Treatment of advanced metastatic lesions of the acetabulum using the saddle prosthesis.

Current methods of treating advanced patients with metastatic periacetabular disease are complex and result in high complication rates. The purpose of this study was to show whether the implantation of the saddle prosthesis would serve as an additional tool to help treat metastatic disease in these patients. From 1991 to 2003, 20 patients with advanced metastatic periacetabular lesions (Harrington Class III) were treated using the saddle prosthesis.

Mechanical environment affects allograft incorporation.

In a bilateral canine tibial model, the mechanical, radiologic, and histologic characteristics of intercalary allografts stabilized with locked intramedullary nails were compared with those of allografts fixed with compression plates. Both methods of fixation achieved healing to host bone. Tibiae that were plated had more callus with statistically greater mean torsional rigidity and strength than those treated with nails (paired t-test, p View Article and Find Full Text PDF

Missense mutations in the beta-myosin heavy-chain gene cause central core disease in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an important cause of sudden death in apparently healthy young individuals. In less than half of kindreds with HCM, the disease is linked to the beta-myosin heavy-chain gene locus (MYH7). We have recently described two missense MYH7 gene mutations [Arg-403 to Gln (R403Q) and Leu-908 to Val (L908V)] and found that the mutant message is present in skeletal muscle soleus) and that the mutant beta-myosin obtained from soleus muscle has abnormal in vitro motility activity.

Differences in clinical expression of hypertrophic cardiomyopathy associated with two distinct mutations in the beta-myosin heavy chain gene. A 908Leu----Val mutation and a 403Arg----Gln mutation.

Background: The disease gene for hypertrophic cardiomyopathy (HCM) has been identified as the beta-myosin heavy chain (beta-MHC) gene in some HCM families. We describe extensive clinical evaluations in two kindreds with two distinct point mutations in the beta-MHC gene.

Methods And Results: We used single-strand confirmation polymorphism (SSCP) gel analysis of polymerase chain reaction-amplified products capturing each of the 40 beta-MHC gene exons to identify distinct missense mutations in two HCM kindreds.

Xenopus transcription factor IIIA. Evidence for heterogeneity of Zn2+ binding affinities and specific labeling of cysteine 287.

The release of Zn2+ from transcription factor IIIA (TFIIIA) was examined with the metallochromic indicator 4-(2-pyridylazo)resorcinol (PAR) in the absence and presence of p-hydroxymercuriphenylsulfonate (PMPS). With 0.5 mM PAR, approximately 5 eq of Zn2+ were released from TFIIIA, but no Zn2+ release was detected from the 7 S ribonucleoprotein.