In vivo detection of the lumbar intraforaminal ligaments by MRI

Purpose

Intraforaminal ligaments (IFL) are of great interest to anatomists and clinicians to fully understand the detailed anatomy of the neuroforamina and to diagnose unclear radicular symptoms. Studies published until now have described radiological imaging of the IFLs using magnetic resonance imaging (MRI) on donor bodies. In the present study, we investigated the detectability of lumbar IFLs in vivo in adults using the high spatial resolution of the constructive interference in steady state (CISS) sequence.

Methods

A total of 14 patients were studied using a 1.5 T MRI scanner. The lumbar spine was imaged using the parasagittal CISS sequence, and the detectability of the IFLs was assessed for each lumbar level. All image datasets were analyzed by a radiologist, an orthopedic surgeon, and an anatomist. Interrater reliability was expressed as Fleiss’ Kappa. Using a single data set, a three-dimensional (3D) model was created to map the location of the IFLs within the intervertebral foramen (IF) and the immediate surrounding vessels.

Results

Overall, the radiologist was able to detect IFLs in 60% of all imaged IFs, the orthopedic surgeon in 62%, and the anatomist in 66%. Fleiss’ Kappa for the various segments varies from 0.71 for L4/5 up to 0.90 for L3/4.

Conclusion

Lumbar IFLs were successfully detected in vivo in every patient. The detection frequency varied from 42–86% per IF. We demonstrated reproducible imaging of the IFLs on MRI, with good interrater reliability. The present study was a launching point for further clinical studies investigating the potential impact of altered IFLs on radicular pain.

     

Nucleotide sequence homology at the 3'' termini of RNA from vesicular stomatitis virus and its defective interfering particles.

Vesicular stomatitis virus (VSV) and defective interfering (DI) particle RNAs were labeled at their 3' ends by using RNA ligase and cytidine 3',5'-bis[32P]phosphate. The RNAs were subjected to partial digestion with alkali and analyzed by oligonucleotide fingerprinting in two dimensions. VSV and DI particle RNAs have complete sequence homology for the first eight bases from the 3' end. The following four positions contain three mismatched nucleotides in which guanosine residues in one strand are replaced by uridine residues in the other. There is again complete homology for the next five bases (positions 13-17). The locations of purine residues within the sequence were confirmed by partial digestion with RNase T1 and RNase U2 and separation by size on 20% acrylamide gels. The latter method also indicated that sequences of VSV and DI particle RNAs diverge beyond the 18th nucleotide from the 3' termini.     

Menetrier’s disease

Opinion statement Menetrier’s disease is a rare acquired disorder of the fundus and body of the stomach (ie, oxyntic mucosa) characterized by giant hyperplastic folds, protein-losing gastropathy, hypoalbuminemia, increased mucus secretion, and hypochlorhydria. Recent research implicates overproduction of transforming growth factor-α with increased signaling of the epidermal growth factor receptor (EGFR) in the pathogenesis. Activation of the EGFR, a transmembrane receptor with tyrosine kinase activity, triggers a cascade of downstream, intracellular signaling pathways that leads to expansion of the proliferative compartment within the isthmus of the oxyntic gland. The diagnosis of Menetrier’s disease is based upon characteristic histologic changes, including foveolar hyperplasia, cystic dilation of pits, and reduced numbers of parietal and chief cells. The best treatment for Menetrier’s disease is not clear. It seems reasonable to test and treat for cytomegalovirus and Helicobacter pylori, as 1) in children, evidence exists that the disease may be due to cytomegalovirus infection in up to one third of patients; and 2) in adults, there are anecdotal reports of resolution upon H. pylori eradication. More recently, therapies targeting increased signaling of the EGFR have shown promise, including somatostatin analogues and monoclonal antibodies (eg, cetuximab) directed against the EGFR. In refractory cases, gastrectomy is curative.     

3D engineered heart tissue for replacement therapy

Myocardial infarction results in irreversible loss of cardiac myocytes and heart failure. Tissue or cell grafting offers the prospect of reintroducing contractile elements into impaired hearts. However, implanted cardiac myocytes remain physically and electrically isolated from the viable myocardium. Accordingly, the proof of increased contractile function attributable specifically to cell grafting procedures is sparse. Over the last few years, we have developed a new method to generate three-dimensional engineered heart tissue (EHTs) in vitro from embryonic chick or neonatal rat cardiac myocytes. EHTs comprise functional and morphological properties of intact myocardium. We hypothesized that EHTs, preformed in vitro into suitable geometric forms, represent appropriate graft material for in vivo tissue repair with advantages over isolated cells. Herein we describe initial results from implantation experiments of EHTs in the peritoneum of Fisher 344 rats. EHTs survived for at least 14 days, maintained a network of differentiated cardiac myocytes, and were strongly vascularized. Thus, the present study provides the first evidence for the general feasibility of EHTs as material for a novel tissue replacement approach.     

Back to the Future with Phenotypic Screening

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