Hemicallotasis for correction of varus deformity of the proximal tibia using a unilateral external fixator.

BACKGROUND: Gradual correction of varus deformity of the proximal tibia is generally accepted and produces good results. However, most studies have used circular external fixators, which are complex and cause patient discomfort. This study was undertaken to determine the efficacy of hemicallotasis with a unilateral external fixator for correction of varus deformity of the proximal tibia. METHODS: Thirteen patients (21 legs, 8 bilateral) were included in this study: 6 with constitutional bowing, 3 with a malunion, 2 with Blount's disease, and 2 with Turner syndrome. There were 7 males and 6 females of mean age 21 years (range 13-40). With an oblique osteotomy on the proximal tibia, a unilateral external fixator was placed on the medial side. Using a distraction of 1 mm/day, the external fixator was removed after consolidation of the callus. RESULTS: Surgery corrected medial proximal tibia angle from a preoperative average of 75.1° (64°-81°) to 88.6° (86°-90°) at final follow-up. Average tibiofemoral angle improved from -7° to 6.8°. The duration of external fixation averaged 101.3 days and the external fixation index was 70 days/cm. No patient had a limited ambulation, and all recovered preoperative range of knee motion (mean 130.1°) at final follow-up. Seven minor complications (pin tract infection, clamp loosening) and 1 major complication (uncorrected genu procurvatum) were observed. CONCLUSIONS: Hemicallotasis using a unilateral external fixator was found to be a safe and simple corrective procedure for varus deformity of the proximal tibia, with few complications.

Ultrasonographic evaluation of the shoulder in elite wheelchair tennis players.

CONTEXT: Wheelchair tennis has been identified as a high-risk sport for shoulder injury, so understanding shoulder pathology in these athletes is important. OBJECTIVE: This study investigated the incidence and pattern of shoulder injuries in wheelchair tennis players using high-resolution ultrasonography. DESIGN: Descriptive study. SETTING: International Wheelchair Tennis Open. PARTICIPANTS: 33 elite-level wheelchair tennis players. OUTCOME MEASURES: Wheelchair tennis players completed a self-administered questionnaire, and shoulders of each athlete were investigated using high-resolution ultrasonography (linear probe 7.5 MHz). RESULTS: The most common pathology in the dominant shoulder was acromioclavicular pathology, in 21 players (63.6%). Full-thickness rotator-cuff tears involving the supraspinatus were found in 8 dominant shoulders and 6 nondominant shoulders. There were no correlations between identified shoulder pathology and the different variables studied, such as age, training time per day, length of wheelchair use, and length of career as a wheelchair tennis player. CONCLUSION: High prevalence of rotator-cuff and acromioclavicular pathology was found by ultrasonographic examination in the elite wheelchair tennis players in both dominant and nondominant shoulders. A high index of suspicion of these pathologies in wheelchair athletes is required.

Downregulation of lipopolysaccharide response in Drosophila by negative crosstalk between the AP1 and NF-kappaB signaling modules.

IkappaB kinase (IKK) and Jun N-terminal kinase (Jnk) signaling modules are important in the synthesis of immune effector molecules during innate immune responses against lipopolysaccharide and peptidoglycan. However, the regulatory mechanisms required for specificity and termination of these immune responses are unclear. We show here that crosstalk occurred between the drosophila Jnk and IKK pathways, which led to downregulation of each other's activity. The inhibitory action of Jnk was mediated by binding of drosophila activator protein 1 (AP1) to promoters activated by the transcription factor NF-kappaB. This binding led to recruitment of the histone deacetylase dHDAC1 to the promoter of the gene encoding the antibacterial protein Attacin-A and to local modification of histone acetylation content. Thus, AP1 acts as a repressor by recruiting the deacetylase complex to terminate activation of a group of NF-kappaB target genes.