Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
M S Hirsch, L E Lunsford, V Trinkaus-Randall, K K Svobod. Chondrocyte survival and differentiation in situ are integrin mediated. Developmental dynamics : an official publication of the American Association of Anatomists. vol 210. issue 3. 1998-02-10. PMID:9389451. |
cephalic chondrocytes become hypertrophic and secrete type x collagen into the extracellular matrix prior to bone deposition. |
1998-02-10 |
2023-08-12 |
chicken |
E Bonucci, G Silvestrini, P Mocett. MC22-33F monoclonal antibody shows unmasked polar head groups of choline-containing phospholipids in cartilage and bone. European journal of histochemistry : EJH. vol 41. issue 3. 1998-01-26. PMID:9359029. |
the mc22-33f mab immunoreaction was found in the cytoplasm of maturing and hypertrophic and, to a lesser extent, proliferating and degenerating chondrocytes; it was strongly positive in matrix vesicles, at the periphery of calcification nodules, and at the periphery of calcified matrix. |
1998-01-26 |
2023-08-12 |
Not clear |
L J Zhou, M Inoue, I Ono, F Kanek. The mode of action of prostaglandin (PG) I1 analog, SM-10906, on fibroblasts of hypertrophic scars is similar to PGE1 in its potential role of preventing scar formation. Experimental dermatology. vol 6. issue 6. 1998-01-22. PMID:9412820. |
the effects of prostaglandin (pg) i1 analog, sm-10906 (sm-6) and pge1 on extracellular matrix formation and the release of cytokines by cultured normal human dermal fibroblasts (ndf) and hypertrophic scar fibroblasts (hsf) were compared in order to evaluate the clinical efficacy of pgs in preventing scar formation. |
1998-01-22 |
2023-08-12 |
human |
G J Breur, M D Lapierre, K Kazmierczak, K M Stechuchak, G P McCab. The domain of hypertrophic chondrocytes in growth plates growing at different rates. Calcified tissue international. vol 61. issue 5. 1998-01-21. PMID:9351885. |
in this study, we tested the hypotheses that (a) both the domain volume (volume of the cell and the matrix it has formed) and matrix volume of juxtametaphyseal hypertrophic chondrocytes in the growth plate is tightly controlled, and that (b) the domain volume of juxtametaphyseal hypertrophic chondrocytes is a strong determinant of the rate of bone length growth. |
1998-01-21 |
2023-08-12 |
rat |
G J Breur, M D Lapierre, K Kazmierczak, K M Stechuchak, G P McCab. The domain of hypertrophic chondrocytes in growth plates growing at different rates. Calcified tissue international. vol 61. issue 5. 1998-01-21. PMID:9351885. |
the data suggest that the domain volume of juxtametaphyseal hypertrophic chondrocytes, as well as the matrix volume produced per cell, may be tightly regulated. |
1998-01-21 |
2023-08-12 |
rat |
N Fujitsuka, A Kurogi, T Hattori, S Shind. [Effects of onpi-to (TJ-8117) and (-)epicatechin-3-O-gallate on the proliferating changes in glomeruli of 5/6 nephrectomized rats]. Nihon Jinzo Gakkai shi. vol 39. issue 7. 1998-01-20. PMID:9396236. |
in the present study, the effects of tj-8117 and (-)epicatechin-3-o-gallate (ecg), which is a component of rhei rhizoma, on glomerular cell proliferation, extracellular matrix accumulation and glomerular hypertrophy were investigated in 5/6 nephrectomized rats. |
1998-01-20 |
2023-08-12 |
rat |
W S Colucc. Molecular and cellular mechanisms of myocardial failure. The American journal of cardiology. vol 80. issue 11A. 1998-01-20. PMID:9412539. |
these alterations include hypertrophy and cellular apoptosis of myocytes, changes in the molecular phenotype of the myocardium with reinduction of a fetal gene program, and alterations in the quantity and composition of the extracellular matrix. |
1998-01-20 |
2023-08-12 |
Not clear |
H Yu, A M Gallagher, P M Garfin, M P Print. Prostacyclin release by rat cardiac fibroblasts: inhibition of collagen expression. Hypertension (Dallas, Tex. : 1979). vol 30. issue 5. 1997-12-10. PMID:9369254. |
cardiac fibroblasts, as the source of extracellular matrix for the left ventricle, subserve important functions to cardiac remodeling and fibrotic development following myocardial infarction or with pressure-overload cardiac hypertrophy. |
1997-12-10 |
2023-08-12 |
rat |
C Shukunami, K Ishizeki, T Atsumi, Y Ohta, F Suzuki, Y Hirak. Cellular hypertrophy and calcification of embryonal carcinoma-derived chondrogenic cell line ATDC5 in vitro. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 12. issue 8. 1997-11-20. PMID:9258747. |
during the process of endochondral bone formation, proliferating chondrocytes give rise to hypertrophic cells, which then deposit a mineralized matrix to form calcified cartilage prior to replacement by bone. |
1997-11-20 |
2023-08-12 |
Not clear |
H Ono, Y On. Nephrosclerosis and hypertension. The Medical clinics of North America. vol 81. issue 6. 1997-11-19. PMID:9356598. |
in the authors' experience, the kidney of an elderly subject, although with normotensive pressure and normal level of cholesterol, shows an increased mesangial matrix and hypertrophic vascular medial smooth muscle cells. |
1997-11-19 |
2023-08-12 |
human |
G Wolf, F N Ziyade. Renal tubular hypertrophy induced by angiotensin II. Seminars in nephrology. vol 17. issue 5. 1997-11-18. PMID:9316213. |
angiotensin ii (ang ii) is a prime agent that has been linked to the progression of renal disease by a host of mechanisms, including the induction of tubular epithelial hypertrophy and stimulation of extracellular matrix biosynthesis. |
1997-11-18 |
2023-08-12 |
Not clear |
N Makino, M Sugano, S Otsuka, T Hat. Molecular mechanism of angiotensin II type I and type II receptors in cardiac hypertrophy of spontaneously hypertensive rats. Hypertension (Dallas, Tex. : 1979). vol 30. issue 4. 1997-11-13. PMID:9336375. |
these results indicate that at1 receptor and ace, but not at2 receptor, play a crucial role in the remodeling of matrix tissue but a smaller role in the development of the hypertrophy of lv myocyte in shr and that the lv/body weight changes do not fully account for the complete suppression of hypertension. |
1997-11-13 |
2023-08-12 |
rat |
K Wong, K R Boheler, M Petrou, M H Yacou. Pharmacological modulation of pressure-overload cardiac hypertrophy: changes in ventricular function, extracellular matrix, and gene expression. Circulation. vol 96. issue 7. 1997-10-31. PMID:9337196. |
pharmacological modulation of pressure-overload cardiac hypertrophy: changes in ventricular function, extracellular matrix, and gene expression. |
1997-10-31 |
2023-08-12 |
rat |
F H Wezeman, M R Bollno. Immunohistochemical localization of fibroblast growth factor-2 in normal and brachymorphic mouse tibial growth plate and articular cartilage. The Histochemical journal. vol 29. issue 6. 1997-10-08. PMID:9248858. |
immunostaining was present only in the territorial extracellular matrix immediately adjacent to the chondrocytes of the proliferating and upper hypertrophic zones. |
1997-10-08 |
2023-08-12 |
mouse |
F H Wezeman, M R Bollno. Immunohistochemical localization of fibroblast growth factor-2 in normal and brachymorphic mouse tibial growth plate and articular cartilage. The Histochemical journal. vol 29. issue 6. 1997-10-08. PMID:9248858. |
in contrast, the reduced size of bm/bm growth plates was accompanied by significantly reduced staining intensity in proliferating and upper hypertrophic chondrocytes, and staining was absent from the territorial extracellular matrix of all zones of the bm/bm growth plate. |
1997-10-08 |
2023-08-12 |
mouse |
J C Woodard, G A Donovan, L W Fishe. Pathogenesis of vitamin (A and D)-induced premature growth-plate closure in calves. Bone. vol 21. issue 2. 1997-10-07. PMID:9267693. |
columnar-zone cartilage cells appeared immature where the matrix became mineralized and lacked the morphology of hypertrophic chondrocytes. |
1997-10-07 |
2023-08-12 |
Not clear |
J C Woodard, G A Donovan, L W Fishe. Pathogenesis of vitamin (A and D)-induced premature growth-plate closure in calves. Bone. vol 21. issue 2. 1997-10-07. PMID:9267693. |
biglycan, type i collagen propeptide, type i collagen, osteopontin, osteocalcin, osteonectin, bone sialoprotein, and alkaline phosphatase were localized within the cytoplasm or surrounding matrix of hypertrophic chondrocytes. |
1997-10-07 |
2023-08-12 |
Not clear |
J C Woodard, G A Donovan, L W Fishe. Pathogenesis of vitamin (A and D)-induced premature growth-plate closure in calves. Bone. vol 21. issue 2. 1997-10-07. PMID:9267693. |
in vitamin-treated calves, these same proteins were found in regions undergoing premature matrix mineralization even though the chondrocytes did not have a hypertrophic morphology. |
1997-10-07 |
2023-08-12 |
Not clear |
J C Woodard, G A Donovan, L W Fishe. Pathogenesis of vitamin (A and D)-induced premature growth-plate closure in calves. Bone. vol 21. issue 2. 1997-10-07. PMID:9267693. |
therefore, vitamin treatment did not cause just a selective expression, but it caused expression of a large number of matrix proteins normally associated with the hypertrophic chondrocyte phenotype. |
1997-10-07 |
2023-08-12 |
Not clear |
S Bord, A Horner, R M Hembry, J J Reynolds, J E Compsto. Distribution of matrix metalloproteinases and their inhibitor, TIMP-1, in developing human osteophytic bone. Journal of anatomy. vol 191 ( Pt 1). 1997-09-18. PMID:9279657. |
chondrocytes demonstrated variable levels of collagenase and stromelysin expression throughout the proliferative and hypertrophic regions, stromelysin showing both cell-associated and strong matrix staining. |
1997-09-18 |
2023-08-12 |
human |