Age and multiparity related urethral sphincter muscle dysfunction in a rabbit model: Potential roles of TGF‐β and Wnt‐β catenin signaling pathways

2018 ◽  
Vol 38 (2) ◽  
pp. 607-614 ◽  
Author(s):  
Mahadevan R. Rajasekaran ◽  
Johnny Fu ◽  
My‐Uyen (Lilly) Nguyen ◽  
Yaozhi Wang ◽  
Michael Albo ◽  
...  
2018 ◽  
Vol 49 (6) ◽  
pp. 2304-2319 ◽  
Author(s):  
Zhenhui Lu ◽  
Qin Liu ◽  
Lei Liu ◽  
Huayu Wu ◽  
Li Zheng ◽  
...  

Background/Aims: 3, 4, 5-trihydroxy-N-{4-[(5-methylisoxazol-3-yl) sulfamoyl] phenyl} benzamide (JEZTC), synthesized from gallic acid (GA) and sulfamethoxazole (SMZ), was reported with chondroprotective effects. However, the effects of JEZTC on osteoarthritis (OA) are still unclear. The goal of this study was to investigate the anti-osteoarthritic properties of JEZTC on interleukin-1-beta (IL-1β) stimulated chondrocytes in vitro and a rabbit anterior cruciate ligament transaction (ACLT) OA model in vivo. Methods: Changes in matrix metalloproteinases (MMPs) and apoptosis genes (bax, caspase 3 and tnf-α) and OA-specific protein (MMP-1) expression in vitro and in vivo were detected by real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemistry. The production of reactive oxygen species (ROS) were investigated upon the treatment of JEZTC in chondrocytes processed with IL-1β in vitro and OA in vivo. Effect of JEZTC on OA was further studied by the macroscopic and histological evaluation and scores. The key proteins in signaling pathways inMAPK/P38, PI3KAkt and NF-κB also determined using western blot (WB) analysis. Results: JEZTC could significantly suppress the expression of MMPs and intracellular ROS, while meaningfully increase the gene expression of tissue inhibitor of metalloproteinase-1 (TIMP-1). Moreover, there was less cartilage degradation in JEZTC group compared with the phosphate-buffered saline (PBS) group in vivo. Results also indicated that JEZTC exerts effect on OA by regulating MAPKs and PI3K/Akt signaling pathways to activate NF-κB pathway, leading to the down-regulation of MMPs. The chondro-protective effect of JEZTC may be related with its ability to inhibit chondrocyte apoptosis by reduction of ROS production. Conclusion: JEZTC may be a possible therapeutic agent in the treatment of OA.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Yukinobu Ito ◽  
Makoto Yoshida ◽  
Hirotake Masuda ◽  
Hiroshi Nanjo ◽  
Akiteru Goto

Aims: Most In vivo angiogenesis studies have been performed by setting an ischemic condition, or by administrating angiogenic factors such as vascular endothelial growth factor. Unexpectedly, we discovered to spontaneously create new blood vessels by just suturing an arterial graft patch in the jugular vein, using a rabbit model. In general, arteriovenous malformations consist of tangles of arteries and veins that are often connected by a fistula. However, the causes and mechanisms of these clinical entities are not fully understood. The purpose of this study is to show the methods used to produce the model, and then to report the chronological processes involved in the development of this neovasculature and the change of endogenous angiogenic factors. Methods and Results: We performed to suture an arterial graft patch into the rabbit vein. Within a month after the surgery, dense (nidus-like) neovasculature was formed around the patch. Angiography and pulse-oximeter analyses demonstrated that the blood, which flew into the new vessels, was arterial blood. It means that arteriovenous shunt has been formed.. Pathological evaluation revealed multiple branching vessels sprouting out from the patch suture site, and numerous dilated vessels devoid of sphincter muscle in the surrounding connective tissue. We determined, by FISH analysis, that these branches had originated from the graft itself. The endogenous angiogenic factors, such as VEGF, have soared immediately after the surgery. Conclusion: This is the first in vivo model of spontaneous arteriovenous fistula formation via the creation of neovasculature. These findings exemplify the difference between the arterial and venous intima, and we believe that this difference could be key to understanding human vascular anomaly diseases and the basic principles of vascular network formation, angiogenesis and/or vasculogenesis.


2020 ◽  
Vol 11 ◽  
pp. S506-S511
Author(s):  
Elizabeth Vinod ◽  
Tephilla Epsibha Jefferson ◽  
Soosai Manickam Amirtham ◽  
Neetu Prince ◽  
Tulasi Geevar ◽  
...  

2016 ◽  
Vol 87 (4) ◽  
pp. 317 ◽  
Author(s):  
Lucio Dell’Atti

Objectives: The purpose of this study was to evaluate preoperatively the results of transrectal ultrasound (TRUS) in the detection of morphological, vascularization status of urethral rhabdosphincter (RS) and evaluate the correlation with urinary continence after radical prostatectomy (RP). Methods: 211 patients who underwent RP were prospectively studied using TRUS scan of the RS thickness. At the end of the examination a study was performed with the use of colour-Doppler for the assessment of the RS vascularity pattern. The level of continence was graded on a 5 point scale as: 1 = complete continence, 2 = 1 pad daily, 3 = 2-3 pads daily, 4 = 4 or more pads daily, and 5 = complete incontinence. Results: It was possible to visualize the rhabdosphincter and its vascularity in all patients. Patients with normal continence (level 1 and 2) showed a sphincter-muscle thickness of 3.5 mm (± 0.4) and a hypoechoic ultrasound pattern. With respect to the other levels 3, 4 and 5 of urinary incontinence RS thickness was 2.8 mm (± 0.5), 2.1 mm (± 0.6), 1.7 (± 0.7) respectively. Incontinence after RP (≥ 3 level) was associated with urethral sphincter deficiency in the great majority of patients. Statistical significant differences were observed in the vascularity between continent and incontinent men in all measured vascularity variables (p < 0.005). Conclusions: This study suggests that RS integrity is a good predictor of urinary continence after RP and this information can be important during the preoperative phase as part of the informed consent.


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