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Articles by S. J Lee
Total Records ( 8 ) for S. J Lee
  S. J Lee , M. C Mahoney and E. Shaughnessy
 

OBJECTIVE. The objective of our study was to present the imaging features, including an MRI example, of dermatofibrosarcoma protuberans of the breast, an uncommon soft-tissue neoplasm of the breast, and review the literature.

CONCLUSION. Dermatofibrosarcoma protuberans is an extremely rare malignancy of the breast, with few published reports. This is the largest collection of such cases in a single institution with analysis of the imaging features.

  O Grauer , D Wolff , H Bertz , H Greinix , J. S Kuhl , A Lawitschka , S. J Lee , S. Z Pavletic , E Holler and I. Kleiter
 

A major obstacle of allogeneic haematopoietic stem cell transplantation is graft-versus-host disease, an immune-mediated disorder that affects multiple tissues and organs with varying severity. Neurological complications of acute and chronic graft-versus-host disease are rare but can produce severe clinical problems with significant morbidity and mortality. In this article, we review neurological manifestations of chronic graft-versus-host disease that comprise immune-mediated neuropathies, myasthenia gravis and myositis in the peripheral nervous system and various cerebrovascular complications, demyelination and immune-mediated encephalitis in the central nervous system. The National Institutes of Health consensus on criteria for clinical trials in chronic graft-versus-host disease recommended that the diagnosis of chronic graft-versus-host disease of the nervous system can be made only when other organs are affected by graft-versus-host disease and frequent neurological differential diagnoses such as drug-induced toxicities or opportunistic infections are excluded. The Consensus Conference on Clinical Practice in chronic graft-versus-host disease, held in autumn 2009 in Regensburg, aimed to summarize the literature and to provide guidelines for the diagnostic approach in children and adults with neurological manifestations of chronic graft-versus-host disease. Moreover, we present therapeutic recommendations and their level of evidence for the management of these complications. Overlapping symptoms and comorbidities after allogeneic haematopoietic stem cell transplantation and the limited knowledge about the underlying biological mechanisms of chronic graft-versus-host disease affecting the nervous system emphasize the need for further experimental and clinical investigations.

  Y Oshima , N Ouchi , M Shimano , D. R Pimentel , K. N Papanicolaou , K. D Panse , K Tsuchida , E Lara Pezzi , S. J Lee and K. Walsh
 

Background— Transforming growth factor-β family cytokines have diverse actions in the maintenance of cardiac homeostasis. Activin A is a member of this family whose regulation and function in heart are not well understood at a molecular level. Follistatin-like 3 (Fstl3) is an extracellular regulator of activin A protein, and its function in the heart is also unknown.

Methods and Results— We analyzed the expression of various transforming growth factor-β superfamily cytokines and their binding partners in mouse heart. Activin βA and Fstl3 were upregulated in models of myocardial injury. Overexpression of activin A with an adenoviral vector (Ad-actβA) or treatment with recombinant activin A protein protected cultured myocytes from hypoxia/reoxygenation-induced apoptosis. Systemic overexpression of activin A in mice by intravenous injection of Ad-actβA protected hearts from ischemia/reperfusion injury. Activin A induced the expression of Bcl-2, and ablation of Bcl-2 by small interfering RNA abrogated its protective action in myocytes. The protective effect of activin A on cultured myocytes was abolished by treatment with Fstl3 or by a pharmacological activin receptor-like kinase inhibitor. Cardiac-specific Fstl3 knockout mice showed significantly smaller infarcts after ischemia/reperfusion injury that was accompanied by reduced apoptosis.

Conclusions— Activin A and Fstl3 are induced in heart by myocardial stress. Activin A protects myocytes from death, and this activity is antagonized by Fstl3. Thus, the relative expression levels of these factors after injury is a determinant of cell survival in the heart.

  S. J Lee , S. S Lee , H. J Jung , H. S Kim , S. J Park , C. W Yeo and J. G. Shin
 

Our objectives were to identify CYP2D6 genetic polymorphisms in a Korean population, to compare the allele frequencies with those of other ethnic groups, and to evaluate variant-induced functional variations in dextromethorphan (DM) metabolism in vitro and in vivo. Thirty-eight single nucleotide polymorphisms of CYP2D6 were identified by direct DNA sequencing in 51 Koreans. An extended set of 707 subjects were screened for the identified variants. A group of 202 healthy subjects was subjected to phenotypic analysis on DM metabolism. CYP2D6*10 was found to be the most frequent allele (45.6%), followed by CYP2D6*1 (32.3%), *2 (9.9%), *5 (5.6%), *41 (2.2%), *49 (1.4%), and some other rare alleles (<1%). The newly identified E418K and S183Stop were assigned as CYP2D6*52 and CYP2D6*60, respectively, by the Human P450 (CYP) Allele Nomenclature Committee. Individuals having the CYP2D6*10/*49 genotype (n = 5) exhibited a significant decrease in CYP2D6 metabolic activity compared with those with the CYP2D6*1/*1 genotype (n = 31) (P < 0.019). Variations in CYP2D6 protein levels in liver tissues (n = 49) were observed with CYP2D6 genotypes, and correlation between the CYP2D6 protein content and the activity was significant (r2 = 0.7). Given the importance of CYP2D6 in drug metabolism, subjects with the CYP2D6*10/*49 genotype may benefit from genotype analysis to achieve optimal drug therapy.

  S. J Lee , S. S Lee , H. J Jung , H. S Kim , S. J Park , C. W Yeo and J. G. Shin
 

Our objectives were to identify CYP2D6 genetic polymorphisms in a Korean population, to compare the allele frequencies with those of other ethnic groups, and to evaluate variant-induced functional variations in dextromethorphan (DM) metabolism in vitro and in vivo. Thirty-eight single nucleotide polymorphisms of CYP2D6 were identified by direct DNA sequencing in 51 Koreans. An extended set of 707 subjects were screened for the identified variants. A group of 202 healthy subjects was subjected to phenotypic analysis on DM metabolism. CYP2D6*10 was found to be the most frequent allele (45.6%), followed by CYP2D6*1 (32.3%), *2 (9.9%), *5 (5.6%), *41 (2.2%), *49 (1.4%), and some other rare alleles (<1%). The newly identified E418K and S183Stop were assigned as CYP2D6*52 and CYP2D6*60, respectively, by the Human P450 (CYP) Allele Nomenclature Committee. Individuals having the CYP2D6*10/*49 genotype (n = 5) exhibited a significant decrease in CYP2D6 metabolic activity compared with those with the CYP2D6*1/*1 genotype (n = 31) (P < 0.019). Variations in CYP2D6 protein levels in liver tissues (n = 49) were observed with CYP2D6 genotypes, and correlation between the CYP2D6 protein content and the activity was significant (r2 = 0.7). Given the importance of CYP2D6 in drug metabolism, subjects with the CYP2D6*10/*49 genotype may benefit from genotype analysis to achieve optimal drug therapy.

  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.

  S. J Lee , Y. S Lee , T. A Zimmers , A Soleimani , M. M Matzuk , K Tsuchida , R. D Cohn and E. R. Barton
 

Myostatin is a TGF-β family member that normally acts to limit skeletal muscle mass. Follistatin is a myostatin-binding protein that can inhibit myostatin activity in vitro and promote muscle growth in vivo. Mice homozygous for a mutation in the Fst gene have been shown to die immediately after birth but have a reduced amount of muscle tissue, consistent with a role for follistatin in regulating myogenesis. Here, we show that Fst mutant mice exhibit haploinsufficiency, with muscles of Fst heterozygotes having significantly reduced size, a shift toward more oxidative fiber types, an impairment of muscle remodeling in response to cardiotoxin-induced injury, and a reduction in tetanic force production yet a maintenance of specific force. We show that the effect of heterozygous loss of Fst is at least partially retained in a Mstn-null background, implying that follistatin normally acts to inhibit other TGF-β family members in addition to myostatin to regulate muscle size. Finally, we present genetic evidence suggesting that activin A may be one of the ligands that is regulated by follistatin and that functions with myostatin to limit muscle mass. These findings potentially have important implications with respect to the development of therapeutics targeting this signaling pathway to preserve muscle mass and prevent muscle atrophy in a variety of inherited and acquired forms of muscle degeneration.

  T. F Tyler , S. J Nicholas , S. J Lee , M Mullaney and M. P. McHugh
  Background

Glenohumeral internal rotation deficit (GIRD) and posterior shoulder tightness have been linked to internal impingement.

Purpose

To determine if improvements in GIRD and/or decreased posterior shoulder tightness are associated with a resolution of symptoms.

Study Design

Cohort study; Level of evidence, 3.

Methods

Passive internal rotation and external rotation (ER) range of motion (ROM) at 90° of shoulder abduction and posterior shoulder tightness (cross-chest adduction in side lying) were assessed in 22 patients with internal impingement (11 men, 11 women; age 41 ± 13 years). Treatment involved stretching and mobilization of the posterior shoulder. The Simple Shoulder Test (SST) was administered on initial evaluation and discharge. Changes in GIRD, ER ROM, and posterior shoulder tightness were compared between patients with complete resolution of symptoms versus patients with residual symptoms using independent t tests.

Results

Patients had significant GIRD (35°), loss of ER ROM (23°), and posterior shoulder tightness (35°) on initial evaluation (all P < .01). Physical therapy (7 ± 2 weeks; range, 3–12 weeks) improved GIRD (26° ± 14°; P < .01), ER ROM loss (14° ± 20°), and posterior shoulder tightness (27° ±19°). The SST improved from 5 ± 3 to 11 ± 1 (P < .01). A greater improvement in posterior shoulder tightness was seen in patients with complete resolution of symptoms (n = 12) compared with patients with residual symptoms (35° vs 18°; P < .05). Improvements in GIRD and ER ROM loss were not different between groups (GIRD, 25° vs 28°, P = .57; ER ROM, 14° vs 15°, P = .84).

Conclusion

Resolution of symptoms after physical therapy treatment for internal impingement was related to correction of posterior shoulder tightness but not correction of GIRD.

 
 
 
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