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21. |
Endothelin‐1 is upregulated during skeletal muscle ischemia and reperfusion |
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Journal of Orthopaedic Research,
Volume 16,
Issue 1,
1998,
Page 128-135
K. Hvaal,
E. Øie,
H. Attramadal,
V. Halvorsen,
A. Svindland,
L. Nordsletten,
S. Skjeldal,
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摘要:
AbstractThe aim of the present study was to test the hypothesis that the vasoconstrictive peptide endothelin‐l is upregulated in ischemia and reperfusion in skeletal muscle. Sixty‐eight Wistar rats were included in the series: 12 served as controls that did not undergo the procedure, 16 underwent sham operations, and 40 were subjected to a modified tourniquet ischemia for 3 hours and 20 minutes. Of the 40 rats, 16 were killed at the end of the ischemic period, 16 underwent reperfusion for 2 hours, and eight underwent reperfusion for 72 hours. Areas of necrosis were measured by morphometry in hematoxylin and eosin‐stained cross sections of the anterior tibial muscles that had been reperfused for 72 hours. Sections from the controls, the muscles that had not been reperfused and the reperfused muscles were immunostained for endothelin‐1. Serum endothelin‐1 levels in blood samples from the aorta were determined with a commercial enzyme immunoassay kit. The anterior tibial muscle was harvested for preproendothelin‐1 mRNA analysis with RNase protection assay. The hematoxylin and eosin‐stained sections showed extensive necrosis with an acellular core of no reperfusion. The muscular core demonstrated weak immunostaining for endothelin‐1 in all sections, a subfascial narrow brim of fibers showed enhanced immunoreactivity at the end of ischemia, and all fibers outside the core stained by 2 hours after the start of reperfusion. After 72 hours of reperfusion. the fibers outside the core stained positive in a checkerboard‐like pattern. There were no differences in serum endothelin‐1 levels between the groups. Preproendothelin‐1 mRNA analysis with RNase protection assay showed 2‐fold upregulation at the end of ischemia and 4‐fold upregulalion'after 2 hours of reperfusion (p = 0.001). This study supports the hypothesis that both ischemia and reperfusion upregulate endoth
ISSN:0736-0266
DOI:10.1002/jor.1100160122
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1998
数据来源: WILEY
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22. |
Quantitative study of the quadriceps muscles and trochlear groove geometry related to instability of the patellofemoral joint |
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Journal of Orthopaedic Research,
Volume 16,
Issue 1,
1998,
Page 136-143
Farzam Farahmand,
Wongwit Sejiavongse,
Andrew A. Amis,
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摘要:
AbstractThis was a quantitative study of the major anatomical structures associated with instability of the patellofemoral joint: the quadriceps muscles and the femoral trochlear groove. The attachments of the muscles to the patella, their lines of action, and their relative sizes (physiological cross‐sectional areas) were found. On the basis of the physiological cross‐sectional areas, it was estimated that the central muscles—the rectus femoris and vastus intermedius—contributed 35% of the quadriceps strength, with 40% from the vastus lateralis and 25% from the vastus medialis. The vastus lateralis had the most variable results, with the ratio of the lateralis to the medialis ranging from 0.90 to 2.18; this may be associated with patellar instability. Both the long and oblique parts of the vastus medialis were more oblique than the corresponding parts of the vastus lateralis. Photographic “skyline” views of the trochlear groove produced data on the sulcus angle and ratio of depth to width. The data showed that the trochlear groove did not deepen in the area contacted by the patella with progressive knee flexion (p>0.53). contrary to popular belief. These data are useful for objective analysis of patellofemoral stability and related surgical in
ISSN:0736-0266
DOI:10.1002/jor.1100160123
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1998
数据来源: WILEY
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23. |
Programmed removal of chondrocytes during endochondral fracture healing |
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Journal of Orthopaedic Research,
Volume 16,
Issue 1,
1998,
Page 144-150
Francis Young‐In Lee,
Yong Won Choi,
Fred F. Behrens,
David O. DeFouw,
Thomas A. Einhorn,
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摘要:
AbstractThis investigation tested the hypothesis that the removal of chondrocytes during endochondral fracture healing involves an ordered process of programmed cell death. To accomplish this, unilateral closed fractures were created in the femora of 36 Sprague‐Dawley rats. The rats were killed in groups of four on days 1, 3, 7, 14, 21, 28, 42, 49, and 56 after fracture. The femora were embedded in paraffin and tested for expression of specific markers of fragmented DNA with use of a terminal deoxyuridyl transferase‐mediated deoxyuridine triphosphatebiotin nick end labeling (TUNEL) technique. To determine the potential for trans–differentiation of chondrocytes to osteoblasts calluses were also hybridized to detect expression of osteocal in mRNA. Cell proliferation was assessed by an immunohistochemical detection method for proliferating cell nuclear antigen. A separate group of four rats was killed on day 28 to represent the later stage of the endochondral ossification, and the calluses were examined for cellular morphology with transmission electron microscopy. The results showed a coordination in both time and space of the activities of cellular proliferation and programmed cell death. Cell proliferation was most active in the earlier phases of fracture healing (days 1 through 14) although TUNEL expression was apparent in hypertrophic chondrocytes on day 14 after fracture and persisted until day 28. In the later stages of fracture healing (days 14 through 28), proliferating cell nuclear antigen was no longer synthesized in hard callus (intramembranous bone) and cell removal was the dominant activity in soft callus chondrocytes. Expression of osteocalcin mRNA was detected in osteoblasts but not in hypertrophic chondrocytes or in any other nonosteoblastic cell type. These findings support the hypothesis that the removal of chondrocytes during endochondral fracture healing is part of an ordered transition of tissue types in which the cellular mechanisms are genetically programmed to involve proliferation, maturation, and apoptotic cell
ISSN:0736-0266
DOI:10.1002/jor.1100160124
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1998
数据来源: WILEY
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24. |
Announcements |
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Journal of Orthopaedic Research,
Volume 16,
Issue 1,
1998,
Page 151-151
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ISSN:0736-0266
DOI:10.1002/jor.1100160125
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1998
数据来源: WILEY
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25. |
Masthead |
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Journal of Orthopaedic Research,
Volume 16,
Issue 1,
1998,
Page -
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PDF (69KB)
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ISSN:0736-0266
DOI:10.1002/jor.1100160101
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1998
数据来源: WILEY
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