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Articles by S. E Kim
Total Records ( 2 ) for S. E Kim
  S. J Lee , C. W Kim , K. J Lee , J. W Choe , S. E Kim , J. H Oh and Y. S. Park
  Background

S100B is a biomarker that reflects injury to the central nervous system. As the spine is an integral part of the spinal cord, a study was undertaken to investigate whether serum S100B levels are associated with acute spinal fracture without head injury.

Methods

The study population consisted of 32 consecutive patients aged ≥18 years in whom the emergency physicians suspected spinal fractures. All the patients underwent CT scans to establish the diagnosis of spinal fracture. MRI was then performed on all the patients to determine the presence of spinal cord injury.

Results

Serum S100B levels were higher in the spinal fracture group than in the non-spinal fracture group, and 19 of the 20 patients in the spinal fracture group (95%) had an S100B level >0.12 µg/l, whereas all 12 of the non-spinal fracture group had an S100B level ≤0.12 µg/l. The S100B level in patients with epidural encroachment of the spinal cord was significantly higher (0.22–4.58 µg/l; mean 2.45 µg/l; 95% CI 0.95 to 3.94) than in those without epidural encroachment (0.114–2.87 µg/l; mean 0.80 µg/l; 95% CI 0.24 to 1.37) (p=0.037). Plain radiography revealed no definite abnormal findings in half of the patients with spinal fracture.

Conclusions

Serum S100B levels are raised in all patients with acute spinal fracture without head injury. Spinal fracture may therefore be one of the extracerebral sources of S100B. Serum S100B levels may be an effective tool for excluding subtle spinal fractures with no clear radiographic findings.

  A. Y Kim , Y. S Lee , K. H Kim , J. H Lee , H. K Lee , S. H Jang , S. E Kim , G. Y Lee , J. W Lee , S. A Jung , H. Y Chung , S Jeong and J. B. Kim
 

In obesity, dysregulation of adipocytokines is involved in several pathological conditions including diabetes and certain cancers. As a member of the adipocytokines, adiponectin plays crucial roles in whole-body energy homeostasis. Recently, it has been reported that the level of plasma adiponectin is reduced in several types of cancer patients. However, it is largely unknown whether and how adiponectin affects colon cancer cell growth. Here, we show that adiponectin suppresses the proliferation of colon cancer cells including HCT116, HT29, and LoVo. In colon cancer cells, adiponectin attenuated cell cycle progression at the G1/S boundary and concurrently increased expression of cyclin-dependent kinase inhibitors such as p21 and p27. Adiponectin stimulated AMP-activated protein kinase (AMPK) phosphorylation whereas inhibition of AMPK activity blunted the effect of adiponectin on the proliferation of colon cancer cells. Furthermore, knockdown of adiponectin receptors such as AdipoR1 and AdipoR2 relieved the suppressive effect of adiponectin on the growth of colon cancer cells. In addition, adiponectin repressed the expression of sterol regulatory element binding protein-1c, which is a key lipogenic transcription factor associated with colon cancers. These results suggest that adiponectin could inhibit the growth of colon cancer cells through stimulating AMPK activity.

 
 
 
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