Autofluorescence imaging and the quantitative intensity of fluorescence for evaluating the dysplastic grade of colonic neoplasms

Background and aims

Autofluorescence imaging (AFI) is a novel technology which can capture fluorescence emitted from intestinal tissues. While AFI is useful for detecting colorectal neoplasms, it is unclear whether AFI can facilitate the diagnosis by differentiating the extent of dysplasia of colorectal neoplasms. This study investigated the efficacy of AFI in discriminating high-grade from low-grade adenoma.

Materials and methods

Sixty-seven patients who underwent colonoscopy with AFI were enrolled in this study. The AFI images obtained from 158 lesions in these patients were visually classified into four categories, namely, green (G), green with magenta spots (GM), magenta with green spots (MG), and magenta (M), according to their color intensities, immediately after the examination. The AFI images of the lesions were quantified using an image-analytical software program (F index). Either the F index or the visual assessment was prospectively compared with the dysplastic grade.

Results

The F index of the high-grade adenomas was significantly lower than that of the low-grade adenomas, hyperplasia, and normal mucosa (p?Conclusions AFI, particularly the F index, is considered to be a useful procedure for estimating the dysplastic grade of colonic adenomas.     

Mechanisms underlying the modulation of L-type Ca2+ channel by hydrogen peroxide in guinea pig ventricular myocytes

Although Cav1.2 Ca²⁺ channels are modulated by reactive oxygen species (ROS), the underlying mechanisms are not fully understood. In this study, we investigated effects of hydrogen peroxide (H₂O₂) on the Ca²⁺ channel using a patch-clamp technique in guinea pig ventricular myocytes. Externally applied H₂O₂ (1 mM) increased Ca²⁺ channel activity in the cell-attached mode. A specific inhibitor of Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) KN-93 (10 μM) partially attenuated the H₂O₂-mediated facilitation of the channel, suggesting both CaMKII-dependent and -independent pathways. However, in the inside-out mode, 1 mM H₂O₂ increased channel activity in a KN-93-resistant manner. Since H₂O₂-pretreated calmodulin did not reproduce the H₂O₂ effect, the target of H₂O₂ was presumably assigned to the Ca²⁺ channel itself. A thiol-specific oxidizing agent mimicked and occluded the H₂O₂ effect. These results suggest that H₂O₂ facilitates the Ca²⁺ channel through oxidation of cysteine residue(s) in the channel as well as the CaMKII-dependent pathway.     

Pathophysiological analysis of nonalcoholic fatty liver disease by evaluation of fatty liver changes and blood flow using xenon computed tomography: can early-stage nonalcoholic steatohepatitis be distinguished from simple steatosis?

Introduction

Effective noninvasive tests that can distinguish early-stage nonalcoholic steatohepatitis (NASH) from simple steatosis (SS) have long been sought. Our aim was to determine the possibility of noninvasively distinguishing early-stage NASH from SS.

Materials and methods

We used Fick’s principle and the Kety–Schmidt equation to determine the hepatic tissue blood flow (TBF) in 65 NASH patients who underwent xenon computed tomography (Xe-CT). We calculated the lambda value (LV), i.e., Xe gas solubility coefficient, in liver and blood. We assessed the histological severity of fatty changes and fibrosis on the basis of Brunt’s classification. Liver biopsy revealed SS in 9 patients and NASH in 56 patients. NASH stages 1 and 2 were classified as early-stage NASH (Ea-NASH; 38 patients) and stages 3 and 4 as advanced-stage NASH (Ad-NASH; 18 patients). We evaluated the differences in LV and TBF among the 3 groups.

Results

LV was significantly lower in the Ad-NASH group than in the SS and Ea-NASH groups. Portal venous TBF (PVTBF) was significantly lower in the Ea-NASH group than in the SS group, and PVTBF was lower in the Ad-NASH group than in the Ea-NASH group. Total hepatic TBF (THTBF) was significantly different between the SS and Ea-NASH groups and between the SS and Ad-NASH groups.

Conclusions

In conclusion, measurements of TBF and LV are useful for evaluating the pathophysiological progression of NASH. In addition, these measurements can facilitate the differential diagnosis of SS and Ea-NASH, which may not be distinguishable by other means.     

Predisposing factors for surgical site infection of spinal instrumentation surgery for diabetes patients

Purpose

Diabetes mellitus (DM) is known as an important risk factor for surgical site infection (SSI) in spine surgery. It is still unclear however which DM-related parameters have stronger influence on SSI. The purpose of this study is to determine predisposing factors for SSI following spinal instrumentation surgery for patients with DM.

Methods

110 DM patients (66 males and 44 females) who underwent spinal instrumentation surgery in one institute were enrolled in this study. For each patient, various preoperative or intraoperative parameters were reviewed from medical records. Patients were divided into two groups (SSI or non-SSI) based on the postoperative course. Each parameter between these two groups was compared. Univariate and multivariate analyses were performed to determine predisposing factor for SSI.

Results

The SSI group consisted of 11 patients (10 %), and the non-SSI group of 99 patients (90 %). Univariate analysis revealed that preoperative proteinuria (p = 0.01), operation time (p = 0.04) and estimated blood loss (p = 0.02) were significantly higher in the SSI group compared to the non-SSI group. Multivariate logistic regression identified preoperative proteinuria as a statistically significant predictor of SSI (OR 6.28, 95 % CI 1.58–25.0, p = 0.009).

Conclusions

Proteinuria is a significant predisposing factor for SSI in spinal instrumentation surgery for DM patients. DM patients with proteinuria who are likely to suffer latent nephropathy have a potential risk for SSI. For them less invasive surgery is recommended for spinal instrumentation. In this retrospective study, there was no significant difference of preoperative condition in glycemic control between the two groups.     

The overexpression of SIRT1 inhibited osteoarthritic gene expression changes induced by interleukin‐1β in human chondrocytes

In this study, we examined the effects of overexpression of SIRT1 on IL‐1β‐induced gene expression changes in human chondrocytes to explore a protective role of SIRT1 in human chondrocytes. SIRT1 was overexpressed in human chondrocytes by expression plasmid under stimulation with IL‐1β. SIRT1 was also inhibited by siRNA under stimulation with IL‐1β. Gene expression changes were examined by real‐time PCR. The interaction of SIRT1 and p65 (NF‐κB) were examined by Western blotting. SIRT1, MMP‐13, and ADAMTS‐5 expressions in human cartilage were examined by immunohistochemistry. IL‐1β stimulation significantly up‐regulated MMP‐1, 2, 9, and 13 and ADAMTS‐5. Overexpression of SIRT1 significantly inhibited the up‐regulation of those genes caused by IL‐1β while the inhibition of SIRT1 further increased them. In addition, the overexpression of SIRT1 markedly reduced the IL‐1β‐induced acetylation of p65. SIRT1 expression was clearly detected in the non‐OA cartilage while MMP‐13 and ADAMTS‐5 were undetectable. In contrast, in the OA cartilage, SIRT1 expression was decreased while MMP‐13 and ADAMTS‐5 were increased. Our observations suggested that SIRT1 can play a protective role by suppressing IL‐1β‐induced expressions of cartilage‐degrading enzymes partially through the modulation of the NF‐κB pathway. SIRT1 overexpression might be a new therapeutic approach for OA. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 531–537, 2013