Citations

Purpose: To identify and compare magnetic resonance imaging (MRI) characteristics, with and without intravenous contrast medium, of cavernous synovial hemangiomas and cystic synovial hyperplasia. Material and Methods: Four cases of cavernous synovial hemangioma and five of cystic synovial hyperplasia of the knee were studied retrospectively. The patients (5 F and 4 M; 15–25 years of age) all had long-standing knee pain. At clinical examination we observed elastic swelling and pain without significant joint effusion. The patients underwent conventional radiography and MRI without and following intravenous contrast medium before arthroscopic biopsy. Results: The radiographs were interpreted as negative in all patients. MRI examination without contrast medium revealed a similar multicystic appearance for both lesions. Following intravenous contrast agent administration, cavernous synovial hemangiomas demonstrated avid, rather homogenous enhancement, whereas cystic synovial hyperplasia demonstrated less intense, peripheral enhancement only. Arthroscopy with histological examination of the lesions confirmed the MRI diagnosis in every case. Conclusion: In our experience, cavernous synovial hemangioma and cystic synovial hyperplasia have a similar appearance on unenhanced MRI, but can be reliably differentiated on the basis of enhancement characteristics following intravenous contrast administration.

Abstract Human long DNA in stool may reflect nonapoptotic exfoliation and has been used as a colorectal cancer (CRC) marker. Targeting human-specific Alu repeats represents a logical but untested approach. A real-time Alu PCR assay was developed for quantifying long human DNA in stool and evaluated in this study. The accuracy and reproducibility of this assay and the stability of long DNA during room temperature fecal storage were assessed using selected patient stools and stools added to human DNA. Thereafter, long DNA levels were determined in blinded fashion from 18 CRC patients and 20 colonoscopically normal controls. Reproducibility of real-time Alu PCR for quantifying fecal long DNA was high (r2 = 0.99; P < 0.01). Long DNA levels in nonbuffered stools stored at room temperature fell a median of 75% by 1 day and 81% by 3 days. An EDTA buffer preserved DNA integrity during such storage. Human long DNA was quantifiable in all stools but was significantly higher in stools from CRC patients than from normal controls (P < 0.05). At a specificity of 100%, the sensitivity of long DNA for CRC was 44%. Results indicate that real-time Alu PCR is a simple method to sensitively quantify long human DNA in stool. This study shows that not all CRCs are associated with increased fecal levels of long DNA. Long DNA degrades with fecal storage, and measures to stabilize this analyte must be considered for optimal use of this marker. (Cancer Epidemiol Biomarkers Prev 2006;15(6):1115–9)

AbstractWe explore the controversial issue of the role of eosinophils in host defense against helminthic parasites using the established Schistosoma mansoni infection model in 2 novel mouse models of eosinophil lineage ablation (ΔdblGATA and TgPHIL). No eosinophils were detected in bone marrow of infected ΔdblGATA or TgPHIL mice, despite the fact that serum IL-5 levels in these infected mice exceeded those in infected wild type by approximately 4-fold. Liver granulomata from infected ΔdblGATA and TgPHIL mice were likewise depleted of eosinophils compared with those from their respective wild types. No eosinophil-dependent differences in granuloma number, size, or fibrosis were detected at weeks 8 or 12 of infection, and differential accumulation of mast cells was observed among the ΔdblGATA mice only at week 12. Likewise, serum levels of liver transaminases, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) increased in all mice in response to S mansoni infection, with no eosinophil-dependent differences in hepatocellular damage observed. Finally, eosinophil ablation had no effect on worm burden or on egg deposition. Overall, our data indicate that eosinophil ablation has no impact on traditional measures of disease in the S mansoni infection model in mice. However, eosinophils may have unexplored immunomodulatory contributions to this disease process.

For fusion to occur the repulsive forces between two interacting phospholipid bilayers must be reduced. In model systems, this can be achieved by increasing the surface tension of at least one of the membranes. However, there has so far been no evidence that the secretory granule membrane is under tension. We have been studying exocytosis by using the patch-clamp technique to measure the surface area of the plasma membrane of degranulating mast cells. When a secretory granule fuses with the plasma membrane there is a step increase in the cell surface area. Some fusion events are reversible, in which case we have found that the backstep is larger than the initial step, indicating that there is a net decrease in the area of the plasma membrane. The decrease has the following properties: (i) the magnitude is strongly dependent on the lifetime of the fusion event and can be extensive, representing as much as 40% of the initial granule surface area; (ii) the rate of decrease is independent of granule size; and (iii) the decrease is not dependent on swelling of the secretory granule matrix. We conclude that the granule membrane is under tension and that this tension causes a net transfer of membrane from the plasma membrane to the secretory granule, while they are connected by the fusion pore. The high membrane tension in the secretory granule may be the critical stress necessary for bringing about exocytotic fusion.

"Snapshot" images of localized Ca2+ influx into patch-clamped chromaffin cells were captured by using a recently developed pulsed-laser imaging system. Transient opening of voltage-sensitive Ca2+ channels gave rise to localized elevations of Ca2+ that had the appearance of either "hotspots" or partial rings found immediately beneath the plasma membrane. When the Ca2+ imaging technique was employed in conjunction with flame-etched carbon-fiber electrodes to spatially map the release sites of catecholamines, it was observed that the sites of Ca2+ entry and catecholamine release were colocalized. These results provide functional support for the idea that secretion occurs from "active zone"-like structures in neuroendocrine cells.

Abstract Skeletal unloading decreases bone formation and osteoblast number in vivo and decreases the number and proliferation of bone marrow osteoprogenitor (BMOp) cells in vitro. We tested the ability of parathyroid hormone (PTH) to stimulate BMOp cells in vivo by treating Sprague Dawley rats (n = 32) with intermittent PTH(1–34) (1 h/day at 8 μ g/100 g of body weight), or with vehicle via osmotic minipumps during 7 days of normal weight bearing or hind limb unloading. Marrow cells were flushed from the femur and cultured at the same initial density for up to 21 days. PTH treatment of normally loaded rats caused a 2.5-fold increase in the number of BMOp cells, with similar increases in alkaline phosphatase (ALP) activity and mineralization, compared with cultures from vehicle-treated rats. PTH treatment of hind limb unloaded rats failed to stimulate BMOp cell number, ALP activity, or mineralization. Hind limb unloading had no significant effect on PTH receptor mRNA or protein levels in the tibia. Direct in vitro PTH challenge of BMOp cells isolated from normally loaded bone failed to stimulate their proliferation and inhibited their differentiation, suggesting that the in vivo anabolic effect of intermittent PTH on BMOp cells was mediated indirectly by a PTH-induced factor. We hypothesize that this factor is insulin-like growth factor-I (IGF-I), which stimulated the in vitro proliferation and differentiation of BMOp cells isolated from normally loaded bone, but not from unloaded bone. These results suggest that IGF-I mediates the ability of PTH to stimulate BMOp cell proliferation in normally loaded bone, and that BMOp cells in unloaded bone are resistant to the anabolic effect of intermittent PTH therapy due to their resistance to IGF-I.