| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| M Smiałek, B Gajkowska, R P Ostrowski, P Piotrowsk. Experimental squalene encephaloneuropathy in the rat. Folia neuropathologica. vol 35. issue 4. 1999-01-19. PMID:9833408. |
accumulation of lipid-like droplets in the myelin sheaths in the pns and in the neurons in the brain cortex, hypertrophy of endothelium, and sometimes endothelial apoptosis in blood vessels, and increased synthesis of collagen in the ischiadic nerve were characteristic for developed squalene encephaloneuropathy. |
1999-01-19 |
2023-08-12 |
rat |
| C van den Bos, S Silverstetter, M Murphy, T Connoll. p21(cip1) rescues human mesenchymal stem cells from apoptosis induced by low-density culture. Cell and tissue research. vol 293. issue 3. 1998-11-24. PMID:9716736. |
the loss of p21 in hypertrophic chondrocytes correlates with the onset of apoptosis during endochondrial ossification. |
1998-11-24 |
2023-08-12 |
human |
| J V Bonventre, T Forc. Mitogen-activated protein kinases and transcriptional responses in renal injury and repair. Current opinion in nephrology and hypertension. vol 7. issue 4. 1998-11-06. PMID:9690043. |
mammalian cells respond to external stimuli by activation of a variety of signal transduction pathways which culminate in stereotypical responses important in renal disease, such as proliferation, growth arrest, hypertrophy, differentiation, or apoptosis. |
1998-11-06 |
2023-08-12 |
Not clear |
| P Bianco, F D Cancedda, M Riminucci, R Cancedd. Bone formation via cartilage models: the "borderline" chondrocyte. Matrix biology : journal of the International Society for Matrix Biology. vol 17. issue 3. 1998-11-03. PMID:9707341. |
hypertrophic chondrocytes located in different cartilage areas are exposed to an inappropriate matrix and endocrine/paracrine environment, cannot differentiate to osteoblast-like cells and therefore undergo apoptosis. |
1998-11-03 |
2023-08-12 |
Not clear |
| Y Shizukuda, P M Buttrick, D L Geenen, A C Borczuk, R N Kitsis, E H Sonnenblic. beta-adrenergic stimulation causes cardiocyte apoptosis: influence of tachycardia and hypertrophy. The American journal of physiology. vol 275. issue 3. 1998-10-01. PMID:9724301. |
beta-adrenergic stimulation causes cardiocyte apoptosis: influence of tachycardia and hypertrophy. |
1998-10-01 |
2023-08-12 |
rat |
| A Enomoto, E P Sandgren, R R Maronpo. Interactive effects of c-myc and transforming growth factor alpha transgenes on liver tumor development in simian virus 40 T antigen transgenic mice. Veterinary pathology. vol 35. issue 4. 1998-09-30. PMID:9684972. |
mice carrying c-myc or tgfalpha alone exhibited centrilobular hypertrophy and increased apoptosis (c-myc mice only) of hepatocytes after 3 or 4 weeks of age, but no detectable changes in cell proliferation or proliferative lesions were observed in either line during the 8 weeks. |
1998-09-30 |
2023-08-12 |
mouse |
| J W Adams, Y Sakata, M G Davis, V P Sah, Y Wang, S B Liggett, K R Chien, J H Brown, G W Dor. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 17. 1998-09-17. PMID:9707614. |
the consequence of cardiomyocyte apoptosis was a transition from compensated hypertrophy to a rapidly progressive and lethal cardiomyopathy. |
1998-09-17 |
2023-08-12 |
mouse |
| J W Adams, Y Sakata, M G Davis, V P Sah, Y Wang, S B Liggett, K R Chien, J H Brown, G W Dor. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 17. 1998-09-17. PMID:9707614. |
progression from hypertrophy to apoptosis in vitro and in vivo was coincident with activation of p38 and jun kinases. |
1998-09-17 |
2023-08-12 |
mouse |
| J W Adams, Y Sakata, M G Davis, V P Sah, Y Wang, S B Liggett, K R Chien, J H Brown, G W Dor. Enhanced Galphaq signaling: a common pathway mediates cardiac hypertrophy and apoptotic heart failure. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 17. 1998-09-17. PMID:9707614. |
these data suggest a mechanism in which moderate levels of gq signaling stimulate cardiac hypertrophy whereas high level gq activation results in cardiomyocyte apoptosis. |
1998-09-17 |
2023-08-12 |
mouse |
| K K Griendling, M Ushio-Fuka. Redox control of vascular smooth muscle proliferation. The Journal of laboratory and clinical medicine. vol 132. issue 1. 1998-07-23. PMID:9665366. |
oxidative stress increases cell proliferation, mediates hormone-induced hypertrophy, and-under some circumstances-induces apoptosis. |
1998-07-23 |
2023-08-12 |
Not clear |
| P Nilsso. [Biological aging and apoptosis--mechanism in cardiovascular disease?]. Nordisk medicin. vol 113. issue 3. 1998-06-25. PMID:9528285. |
studies of apoptosis regulation can yield improved understanding of such phenomena as atherosclerotic plaque rupture and such structural cardiovascular changes as left ventricular hypertrophy. |
1998-06-25 |
2023-08-12 |
Not clear |
| T H Vu, J M Shipley, G Bergers, J E Berger, J A Helms, D Hanahan, S D Shapiro, R M Senior, Z Wer. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. Cell. vol 93. issue 3. 1998-05-29. PMID:9590175. |
mmp-9/gelatinase b is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. |
1998-05-29 |
2023-08-12 |
mouse |
| T H Vu, J M Shipley, G Bergers, J E Berger, J A Helms, D Hanahan, S D Shapiro, R M Senior, Z Wer. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. Cell. vol 93. issue 3. 1998-05-29. PMID:9590175. |
although hypertrophic chondrocytes develop normally, apoptosis, vascularization, and ossification are delayed, resulting in progressive lengthening of the growth plate to about eight times normal. |
1998-05-29 |
2023-08-12 |
mouse |
| N C Rath, W E Huff, G R Bayyari, J M Balo. Cell death in avian tibial dyschondroplasia. Avian diseases. vol 42. issue 1. 1998-05-26. PMID:9533083. |
normal growth plates, under similar conditions, showed no significant apoptosis of chondrocytes from hypertrophic and chondrolyzing zones. |
1998-05-26 |
2023-08-12 |
Not clear |
| Y Y Zhao, D R Sawyer, R R Baliga, D J Opel, X Han, M A Marchionni, R A Kell. Neuregulins promote survival and growth of cardiac myocytes. Persistence of ErbB2 and ErbB4 expression in neonatal and adult ventricular myocytes. The Journal of biological chemistry. vol 273. issue 17. 1998-05-22. PMID:9553078. |
rhggf2 also promoted survival and inhibited apoptosis of subconfluent, serum-deprived myocyte primary cultures and also induced hypertrophic growth in both neonatal and adult ventricular myocytes, which was accompanied by enhanced expression of prepro-atrial natriuretic factor and skeletal alpha-actin. |
1998-05-22 |
2023-08-12 |
mouse |
| S J Shankland, R J Johnso. TGF-beta in glomerular disease. Mineral and electrolyte metabolism. vol 24. issue 2-3. 1998-05-01. PMID:9525701. |
however, tgf-beta may also have other important functions in the glomerulus, including the regulation of cell proliferation, hypertrophy, and survival (apoptosis), as well as modulation of the local and systemic immune response. |
1998-05-01 |
2023-08-12 |
Not clear |
| Y Wang, S Huang, V P Sah, J Ross, J H Brown, J Han, K R Chie. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. The Journal of biological chemistry. vol 273. issue 4. 1998-03-03. PMID:9442057. |
cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. |
1998-03-03 |
2023-08-12 |
mouse |
| Y Wang, S Huang, V P Sah, J Ross, J H Brown, J Han, K R Chie. Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. The Journal of biological chemistry. vol 273. issue 4. 1998-03-03. PMID:9442057. |
the direct involvement of p38 pathways in cardiac hypertrophy and apoptosis suggests a significant role for p38 signaling in the pathophysiology of heart failure. |
1998-03-03 |
2023-08-12 |
mouse |
| T Force, J V Bonventr. Growth factors and mitogen-activated protein kinases. Hypertension (Dallas, Tex. : 1979). vol 31. issue 1 Pt 2. 1998-02-20. PMID:9453296. |
mammalian cells respond to external stimuli by activation of a variety of signal transduction pathways, which culminate in stereotypical responses, such as proliferation, growth arrest, hypertrophy, differentiation, or apoptosis. |
1998-02-20 |
2023-08-12 |
Not clear |
| R Venezian, B J Shenker, S Datar, P S Lebo. Modulation of chondrocyte proliferation by ascorbic acid and BMP-2. Journal of cellular physiology. vol 174. issue 3. 1998-02-13. PMID:9462695. |
when prehypertrophic chondrocytes from the cephalic region of embryonic sternae were stimulated to undergo hypertrophy with rhbmp-2 + ascorbate, levels of apoptosis were similar to that seen with ascorbate alone. |
1998-02-13 |
2023-08-12 |
chicken |