecting the risk of abdominal aortic aneurysm (AAA) rupture relative to the physical properties of the aneurysm sac. METHODS: Three latex AAAs with different wall elasticities were tested in a validated pulsatile flow model (PFM). Strain gauges were wired to each AAA model at the neck, inflection point, and at the maximum diameter. In initial studies, the influence of pressurization and the mechanical properties of AAA wall stress were evaluated. In subsequent studies, the latex AAAs were excluded with a tube graft and retested in the PFM. After creation of either a type I or II endoleak of known size and pressure, the systemic/intrasac pressure and the AAA wall stress were measured. RESULTS: Each model had a complex wall-stress pattern comprising radial, longitudinal, and shear components. The peak wall stress at any point, in the presence of systemic pressurization or endoleak pressure, only reached 1% of the failure strength. In an AAA with a reinforced wall, the peak stress was significantly greater. Statistical analysis showed that wall strength contributed more significantly to wall stress than increasing pressurization within the AAA sac. CONCLUSIONS: AAA wall mechanics contribute more significantly to peak wall stress than pressure variations within the system. In particular, increased stiffness (analogous to collagen deposition) significantly increased peak wall stress, which was located at the inflection point rather than at the maximum diameter. Techniques to measure the AAA wall mechanics and the rate of deterioration may predict AAA rupture in the untreated state or in the presence of an endoleak following endovascular repair.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12431152&dopt=Abstract
Am J Reprod Immunol. 2000 Sep;44(3):136-42.
Anti-DNA antibodies cross-reacting with laminin inhibit trophoblast attachment and migration: implications for recurrent pregnancy loss in SLE patients.
Qureshi F, Yang Y, Jaques SM, Johnson MP, Naparstek Y, Ulmansky R, Schuger L.
Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA.
PROBLEM: Systemic lupus erythematosus (SLE), an autoimmune disease, is associated with reduced fetal survival, recurrent abortions, and other pregnancy complications. Some of the autoantibodies found in SLE bind to laminins (LNs), which play an important role in the implantation of the fertilized ovum in humans. METHOD OF STUDY: To elucidate the role of these specific autoantibodies, chorionic villous explants from 6 7-week-old human placentas were established as organ cultures on laminin-1 (LN-1), collagen IV (CN-IV) or uncoated culture dishes. The cultures were then exposed to a mouse monoclonal anti-DNA/anti-LN-1 antibody, to human polyclonal lupus antibodies cross-reacting with LN-1, a function-blocking polyclonal antibody to LN-1, polyclonal antibodies to CN-IV, or IgG control. RESULTS: The explants attached to LN-1 and CN-IV, but not to uncoated culture dishes. LN-1 promoted migration of trophoblast, whereas CN-IV promoted migration of fibroblast-like cells. Trophoblast attachment and migration were abolished in a dose-dependent manner by all three antibodies to LN-1, but not by antibodies to CN-IV or IgG control. Furthermore, the effect of anti-LN antibodies was abolished by preincubating them with LN-1. CONCLUSIONS: These studies suggest that anti-DNA antibodies cross-reacting with LNs may play a role in early pregnancy failure in SLE patients by interfering with placental implantation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11028899&dopt=Abstract
Mol Biol Cell. 2000 Oct;11(10):3353-64.
Matricellular proteins as modulators of cell-matrix interactions: adhesive defect in thrombospondin 2-null fibroblasts is a consequence of increased levels of matrix metalloproteinase-2.
Yang Z, Kyriakides TR, Bornstein P.
Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
Thrombospondin 2 (TSP2)-null mice, generated by disruption of the Thbs2 gene, display a variety of connective tissue abnormalities, including fragile skin and the presence of abnormally large collagen fibrils with irregular contours in skin and tendon. In this study we demonstrate that TSP2-null skin fibroblasts show a defect in attachment to a number of matrix proteins, and a reduction in cell spreading. To investigate the molecular mechanisms responsible for these abnormal cell-matrix interactions, we compared the levels of matrix metalloproteinases (MMPs) in wild-type and mutant fibroblasts. Isolation and analysis of gelatinases from conditioned media by gelatin-agarose affinity chromatography and gelatinolytic assays demonstrated that TSP2-null fibroblasts produce a 2-fold increase in gelatinase A (MMP2) compared with wild-type cells. The adhesive defect was corrected by treatment of TSP2-null fibroblasts with soluble TSP2, with the MMP inhibitors BB94 and tissue inhibitor of metalloproteinase-2, and with a neutralizing antibody to MMP2. Moreover, stable transfection of TSP2-null fibroblasts with mouse TSP2 cDNA corrected both the adhesive defect and the altered expression of MMP2. Finally, MMP2 was shown to interact with TSP2 in a direct-binding plate assay. We conclude that TSP2 plays an important role in cell-matrix interactions, and that a deficiency in the protein results in increased levels of MMP2 that contribute to the adhesive defect in TSP2-null fibroblasts and could play a role in the complex phenotype of TSP2-null mice.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11029041&dopt=Abstract
Abdom Imaging. 2000 Nov-Dec;25(6):658-62.
Injected periurethral collagen for postprostatectomy urinary incontinence: MR and CT appearance.
Maki DD, Banner MP, Ramchandani P, Stolpen A, Rovner ES, Wein AJ.
Department of Radiology, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA.
BACKGROUND: Urinary incontinence, a disturbing complication of radical prostatectomy, is often treated with periurethral collagen injections to increase urethral closure and resistance to urinary outflow. METHODS: Using magnetic resonance imaging and computed tomography, we studied the appearance of glutaraldehyde cross-lined bovine collagen endoscopically injected into the periurethral tissues in four men who developed urinary incontinence after radical prostatectomy. Collagen was also scanned in vitro to verify its magnetic resonance appearance. RESULTS: Collagen deposits appear as well-circumscribed nodules of low to intermediate signal intensity on both T1- and T2-weighted images in the periurethral tissues or in the base of the subjacent penile bulb (base of corpus spongiosum). On contrast-enhanced computed tomography, collagen appears as a hypoattenuating nodular-filling defect within the penile bulb. CONCLUSION: These imaging characteristics should allow differentiation of collagen from locally recurrent prostate carcinoma and avoid inappropriate work-up of benign findings.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11029103&dopt=Abstract
The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes
Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs.
However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals.
The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime.
Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.
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