Prognostic value of changes in spinal cord signal intensity on magnetic resonance imaging in patients with cervical compressive myelopathy

Background contextSignal intensity on preoperative cervical magnetic resonance imaging (MRI) of the spinal cord has been shown to be a potential predictor of outcome of surgery for cervical compressive myelopathy. However, the prognostic value of such signal remains controversial. One reason for the controversy is the lack of proper quantitative methods to assess MRI signal intensity.PurposeTo quantify signal intensity and to correlate intramedullary signal changes on MRI T1- and T2-weighted images (WIs) with clinical outcome and prognosis.Study designRetrospective case study.Patient samplePatients (n=148; cervical spondylotic myelopathy, n=102 and ossified posterior longitudinal ligament, n=46) who underwent surgery for cervical compressive myelopathy and had high signal intensity change on sagittal T2-WI MRI before surgery between 2006 and 2010.Outcome measureNeurologic assessment was conducted with the Japanese Orthopedic Association (JOA) scoring system for cervical myelopathy. The rate of neurologic improvement was calculated with the use of preoperative and postoperative JOA scores.MethodsQuantitative analysis of MRI signal on both T1- and T2-WIs via use of the signal intensity ratio (SIR; signal intensity of lesion relative to that at C7-T1 disc level) was performed. Correlations between SIR on T1- and T2-WIs and preoperative JOA score, JOA improvement rate, disease duration, and MRI morphologic classification (cystic or diffuse type) were analyzed. Multivariate regression analysis for JOA improvement rate was also analyzed. In a substudy, 25 patients underwent follow-up MRI starting from 6 months after surgery to analyze the relationship between changes in SIR on follow-up MRI and clinical outcome.ResultsSIR on T1-WIs, but not SIR on T2-WIs, correlated with postoperative neurologic improvement. The disease duration correlated negatively with SIR on T1-WIs and JOA improvement rate but not with SIR on T2-WIs. SIR on T2-WIs of “cystic type” was significantly greater than of “diffuse type,” but SIR on T1-WI and JOA improvement rate were not different in the two types. Stepwise multivariate regression analysis indicated that SIR on T1-WIs and long disease duration were significant predictors of postoperative neurologic outcome. SIR on follow-up T1-WI and changes in SIR on T1-WI after surgery correlated positively with postoperative improvement rate. SIR on follow-up T2-WI and changes on T2-WI correlated negatively with postoperative neurologic improvement.ConclusionsOur results suggest that low intensity signal on preoperative T1-WIs but not T2-WIs correlated with poor postoperative neurologic outcome. Furthermore, decreased signal intensity on postoperative T1-WIs and increased signal intensity on postoperative T2-WIs are predictors of poor neurologic outcome.     

Suppression and acceleration of cell elongation by integration of xyloglucans in pea stem segments

Xyloglucan is a key polymer in the walls of growing plant cells. Using split pea stem segments and stem segments from which the epidermis had been peeled off, we demonstrate that the integration of xyloglucan mediated by the action of wall-bound xyloglucan endotransglycosylase suppressed cell elongation, whereas that of its fragment oligosaccharide accelerated it. Whole xyloglucan was incorporated into the cell wall and induced the rearrangement of cortical microtubules from transverse to longitudinal; in contrast, the oligosaccharide solubilized xyloglucan from the cell wall and maintained the microtubules in a transverse orientation. This paper proposes that xyloglucan metabolism controls the elongation of plant cells.     

Efficacy of combination therapy of interferon-α with ursodeoxycholic acid in chronic hepatitis C: A randomized controlled clinical trial

The efficacy of interferon- therapy in the treatment of chronic hepatitis C is still limited. A combination therapy of interferon- with ursodeoxycholic acid (UDCA) was tested for its efficacy in the treatment of chronic hepatitis C by a randomized controlled study. Eighty consecutive Japanese patients with chronic hepatitis C were randomly divided into two groups: one group was treated with interferon- (group A,n=40) and the other with a combination of interferon- and UDCA (group B,n=40). In both groups, human interferon- (6 million units per day) was intramuscularly injected daily for 2 weeks and then three times a week for 22 weeks: this 24-week period was followed by 24 weeks of observation. In group B, UDCA was also administered, daily at a dose of 600mg orally, from the beginning of the interferon therapy and administration was continued for 48 weeks. The rates for ALT normalization and clearance of hepatitis C virus (HCV) viremia at the end of the 24-week interferon therapy were similar for groups A and B (58% vs 60% and 55% vs 48%, respectively). At the end of the 24-week follow-up, the sustained normalization rates for ALT levels for the two groups were not different (35% vs 43%), while the rate of clearance was higher in group B (40%) than in group A (23%), but the difference was not significant (P=0.14). The sustained complete response, i.e., HCV RNA negativity at the end of the follow-up, as well as the maintenance of ALT normalization during the follow-up period, was more frequent in group B (38%) than in group A (18%) although the difference was not significantP=0.08). The rate of HCV reactivation after interferon was discontinued was significantly lower in group B (16%) than in group A (59%) (P<0.01). Although this combination therapy did not lead to a sufficiently sustained complete response, it could serve as adjuvant antiviral therapy when a suitable dosage and administration period are determined.     

Both a Calcium Antagonist and ACE Inhibitor Reverse Hypertrophy in Hypertension But a Calcium Antagonist also Depresses Contractility

The aim of this study was to compare the effects of a calcium antagonist, nicardipine SR, with an angiotensin-converting enzyme (ACE) inhibitor, alacepril, on the regression of left ventricular hypertrophy (LVH) and function. Twenty patients with LVH, aged 42–73 years, were treated with nicardipine SR or alacepril. Ten patients were treated with nicardipine SR (40–80 mg) for 21 months, and the other 10 patients were treated with alacepril (25–100 mg) for 18 months. All patients underwent echocardiography to assess left ventricular structure and function before and after the treatment. After nicardipine SR or alacepril treatment, blood pressure was decreased significantly from 176.0 ± 13.9/97.0 ± 5.3 mmHg to 140.0 ± 14.0/77.4 ± 7.2 mmHg and from 168.2 ± 22.3/99.0 ± 5.5 mmHg to 138.4 ± 12.5/85.2 ± 9.7 mmHg, respectively (both p < 0.01), whereas heart rate did not change (73.8 ± 14.6 beats/min vs. 69.9 ± 13.5 beats/min and 71.6 ± 9.7 vs. 65.8 ± 8.1 beats/min, respectively). The left ventricular mass index decreased significantly from 133.2 ± 11.7 g/m2 to 114.4 ± 15.7 g/m2 with nicardipine SR and from 137.1 ± 14.8 g/m2 to 99.3 ± 23.0 g/m2 with alacepril (both p < 0.01). The fractional shortening, peak shortening rate, and peak lengthening rate all improved significantly after each treatment. The end-systolic wall stress/left ventricular end-systolic volume index, as an index of left ventricular contractility, was decreased significantly after treatment with nicardipine SR but was not changed after treatment with alacepril. In conclusion, both nicardipine SR and alacepril similarly reduced LVH and improved left ventricular systolic and diastolic function. However, alacepril did not alter left ventricular contractility, whereas nicardi-pine SR decreased left ventricular contractility.     

Generation of transgenic mice with elevated blood pressure by introduction of the rat renin and angiotensinogen genes.

The role of the renin-angiotensin system in blood pressure control and in the development of hypertension was investigated by generating transgenic mice carrying the rat renin or angiotensinogen gene or both genes under the control of the mouse metallothionein I promoter. The systolic blood pressure was significantly elevated in transgenic mice carrying both transgenes but was maintained normally in those bearing either of the transgenes. The transgene was effectively and properly transcribed to form the mature mRNA in the transgenic mice. The production of rat renin and angiotensinogen in the transgenic mice carrying the corresponding transgene was also verified by immunoanalyses of these proteins. Furthermore, the specific angiotensin-converting enzyme inhibitor captopril was effective in reducing the elevated blood pressure of the hypertensive transgenic mice. These results indicate that the combined action of the exogenous rat renin and angiotensinogen is responsible and necessary for elevation of blood pressure in the hypertensive transgenic mice.