Objective To investigate the relationship between tendinopathy and higher production of prostaglandins E2 (PGE2) and leukotriene B4 (LTB4) induced by cyclic stretching of human patellar tendon fibroblasts. Methods We used a novel in vitro model system to mimic in vivo conditions, where human patellar tendon fibroblasts (HPTFs) were uniaxially stretched with different magnitudes of stretching (4%, 8% and 12%). Non-stretched fibroblasts were used as control. The productions of PGE2 and LTB4 as well as the expression of cycloxygenase (COX) and 5-lipoxygenase (5-LO) were then measured every four hours of cyclic stretching. In addition, we treated the cells with inhibitors of COX or 5-LO. Results It was found that cyclic stretching of fibroblasts at 8% and 12% of stretching increased PGE2 and LTB4 levels. Blocking the COX enzyme with indomethacin (25 mol/L) decreased PGE2 levels but increased LTB4 production and vice versa. Whereas decreasing LTB4 production with MK-886 (10 ?mol/L) could increase PGE2 levels compared to cells stretched without inhibitors. Conclusions Cyclic stretching of HPTFs produces high levels of PGE2 and LTB4, where a balance exists: blocking PGE2 production increases the production of LTB4, and vice versa. Therefore, this study raises the possibility that the routine use of COX inhibitors in clinical treatment of tendinopathy may exacerbate the condition by causing neutrophil-mediated inflammatory and degenerative changes in the tendon due to increased levels of LTB4, which is a potent chemoattractant for neutrophils.

Tendinopathy refers to a syndrome of pain, swelling, and impaired performance of tendon and paratenon that is caused by overuse of tendon and paratenon. In the past three decades, the incidence of tendinopathy increased obviously. Although extensive researches have been done, we still do not know much about its pathogenesis, pathology and therapy. In this paper, the authors review its pathological classification, its macroscopic, light microscopic and electron microscopic features, and the morphology of apoptotic cells under light microscopy. The paper also highlights the recent research on how stimulation leads to apoptosis and further to tendinosis.

[Objective]To examine the difference of proliferation and ?-smooth muscle actin(?-SMA) expression between healing and normal medial collateral ligament(MCL) fibroblasts.[Method]Ten adult,male,Sprague-Dawley rats weighing between 350 and 375 g were used in this study.Normal and healing MCL were cut into small pieces in aseptic conditions,and then placed and cultured in culture chamber.Fibroblasts were passaged with 0.25% trypsin.After 24 and 48 hours incubation,MTT was used to measure the cell proliferation.The production of ?-SMA was measured by Western Blot.[Result]After 24 and 48 hours incubation,healing fib roblasts showed absorbency values of 0.49?0.080 and 0.53?0.07 respectively.II was found that healing fibroblasts proliferated faster than normal fibroblasts(P

[Objective]To examine the effects of TGF-?1 on the production of ?-SMA and extracellular matrix in flexor tendon sheath fibroblasts. [Methods]Sheath fibroblasts were obtained from rabbit flexor tendons.Cell culture was supplemented with 5ng/ml of TGF-?1.After 48 hours incubation,the production of a-SMA was assayed by Western-Blot.The productions of collagen I and fibronectin in supernatants culture were examined using ELISA.[Results]Treatment with TGF-?1 significantly stimulated a-SMA production in flexor tendon sheath fibroblasts (P

Objective To summarize the clinical characteristic and therapeutic efficacy of lacunar infarction after craniocerebral trauma.Methods 37 cases of children with lacunar infarction after craniocerebral trauma from December 2000 to December 2004 were retrospectively analyzed.Results All of the 37 sufferers received the expectant treatment in hospital.Among the 37 cases,30(81.1%) were well-healed and 7(18.9%) were light maimed when leaving hospital.The clinical symptom of the 29 sufferers completely faded and 7 patients who were light maimed recoverd during the follow-up visit for 6 to 12 months.Conclusions Lacunar infarction after craniocerebral trauma is the syndrome of the damage of the nervous system.Its' major manifestation is the disorder of half body movement.Children with light craniocerebral trauma get this kind of disesase easily.CT scanning and regular re-X can predominantly raise the of the final diagnosis.Most of the sufferers can receive good long-term therapeutic efficacy.

The research of bone tissue engineering bases on three basic directions of seed cells, scaffold materials and growth information. Stem cells have been widely studied as seed cells. Human urine-derived stem cell (hUSC) is extracted from urine and described to be adhesion growth, cloning, expression of the majority of mesenchymal stem cell markers and peripheral cell markers, multi-potential and no tumor but stable karyotype with passaging many times. Some researches proposed that hUSC might be a new source of seed cells in tissue engineering because of their invasive and convenient obtention, stable culture and multiple differentiation potential.
Bone and Bones ; Cell Differentiation ; Humans ; Mesenchymal Stromal Cells ; Stem Cells ; cytology ; Tissue Engineering ; Urine ; cytology

Objective To examine the effectiveness of HGF in blocking TGF-β1 induced α-SMA and extracellular matrix production in fibroblasts of the flexor tendon sheath. Methods Seven adult male New Zealand white rabbits (3.75-4.00 kg) were used for this study. Both of their front feet were sterilised and the middle digit flexor digitorum profundus tendon equivalents were identified and isolated. These specimens were used to establish primary cell cultures. Sheath fibroblasts were obtained from rabbit flexor tendons. After the cells reached confluence, cells were detached with trypsin/ethylenediamine tetra-acetic acid. All experiments were performed using the cells at the third passage. At 70% confluence the medium was supplemented with 5 ng/ml of TGF-β1 along with increasing doses of HGF (10-40 ng/ml). After 72 hours incubation, the productions of α-SMA were assayed by Western-Blot. The productions of collagen Ⅰ and fibronectin in supernatants culture were examined using ELISA. Results Evaluation of protein expression revealed that TGF-β1 markedly induced α-SMA expression in cultured rabbit flexor tendon sheath fibroblasts. TGF-β1 treated fibroblasts expressed 1.8-fold more protein compared to non-treated fibroblasts (P ＜ 0.05). However, simultaneous incubation of HGF significantly abrogated TGF-β1 induced α-SMA expression in a dose-dependent manner (P＜ 0.05). Treatment with TGF-β1 significantly stimulated collagen Ⅰ and fibronectin production in flexor tendon sheath fibroblasts (P ＜ 0.01). Remarkably, the addition of HGF reduced productions of all components induced by TGF-β1 in a dose-dependent manner (P ＜ 0.05). Conclusion HGF antagonizes TGF-β1 induced α-SMA, collagen Ⅰ, and fibronectin production in flexor tendon sheath fibroblasts. The findings provide a cellular and molecular basis for HGF's acting as a therapeutic agent for adhesions in flexor tendons.

Ureteral stents play an important role in the treatment of ureteral strictures. It supports the narrow urethra and ensures the smooth flow of urine, thus alleviating the impact of ureteral stricture on kidney function. Traditional ureteral stents are prone to complications such as stones, bacterial infections, inflammation, and restenosis when indwelling in the body. This paper reviews the performance requirements of ureteral stents, introduces ureteral stents of different structures, functions, materials, and preparation as well as processing techniques, and analyzes the key problems and future research directions of ureteral stents, which provides a reference basis for the research of ideal ureteral stents.