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1.  Atypical Mycobacterial Exit-Site Infection and Peritonitis in Peritoneal Dialysis Patients on Prophylactic Exit-Site Gentamicin Cream 
We report 9 cases of exit-site infection and continuous ambulatory peritoneal dialysis peritonitis associated with atypical mycobacteria. All patients had been using topical gentamicin cream as prophylaxis for exit-site infection before the onset of these infections. Gentamicin cream is postulated to be a potential risk factor for atypical mycobacterial infection because of selective pressure on other micro-organisms. The microbiology of atypical mycobacteria and the treatment for atypical mycobacterial infections are discussed.
PMCID: PMC3649895  PMID: 23032088
Atypical mycobacterial infection; exit site; peritonitis
2.  Polymorphism at the TNF superfamily gene TNFSF4 confers susceptibility to systemic lupus erythematosus 
Nature genetics  2007;40(1):83-89.
Systemic lupus erythematosus (SLE) is a multisystem complex autoimmune disease of uncertain etiology (OMIM 152700). Over recent years a genetic component to SLE susceptibility has been established1–3. Recent successes with association studies in SLE have identified genes including IRF5 (refs. 4,5) and FCGR3B6. Two tumor necrosis factor (TNF) superfamily members located within intervals showing genetic linkage with SLE are TNFSF4 (also known as OX40L; 1q25), which is expressed on activated antigen-presenting cells (APCs)7,8 and vascular endothelial cells9, and also its unique receptor, TNFRSF4 (also known as OX40; 1p36), which is primarily expressed on activated CD4+ T cells10. TNFSF4 produces a potent co-stimulatory signal for activated CD4+ T cells after engagement of TNFRSF4 (ref. 11). Using both a family-based and a case-control study design, we show that the upstream region of TNFSF4 contains a single risk haplotype for SLE, which is correlated with increased expression of both cell-surface TNFSF4 and the TNFSF4 transcript. We hypothesize that increased expression of TNFSF4 predisposes to SLE either by quantitatively augmenting T cell–APC interaction or by influencing the functional consequences of T cell activation via TNFRSF4.
PMCID: PMC3705866  PMID: 18059267
3.  Natural history of multiple meningiomas 
Asymptomatic solitary meningiomas are typically managed with clinical and radiographic follow-up. Multiple meningiomas represents a clinical entity distinct from solitary meningiomas and can be sporadic, radiation-induced, associated with neurofibromatosis, or exhibit other familial inheritance. The growth rate for multiple meningiomas is not known and therefore management of these complicated patients can be difficult.
A retrospective chart review was performed on 12 patients with a total of 55 meningiomas. Patients with neurofibromatosis were not included. Serial enhanced magnetic resonance imaging was used to determine tumor growth rates. Treatment history was also reviewed and included for analysis.
Analysis of all 55 tumors demonstrated an average rate of growth of 0.46 cm3/year (range: −0.57-2.94 cm3/year). In the 23 tumors that received no treatment, the average rate of growth was 0.34 cm3/year (range: −0.03-1.8 cm3/year). Ten of the 23 tumors that received no treatment had no history of cranial irradiation. This group demonstrated a growth rate of 0.44 cm3/year (range: −0.01-1.8 cm3/year). Linear regression analysis did not yield any significant relationship between tumor burden and rates of growth.
Tumor growth rates in patients with multiple meningiomas did not appear to be higher than reported rates for incidentally found solitary meningiomas. As such, asymptomatic multiple meningioma patients should be managed with clinical and radiographic follow-up.
PMCID: PMC3683641  PMID: 23776757
Meningioma; multiple meningioma; natural history
4.  IRF5 haplotypes demonstrate diverse serological associations which predict serum interferon alpha activity and explain the majority of the genetic association with systemic lupus erythematosus 
Annals of the Rheumatic Diseases  2011;71(3):463-468.
High serum interferon α (IFNα) activity is a heritable risk factor for systemic lupus erythematosus (SLE). Auto-antibodies found in SLE form immune complexes which can stimulate IFNα production by activating endosomal Toll-like receptors and interferon regulatory factors (IRFs), including IRF5. Genetic variation in IRF5 is associated with SLE susceptibility; however, it is unclear how IRF5 functional genetic elements contribute to human disease.
1034 patients with SLE and 989 controls of European ancestry, 555 patients with SLE and 679 controls of African–American ancestry, and 73 patients with SLE of South African ancestry were genotyped at IRF5 polymorphisms, which define major haplotypes. Serum IFNα activity was measured using a functional assay.
In European ancestry subjects, anti-double-stranded DNA (dsDNA) and anti-Ro antibodies were each associated with different haplotypes characterised by a different combination of functional genetic elements (OR > 2.56, p >003C; 1.9×10−14 for both). These IRF5 haplotype-auto-antibody associations strongly predicted higher serum IFNα in patients with SLE and explained > 70% of the genetic risk of SLE due to IRF5. In African–American patients with SLE a similar relationship between serology and IFNα was observed, although the previously described European ancestry-risk haplotype was present at admixture proportions in African–American subjects and absent in African patients with SLE.
The authors define a novel risk haplotype of IRF5 that is associated with anti-dsDNA antibodies and show that risk of SLE due to IRF5 genotype is largely dependent upon particular auto-antibodies. This suggests that auto-antibodies are directly pathogenic in human SLE, resulting in increased IFNα in cooperation with particular combinations of IRF5 functional genetic elements.
SLE is a systemic autoimmune disorder affecting multiple organ systems including the skin, musculoskeletal, renal and haematopoietic systems. Humoral autoimmunity is a hallmark of SLE, and patients frequently have circulating auto-antibodies directed against dsDNA, as well as RNA binding proteins (RBP). Anti-RBP autoantibodies include antibodies which recognize Ro, La, Smith (anti-Sm), and ribonucleoprotein (anti-nRNP), collectively referred to as anti-retinol-binding protein). Anti-retinol-binding protein and anti-dsDNA auto-antibodies are rare in the healthy population.1 These auto-antibodies can be present in sera for years preceding the onset of clinical SLE illness2 and are likely pathogenic in SLE.34
PMCID: PMC3307526  PMID: 22088620
5.  Transtibial ACL reconstruction technique fails to position drill tunnels anatomically in vivo 3D CT study 
The purpose of this study was to visualize and quantify the positions of femoral and tibial tunnels in patients who underwent traditional transtibial single-bundle ACL reconstruction, as performed by multiple surgeons, utilizing 3D CT models, and to compare these positions to our previously reported anatomical tunnel positions.
Fifty-eight knee computed tomography (CT) scans were performed on patients who underwent primary or revision transtibial single-bundle ACL reconstruction, and three-dimensional reconstructions of the CT scans were aligned within an anatomical coordinate system. The position of femoral tunnel aperture centers was measured with (1) the quadrant method and (2) in the anatomic posterior-to-anterior and proximal-to-distal directions. The position of tibia tunnel aperture centers were measured similarly, in the anterior-to-posterior and medial-to-lateral dimensions on the tibial plateau. Comparisons were made to previously established anatomical tunnel positions, and data were presented as “mean value ± standard deviation (range).”
The location of tibial tunnels was at 48.0 ± 5.4% (35.6–59.5%) of the anterior-to-posterior plateau depth and at 47.9 ± 2.9% (42.2–57.4%) of the medial-to-lateral plateau width. The location of femoral tunnels was at 55.8 ± 8.0% (41.5–79.5%) in the anatomic posterior-to-anterior direction and at 41.2 ± 10.4% (15.1–67.4%) in the proximal-to-distal directions. Utilizing a quadrant method, femoral tunnels were positioned at 37.4 ± 5.1% (24.9–50.6%) from the proximal condylar surface, parallel to Blumensaat line, and at 11.0 ± 7.3% (−6.0–28.7%) from the notch roof, perpendicular to Blumensaat line. In summary, tibial tunnels were positioned medial to the anatomic PL position (p < 0.001), and femoral tunnels were positioned anterior to both AM and PL anatomic tunnel locations (p < 0.001 and p < 0.001).
ACL reconstruction via traditional transtibial technique fails to accurately position femoral and tibial tunnels within the native ACL insertion site. To achieve anatomical graft placement, other surgical techniques should be considered.
Level of evidence
Electronic supplementary material
The online version of this article (doi:10.1007/s00167-011-1851-z) contains supplementary material, which is available to authorized users.
PMCID: PMC3477486  PMID: 22210518
ACL; Anatomy; Transtibial; Anterior cruciate ligament; 3D CT
6.  Meniscus tear developed by pulling of the anomalous insertion of medial meniscus on anterior cruciate ligament 
There is no report regarding a medial meniscus tear arising from an anomalous insertion of medial meniscus on the ACL, which seemed to be developed by the same mechanism as ACL tear. A case of a combined medial meniscus tear with ACL tear in the presence of an anomalous insertion of the medial meniscus on the ACL is reported.
PMCID: PMC3176407  PMID: 21468619
Anomalous insertion of medial meniscus; Anterior cruciate ligament; Meniscus tear; Knee; Arthroscopy
7.  Genetic Variants Near TNFAIP3 on 6q23 are Associated with Systemic Lupus Erythematosus (SLE) 
Nature genetics  2008;40(9):1059-1061.
SLE is an autoimmune disease influenced by genetic and environmental components. We performed a genome-wide association scan (GWAS) and observed novel association evidence with a variant inTNFAIP3(rs5029939, P = 2.89×10−12, OR = 2.29). We also found evidence of two independent signals of association to SLE risk, including one described in Rheumatoid Arthritis. These results establish that genetic variation inTNFAIP3contributes to differential risk for SLE and RA.
PMCID: PMC2772171  PMID: 19165918

Results 1-7 (7)