Nomogram predicting the efficacy of transurethral surgery in benign prostatic hyperplasia patients.

PURPOSE: This study aimed to develop and validate a nomogram for predicting the efficacy of transurethral surgery in benign prostatic hyperplasia (BPH) patients. METHODS: Patients with BPH who underwent transurethral surgery in the West China Hospital and West China Shang Jin Hospital were enrolled. Patients were retrospectively involved as the training group and were prospectively recruited as the validation group for the nomogram. Logistic regression analysis was utilized to generate nomogram for predicting the efficacy of transurethral surgery. The discrimination of the nomogram was assessed using the area under the receiver operating characteristic curve (AUC) and calibration plots were applied to evaluate the calibration of the nomogram. RESULTS: A total of 426 patients with BPH who underwent transurethral surgery were included in the study, and they were further divided into a training group (n = 245) and a validation group (n = 181). Age (OR 1.07, 95% CI 1.02-1.15, P < 0.01), the compliance of the bladder (OR 2.37, 95% CI 1.20-4.67, P < 0.01), the function of the detrusor (OR 5.92, 95% CI 2.10-16.6, P < 0.01), and the bladder outlet obstruction (OR 2.21, 95% CI 1.07-4.54, P < 0.01) were incorporated in the nomogram. The AUC of the nomogram was 0.825 in the training group, and 0.785 in the validation group, respectively. CONCLUSION: The nomogram we developed included age, the compliance of the bladder, the function of the detrusor, and the severity of bladder outlet obstruction. The discrimination and calibration of the nomogram were confirmed by internal and external validation.

Left Ventricular Outflow Tract Obstruction in Hypertrophic Cardiomyopathy: The Utility of Myocardial Strain Based on Cardiac MR Tissue Tracking.

BACKGROUND: Myocardial strain for assessment of hypertrophic cardiomyopathy (HCM) is of importance and may play a role in identifying obstruction in HCM patients. PURPOSE: To evaluate the utility of myocardial strain for detecting left ventricular (LV) outflow tract (LVOT) obstruction in HCM patients based on magnetic resonance tissue tracking. STUDY TYPE: Retrospective. POPULATION: In all, 44 adult HCM patients with LVOT obstruction and 108 adult HCM patients without LVOT obstruction. FIELD STRENGTH/SEQUENCE: 1.5 T; Steady-state free-precession cine sequence; phase-sensitive inversion-prepared segmented gradient echo sequence for late gadolinium enhancement (LGE) imaging. ASSESSMENT: Strain parameters including the local and global levels of LV myocardium and the subtraction (Sub) of myocardial strain variables between interventricular septal segments (IVSS) and noninterventricular septal segments (NIVSS) were measured for differentiating HCM with obstruction from nonobstruction. Average and maximum LV wall thickness (Average and Maximum LVWT) were also analyzed. STATISTICAL TESTS: Univariate and multivariate logistic regression analysis, area under the receiver operating characteristic (ROC) curve (AUC), intraclass correlation coefficient. RESULTS: In multivariate analysis, Average LVWT, Maximum LVWT, and the subtraction of radial peak strain (Sub Radial PS) between NIVSS and IVSS were independently associated with LVOT obstruction. The AUCs were 0.731, 0.840, and 0.890 for Average LVWT, Maximum LVWT, and Sub Radial PS, respectively. Sub Radial PS (cutoff value: 8.1%) demonstrated the highest sensitivity of 75.0% and a high specificity of 87.9% for identifying LVOT; Maximum LVWT (cutoff value: 22.9 mm) showed good sensitivity (72.7%) and specificity (83.3%). Combining Maximum LVWT >22.9 mm and Sub Radial PS > 8.1% achieved a better diagnostic performance (specificity 95.4%, sensitivity 70.5%). DATA CONCLUSION: Combining Maximum LVWT >22.9 mm and Sub Radial PS >8.1% holds promise for objectively evaluating LVOT obstruction in HCM patients with very high specificity and acceptable sensitivity. LEVEL OF EVIDENCE: 3 TECHNICAL EFFICACY STAGE: 2.

Autophagy protects end plate chondrocytes from intermittent cyclic mechanical tension induced calcification.

Calcification of end plate chondrocytes is a major cause of intervertebral disc (IVD) degeneration. However, the underlying molecular mechanism of end plate chondrocyte calcification is still unclear. The aim of this study was to clarify whether autophagy in end plate chondrocytes could protect the calcification of end plate chondrocytes. Previous studies showed that intermittent cyclic mechanical tension (ICMT) contributes to the calcification of end plate chondrocytes in vitro. While autophagy serves as a cell survival mechanism, the relationship of autophagy and induced end plate chondrocyte calcification by mechanical tension in vitro is unknown. Thus, we investigated autophagy, the expression of the autophagy genes, Beclin-1 and LC3, and rat end plate chondrocyte calcification by ICMT. The viability of end plate chondrocytes was examined using the LIVE/DEAD viability/cytotoxicity kit. The reverse transcription-polymerase chain reaction and western blotting were used to detect the expression of Beclin-1; LC3; type I, II and X collagen; aggrecan; and Sox-9 genes. Immunofluorescent and fluorescent microscopy showed decreased autophagy in the 10- and 20-day groups loaded with ICMT. Additionally, Alizarin red and alkaline phosphatase staining detected the palpable calcification of end plate chondrocytes after ICMT treatment. We found that increased autophagy induced by short-term ICMT treatment was accompanied by an insignificant calcification of end plate chondrocytes. To the contrary, the suppressive autophagy inhibited by long-term ICMT was accompanied by a more significant calcification. The process of calcification induced by ICMT was partially resisted by increased autophagy activity induced by rapamycin, implicating that autophagy may prevent end plate chondrocyte calcification.

[Autophagy expression and its significance in chondrocytes from a degenerate model of human cervical endplate].

OBJECTIVE: To explore the autophagy expression and examine its significance in chondrocytes in a degenerate model of human cervical vertebrae endplate. METHODS: Cartilage endplates were obtained from 48 hospitalized patients with cervical vertebral fracture or dislocation at our hospital between February 2012 to August 2012. They were divided into cervical spondylosis group with cervical spondylotic myelopathy (n = 31) and control group (n = 17).Endplate chondrocytes were isolated by enzyme digestion and cultured in vitro. The cells were stained with toluidine blue and hematoxylin and eosin; laser scanning confocal microscope and monodansylcadaverine (MDC) were used to observe autophagy in endplate chondrocytes; reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of typeIIcollagen and aggrecan and Western blot for the protein of LC3. RESULTS: A degenerative cell model of human cervical endplate chondrocytes was established successfully in vitro. Compared with the common group, the cellular morphologies of degenerative group showed spindle changes. Autophagic body was stained with MDC.Intracellular and perinuclear LC3 protein was detected by laser confocal microscopy. Compared with the control group, the mRNA expressions of aggrecan (0.715 ± 0.194) and typeII collagen (0.628 ± 0.254) markedly decreased (0.845 ± 0.186,0.913 ± 0.254, P < 0.05) and LC3-II/LC3-I declined in cervical spondylosis group. CONCLUSION: Autophagy plays an important pathogenic role in the process of human cervical disc degeneration. And regulating its expression may improve disc degeneration in endplate cartilage cells.

[Change of autophagy in endplate chondrocytes of rats during aging process].

OBJECTIVE: To explore the expression and significance of autophagy in endplate cartilage of rats during aging process. METHODS: The end-plate chondrocytes were isolated from 3, 6 and 12-month SD rats respectively. And the natural culture and rapamycin groups were assigned. Alizarin red staining was used to observe the morphological changes of cells. And RT-PCR was employed to detect the expressions of type II collagen, proteoglycan, SOX-9 and matrix metalloproteinase (MMP-13). The expressions of Beclin-I and LC3 were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The rate of autophagy was observed by monodansylcadaverine (MDC) staining and methyl thiazolyl tetrazolium (MTT) for cell survival rate. RESULTS: Alizarin red staining showed that cells might reflect the process of intervertebral disc degeneration. The expressions of polysaccharide, Sox-9, type II collagen, Beclin-1 and LC3 in endplate chondrocytes significantly decreased with advancing age (P < 0.05). The incidence of autophagy significantly decreased (P < 0.05). The cell viability of each group significantly decreased (P < 0.05). Compared with control group, the cell viability of rapamycin group significantly increased (P < 0.05). CONCLUSION: During aging process, the expressions of autophagy related-gene LC3 and Beclin-1 significantly decrease with the reduced activity of end-plate chondrocyte. And autophagy activity may be correlated with the development and degeneration of intervertebral disc.