Perioperative complications of anterior cervical decompression with fusion in patients with ossification of the posterior longitudinal ligament: a retrospective, multi-institutional study

BackgroundAnterior decompression with fusion (ADF) for patients with cervical ossification of the posterior longitudinal ligament (OPLL) is reportedly associated with a higher incidence of complications than is laminoplasty. However, the frequency of perioperative complications associated with ADF for cervical OPLL has not been fully established. The purpose of this study was to investigate the incidence of perioperative complications, especially neurological complications, following ADF performed to relieve compressive cervical myelopathy due to cervical OPLL.MethodsStudy participants comprised 150 patients who had undergone ADF for cervical OPLL at 27 institutions between 2005 and 2008. Perioperative—especially neurological—complications occurring within 2 weeks after ADF were analyzed. Preoperative imaging findings, including Cobb angle, between C2 and C7 and occupying ratio of OPLL were investigated. Multivariate analysis with logistic regression was performed to identify independent risk factors for neurological complications.ResultThree patients (2.0 %) showed deterioration of lower-extremity function after ADF. One of the three patients had not regained their preoperative level of function 6 months after surgery. Upper-extremity paresis occurred in 20 patients (13.3 %), five of whom had not returned to preoperative levels 6 months after surgery. Patients with upper-extremity paresis showed significantly higher occupying ratios of OPLL, greater blood loss, longer operation times, fusion of more segments, and higher rates of cerebrospinal fluid leakage than those without paresis. Independent risk factors for upper-extremity paresis were a high occupying ratio of OPLL and large blood loss during surgery.ConclusionsThe incidences of deterioration in upper- and lower-extremity functions were 13.3 % and 2.0 %, respectively. Patients with a high occupying ratio of OPLL are at higher risk of developing neurological deterioration.     

Trimebutine maleate has inhibitory effects on the voltage-dependent Ca2+ inward current and other membrane currents in intestinal smooth muscle cells

We examined effects of trimebutine maleate on the membrane currents of the intestinal smooth muscle cells by using the tight-seal whole cell clamp technique. Trimebutine suppressed the Ba2+ inward current through voltage-dependent Ca2+ channels in a dose-dependent manner. The inhibitory effect of trimebutine on the Ba2+ inward current was not use-dependent. It shifted the steady-state inactivation curve to the left along the voltage axis. Trimebutine also had inhibitory effects on the other membrane currents of the cells, such as the voltage-dependent K+ current, the Ca2(+)-activated oscillating K+ current and the acetylcholine-induced inward current. These relatively non-specific inhibitory effects of trimebutine on the membrane currents may explain, at least in part, the dual actions of the drug on the intestinal smooth muscle contractility, i.e. inhibitory as well as excitatory.     

Both estrogen and raloxifene cause G1 arrest of vascular smooth muscle cells

The proliferation of vascular smooth muscle cells (VSMC) is a crucial pathophysiological process in the development of atherosclerosis. Although estrogen is known to inhibit the proliferation of VSMC, the mechanism responsible for this effect remains to be elucidated. In addition, the effect of raloxifene on VSMC remains unknown. We have shown here that 17beta-estradiol (E(2)) and raloxifene significantly inhibited the platelet-derived growth factor (PDGF)-stimulated proliferation of cultured human VSMC. Flow cytometry demonstrated that PDGF-stimulated S-phase progression of the cell cycle in VSMC was also suppressed by E(2) or raloxifene. We found that PDGF-induced phosphorylation of retinoblastoma protein (pRb), whose hyperphosphorylation is a hallmark of the G1-S transition in the cell cycle, was significantly inhibited by E(2) and raloxifene. These effects were associated with a decrease in cyclin D1 expression, without a change in cyclin-dependent kinase 4 or cyclin-dependent kinase inhibitor, p27(kip1) expression. ICI 182,780 abolished the inhibitory effects of E(2) and raloxifene on PDGF-induced pRb phosphorylation. Next, we examined which estrogen receptor (ER) is necessary for these effects of E(2) and raloxifene. Since VSMC express both ERalpha and ERbeta, A10, a rat aortic smooth muscle cell line that expresses ERbeta but not ERalpha, was used. The dose-dependent stimulation of A10 cell proliferation by PDGF was not inhibited by E(2) or raloxifene in contrast to the results obtained in VSMC. Moreover, E(2) and raloxifene significantly inhibited the PDGF-induced cyclin D1 promoter activity in A10 cells transfected with cDNA for ERalpha but not in the parental cells. These results suggested that E(2) and raloxifene exert an antiproliferative effect in VSMC treated with PDGF, at least in part through inhibition of pRb phosphorylation, and that the inhibitory effects of E(2) and raloxifene may be mainly mediated by ERalpha.     

High concentration of glucose decreases glucose transporter-1 expression in mouse placenta in vitro and in vivo

Facilitative glucose transporter-1 (GLUT1) is expressed abundantly and has an important role in glucose transfer in placentas. However, little is known about the regulation of GLUT1 expression in placental cells. We studied the changes in placental GLUT1 levels in relation to changes in glucose concentration in vitro and in vivo. In in vitro experiments, dispersed mouse placental cells were incubated under control (5.5 mM) and moderately high (22 mM) glucose concentrations, and 2-deoxyglucose uptake into cells was studied on days 1-5 of culture. After 4 days of incubation under both conditions, GLUT1 mRNA and proten levels were examined by Northern and immunoblot analyses. Treatment of cells with 22 mM glucose resulted in a significant decrease in 2-deoxyglucose uptake compared with control, from day 2 to day 5 of culture. Moreover, GLUT1 mRNA and protein levels on day 4 of culture were significantly reduced in cells incubated with 22 mM glucose compared with control. Next, we rendered mice diabetic by administering 200 micrograms/g body weight streptozotocin (STZ) on day 8 of pregnancy. Animals were killed on day 12 of pregnancy and placental tissues were obtained. [3H]Cytochalasin B binding study was carried out to assess total GLUTs, and GLUT1 mRNA and protein were measured as above. [3H]Cytochalasin B binding sites in placentas from STZ-treated mice were significantly less than those in control mice. Northern and immunoblot analyses revealed a significant decrease in GLUT1 mRNA and protein levels in diabetic mice compared with the controls. These findings suggest that the glucose concentration may regulate the expression of placental GLUT1.