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Lateral unicompartmental knee arthroplasty affords excellent functional results and implant survivorship for properly selected patients. More high-quality studies are necessary to determine whether expanded indications for medial unicompartmental knee arthroplasty also apply to lateral unicompartmental knee arthroplasty. Operative adjuncts such as robotics, custom implants, and navigation technology hold promise in minimizing the technical burden and unfamiliarity of lateral unicompartmental knee arthroplasty. Improvements in lateral-specific implants may translate to operational efficiency and improved outcomes, but few lateral-specific implants currently exist. Mobile-bearing devices have increased rates of failure due to bearing dislocation, and further studies are warranted to evaluate this complication with newer designs. Future registry and cohort studies should show medial unicompartmental knee arthroplasty and lateral unicompartmental knee arthroplasty separately to allow for better understanding of the nuances and technical differences between these uniquely different procedures.

Wear, instability, leg length, and muscle recovery are the major obstacles in total hip arthroplasty (THA). The direct anterior approach with fluoroscopic assistance has been proposed to address all four of these issues. The goal of this study was to assess the learning curve, safety, and accuracy of direct anterior THA. A retrospective review was completed on a single surgeon's initial consecutive series of 300 THAs performed via a direct anterior approach. Cases were grouped based on chronologic order (1-100, 101-200, 201-300). Operative time, fluoroscopy time, estimated blood loss, radiographic leg length discrepancy (LLD), radiographic cup abduction angle, and complications were recorded. Data were analyzed using an analysis of variance. Postoperatively, all patients were managed without dislocation precautions. The average age for the cohort was 58.9 years, and the average BMI was 29. All groups were similar with respect to age and BMI. Direct anterior THA demonstrated significant reductions inoperative and fluoroscopy after the first 100 cases. Mean surgery time was 132.8 minutes for group 1, 109.9 for group 2, and 106.1 for group 3 (P.001). Mean fluoroscopy time was 32.1 seconds for group 1, 14.5 for group 2, and 14.5 for group 3 (P.001). There was one dislocation in group 3 and three intraoperative calcar fractures in the first 100 cases. There were no infections. Direct anterior THA demonstrated a reduction in operative time and fluoroscopy time after the initial 100 cases. Calcar fracture did not occur after the first 62 cases. Cup abduction angle, dislocation rate, and LLD were excellent in all groups.

The behaviour of herpes simplex virus type 1 (HSV-1) strain 17 in tissue cultures of PC12 cells treated with nerve growth factor (NGF) was studied. PC12 cells respond to NGF by ceasing to proliferate and extending long neurites. After differentiation with NGF, cultures were infected with HSV-1 and maintained in the presence of the hormone for several weeks. These long-term infected cultures were tested for HSV DNA, transcripts and the ability to produce virus, before and after NGF removal. Before NGF removal, the cultures were characterized by little or no virus production and the presence of HSV-1 DNA in a predominantly endless form. In situ analysis of long-term infected cultures revealed latency-associated transcript expression in only a portion of the cells. However, as shown by an infectious centre assay, virus was present in almost all cells in the population. Moreover, removal of NGF from long-term cultures resulted in the appearance of significantly increased amounts of virus in the media. The degree to which this system resembles HSV latency in vivo is discussed.

A Herpes simplex virus type I (HSV-I) strain 17 mutant deleted between the Not l and Hpa l restriction sites of the latency associated transcript (LAT) region has been constructed. The mutant, therefore, contains a deletion of the putative LAT promoter and is called 17N/H. The 17N/H isolate established latent infections in mice nearly as efficiently as its wildtype parent. However, like other LAT null mutants, 17N/H reactivates from explanted ganglia with much slower kinetics than its LAT competent parent. In tissue culture, although 17N/H produces as much virus per cell as its strain 17 parent, it produces small plaques. The small plaque phenotype appears to be due to the inability of the virus to be released from the infected cell into the medium, following low but not high multiplicities of infection (m.o.i.). The mutant was also shown to produce an aberrant LAT homologous transcript of 1.1 kb as well as overproduce an approximately 29,000-Da HSV-specific polypeptide, which is barely detectable in wildtype infected cells. Rescuants of the 17N/H defect were constructed using a 10-kb restriction fragment containing viral sequences spanning the deletion, make large plaques, and have reactivation patterns and infected cell gene product profiles indistinguishable from the 17 parent. This shows that the phenotypes observed in 17N/H are reversed when the deletion, or at most sequences within 5 kb of each side of the deletion, is corrected. The possibilities that the defect in vital egress from infected cell, the small LAT homologous transcript, and the accumulation of the 29,000 Da polypeptide are related to the delayed reactivation kinetics are discussed.