Interbody Fusion in Low Grade Lumbar Spondylolsithesis: Clinical Outcome Does Not Correalte with Slip Reduction and Neural Foraminal Dimension

Study DesignProspective nonrandomized study.PurposeTo find a possible correlation between clinical outcome and extent of lumbar spondylolisthesis reduction.Overview of LiteratureThere is no consensus in the literature concerning whether a beneficial effect of reduction on outcome can be expected following reduction and surgical fusion for low grade lumbar spondylolisthesis.MethodsForty six patients with a mean age of 37.5 years (age, 17–48 years) with isthmic spondylolisthesis underwent interbody fusion with cages with posterior instrumentation (TLIF). Clinical outcome was measured using visual analogue score (VAS) and Oswestry disability index (ODI). Foraminal dimensions and disc heights were measured in standard digital radiographs. These were analyzed at baseline and 1 year after surgery and changes were compared. Radiographic fusion was judged with computed tomography scans at 1 year.ResultsNinety percent of the patients had good or very good clinical results with fusion and instrumentation. Baseline and one-year postoperative mean VAS score was 6.33 (range, 5–8) and 0.76 (range, 0–3), respectively (p=0.004). Baseline and one-year postoperative, mean ODI score was 48 (range, 32–62) and 10 (range, 6–16), respectively (p<0.001). A mean spondylolisthesis slip of 32.1% was reduced to 6.7% at 1 year. Average anterior disc height, posterior disc height, vertical foraminal dimension), and foraminal) diameter improved from 9.8 to 11.7 mm (p=0.005), 4.5 to 5.8 mm (p=0.004), 11.3 to 12.6 mm (p=0.002), and 18.6 to 20.0 mm (p<0.001), respectively. The fusion rate was 75% with TLIF. There is no significant correlation between the improvements of ODI scores and the extent of slip reduction.ConclusionsNeural decompression and interbody fusion can significantly improve pain and disability but the clinical outcome does not correlate with radiological improvement in the neural foraminal dimension

Characterization of Yeast Extracellular Vesicles: Evidence for the Participation of Different Pathways of Cellular Traffic in Vesicle Biogenesis

Background: Extracellular vesicles in yeast cells are involved in the molecular traffic across the cell wall. In yeast pathogens, these vesicles have been implicated in the transport of proteins, lipids, polysaccharide and pigments to the extracellular space. Cellular pathways required for the biogenesis of yeast extracellular vesicles are largely unknown. Methodology/Principal Findings: We characterized extracellular vesicle production in wild type (WT) and mutant strains of the model yeast Saccharomyces cerevisiae using transmission electron microscopy in combination with light scattering analysis, lipid extraction and proteomics. WT cells and mutants with defective expression of Sec4p, a secretory vesicleassociated Rab GTPase essential for Golgi-derived exocytosis, or Snf7p, which is involved in multivesicular body (MVB) formation, were analyzed in parallel. Bilayered vesicles with diameters at the 100–300 nm range were found in extracellular fractions from yeast cultures. Proteomic analysis of vesicular fractions from the cells aforementioned and additional mutants with defects in conventional secretion pathways (sec1-1, fusion of Golgi-derived exocytic vesicles with the plasm

The RNA polymerase-binding protein RbpA confers basal levels of rifampicin resistance on Streptomyces coelicolor

RbpA is an RNA polymerase-binding protein that occurs in the actinomycete family of bacteria and is regulated by the disulphide stress-response sigma factor, sigma(R), in Streptomyces coelicolor. Here we demonstrate that rbpA null mutants exhibit a slow-growth phenotype and are particularly sensitive to the transcription inhibitor rifampicin. Strikingly, transcription mapping experiments revealed that rbpA expression is induced upon exposure of S. coelicolor to rifampicin and that this, in part, involves an increase in the activity of sigma(R). In contrast, the ribosomal RNA operon promoter rrnDp3, which is recognized by the vegetative sigma factor sigma(HrdB), was strongly inhibited by rifampicin. Reconstitution of RNAP from an rbpA null mutant with purified RbpA revealed that RbpA stimulates transcription from rrnDp3, even in the presence of rifampicin. The data presented suggest that RbpA confers basal levels of rifampicin resistance and is a novel regulator of rRNA synthesis in S. coelicolor

Evolutionary Divergence of an Elongation Factor 3 from Cryptococcus neoformans

Elongation factor 3 (EF3) is considered a promising drug target for the control of fungal diseases because of its requirement for protein synthesis and survival of fungi and a lack of EF3 in the mammalian host. However, EF3 has been characterized only in ascomycete yeast. In order to understand the role of EF3 in a basidiomycete yeast, we cloned the gene encoding EF3 from Cryptococcus neoformans (CnEF3), an important fungal pathogen in immunocompromised patients, including those infected with human immunodeficiency virus. CnEF3 was found to encode a 1,055-amino-acid protein and has 44% identity with EF3 from Saccharomyces cerevisiae (YEF3). Expressed CnEF3 exhibited ATPase activity that was only modestly stimulated by ribosomes from S. cerevisiae. In contrast, CnEF3 showed tight binding to cryptococcal ribosomes, as shown by an inability to be removed under conditions which successfully remove Saccharomyces EF3 from ribosomes (0.5 M KCl or 2 M LiCl). CnEF3 also poorly complemented a YEF3 defect in a diploid null mutant and two temperature-sensitive mutants which have been shown previously to be complemented well by EF3 from other ascomycetes, such as Candida albicans. These data clearly identify the presence of a functioning EF3 in the basidiomycete yeast C. neoformans, which demonstrates an evolutionary divergence from EF3 of ascomycete yeast