BackgroundThe pathogenesis for colorectal cancer remains unresolved. A growing body of evidence suggests a direct correlation between cyclooxygenase enzyme expression, prostaglandin E2 metabolism and neoplastic development. Thus further understanding of the regulation of epithelial functions by prostaglandin E2 is needed. We hypothesized that patients with colonic neoplasia have altered colonic epithelial ion transport and express functionally different prostanoid receptor levels in this respect.MethodsPatients referred for colonoscopy were included and grouped into patients with and without colorectal neoplasia. Patients without endoscopic findings of neoplasia served as controls. Biopsy specimens were obtained from normally appearing mucosa in the sigmoid part of colon. Biopsies were mounted in miniaturized modified Ussing air-suction chambers. Indomethacin (10 μM), various stimulators and inhibitors of prostanoid receptors and ion transport were subsequently added to the chamber solutions. Electrogenic ion transport parameters (short circuit current and slope conductance) were recorded. Tissue pathology and tissue damage before and after experiments was assessed by histology.ResultsBaseline short circuit current and slope conductance did not differ between the two groups. Patients with neoplasia were significantly more sensitive to indomethacin with a decrease in short circuit current of 15.1 ± 2.6 μA·cm-2 compared to controls, who showed a decrease of 10.5 ± 2.1 μA·cm-2 (p = 0.027). Stimulation or inhibition with theophylline, ouabain, bumetanide, forskolin or the EP receptor agonists prostaglandin E2, butaprost, sulprostone and prostaglandin E1 (OH) did not differ significantly between the two groups. Histology was with normal findings in both groups.ConclusionsEpithelial electrogenic transport is more sensitive to indomethacin in normal colonic mucosa from patients with previous or present colorectal neoplasia compared to colonic mucosa from control patients. Stimulated epithelial electrogenic transport through individual prostanoid subtype receptors EP1, EP2, EP3, and EP4 is not significantly different between neoplasia diseased patients and controls. This indicates that increased indomethacin-sensitive mechanisms in colonic mucosa from neoplasia diseased patients are not related to differences in functional expression of EP receptor subtypes.
Objective Magnetic resonance imaging (MRI)-verified neural axis abnormalities (NAAs) have been described in adolescent idiopathic scoliosis (AIS), and several risk factors have been associated with the presence of NAAs in AIS patients. However, the clinical significance of these findings is unclear. The purpose of the present study was to determine the prevalence of NAAs in a large consecutive cohort of AIS patients and to evaluate the clinical significance of previously proposed risk factors. Methods We prospectively included AIS patients referred to a tertiary facility for evaluation. Full-spine MRI scans were performed on all included patients irrespective of curve magnitude or proposed treatment modality. MRI scans were prospectively analyzed by a neuroradiologist and the pathologic findings were confirmed by a second independent radiologist. Results NAA was observed in 34 of the 381 patients (8.9%): 32 patients had a syrinx, 1 patient had an arachnoid cyst, and 1 patient had a Chiari malformation. Four patients were referred for a neurosurgical evaluation but none received any neurosurgical treatment. No statistically significant difference was observed between the NAA and non-NAA groups in terms of sex, major curve size, thoracic kyphosis, left thoracic curve, curve convexity, curve progression, or level of pain (p>0.05). Conclusion In this prospective study examining the risk factors for NAA in AIS patients, we found that previously proposed risk factors could not predict the MRI outcomes. The finding of an NAA had no clinical implications and we do not support MRI scans as a routine diagnostic modality in all AIS patients.
Substitutes for bone grafts experience increasing popularity, but the need for defect-filling following simple curettage of benign bone lesions is controversial. In this study, we wish to objectively report the radiological changes following bone defect-filling using a composite ceramic bone graft substitute, as well as the clinical results and complications. We evaluated 35 surgically treated benign bone lesions with subsequent defect-filling using two variants of a composite ceramic bone graft substitute (CERAMENT|BONE VOID FILLER or CERAMENT|G, BONESUPPORT AB, SWEDEN). After one year, a normal cortical thickness surrounding the defect was seen in approximately 80% of patients. Inside the defect-cavity, an almost complete product-resorption was seen after one year. The most common complication was a post-operative inflammatory soft-tissue reaction, seen in 7 patients (20%), which resolved without further treatment, although short-term antibiotic treatment was initiated at a local hospital in 6 patients, due to suspected wound infection. In summary, cortical thickness most commonly normalizes after bone tumor removal and filling of the bone defect using this particular composite ceramic bone graft substitute. The ceramic substitute undergoes resorption, which causes progressive changes in the radiological appearance inside the bone defect.
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