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Zheng Y.,Shanghai JiaoTong University | Shi D.,Shanghai Jiading Central Hospital | Wu X.,Shanghai First Rehabilitation Hospital | Gu M.,Shanghai Jiading Hospital of Traditional Chinese Medicine | And 4 more authors.
Evidence-based Complementary and Alternative Medicine | Year: 2014

Objective. To compare ultrasound-guided miniscalpel-needle (UG-MSN) release versus ultrasound-guided dry needling (UG-DN) for chronic neck pain.Methods. A total of 169 patients with chronic neck pain were randomized to receive either UG-MSN release or UG-DN. Before treatment and at 3 and 6 months posttreatment, pain was measured using a 10-point visual analogue scale (VAS). Neck function was examined using the neck disability index. Health-related quality of life was examined using the physical component score (PCS) and mental component score (MCS) of the SF-36 health status scale.Results. Patients in the UG-MSN release had greater improvement on the VAS (by 2 points at 3 months and 0.9 points at 6 months) versus in the UG-DN arm; (both P < 0.0001). Patients receiving UG-MSN release also showed significantly lower scores on the adjusted neck disability index, as well as significantly lower PCS. No severe complications were observed.Conclusion. UG-MSN release was superior to UG-DN in reducing pain intensity and neck disability in patients with chronic neck pain and was not associated with severe complications. The procedural aspects in the two arms were identical; however, we did not verify the blinding success. As such, the results need to be interpreted with caution. © 2014 Yongjun Zheng et al.

Ye L.,Shanghai JiaoTong University | Mei Q.,Shanghai University | Li M.,Shanghai First Rehabilitation Hospital | Gu M.,Shanghai Jiading Hospital of Traditional Chinese Medicine | And 6 more authors.
Pain Medicine (United States) | Year: 2015

Objective: The treatment of plantar heel pain is highly challenging. We report ultrasound-guided pulsed radiofrequency treatment (UG-PRF) in the gastrocnemius to treat plantar heel pain and minimize the safety issues. Design: This study compared UG-PRF with sham treatment in 100 patients with plantar heel pain. Primary outcome measures include the pain subscale of the Foot Health Status Questionnaire (FHSQ-pain) and "first step" pain as measured on a visual analogue scale (VAS-"first-step" pain). The secondary outcome measures include the FHSQ-foot function and general foot health, and health related quality of life (assessed using the Short Form-36 questionnaire [SF-36]). All outcomes were measured at 3 and 6 months post-treatment. Results: The results showed the efficacy of UG-PRF in terms of pain management, as reflected by higher FHSQ-pain score (increased by 20.0 (P<0.0001) and 17.9 (P = 0.001) compared with the sham treatment at 3 or 6 months, respectively) and lower VAS-"first-step" pain (reduced by 26.1 (P<0.0001) and 14.3 (P = 0.01) compared with the sham group at 3 or 6 months, respectively). The FHSQ-foot function and FHSQ-general foot health were increased by the UG-PRF (P<0.05, vs sham treatment at 3 or 6 months). The SF-36 physical component score in the sham group was 10.8 (P = 0.042) and 10.4 (P = 0.044) lower than the UG-PRF group at 3 or 6 months, respectively. No severe complications were observed. Conclusions: We conclude that the UG-PRF is both safe and efficacious in managing plantar heel pain. Wiley Periodicals, Inc.

Luo L.-J.,Shanghai Jiading Central Hospital | Luo L.-J.,CAS Shanghai Institutes for Biological Sciences | Liu F.,CAS Shanghai Institutes for Biological Sciences | Wang X.-Y.,Tongji University | And 5 more authors.
Cellular Signalling | Year: 2012

The uptake of oxidized low density lipoprotein (ox-LDL) by macrophages usually leads to the formation of lipid-laden macrophages known as "foam cells," and this process plays an important role in the development of atherosclerosis. Ox-LDL activates mitogen-activated protein kinase (MAP) kinases and nuclear factor (NF)-κB, and activations of p38 and NF-κB are important for the formation of foam cells. MAP kinase phosphatase (MKP) 5 is a member of the dual specificity phosphatases (DUSPs) family that can selectively dephosphorylate activated MAPKs to regulate innate and adaptive immune responses. However, the role of MKP5 in the formation of foam cells remains unknown. Here, we found that stimulation of ox-LDL induces the expression of MKP5 in macrophages. MKP5 deficiency blocked the uptake of ox-LDL and the formation of foam cells. Further analysis revealed that deletion of MKP5 reduced the ox-LDL-induced activation of NF-κB. Also, MKP5 deficiency markedly inhibited the production of TNF-α, but enhanced the levels of TGF-β1 in ox-LDL-stimulated macrophages. Moreover, inhibition of NF-κB by p65 RNAi significantly reduced foam cell formation in macrophages from WT mice relative to MKP5-deficient mice. Thus, MKP5 has an essential role in the formation of foam cells through activation of NF-κB, and MKP5 represents a novel target for the therapeutic intervention of atherosclerosis. © 2012 Elsevier Inc.

Chen Z.,Shanghai University | Fu Q.,Tongji University | Shen B.,Shanghai Jiading Central Hospital | Huang X.,Shanghai University | And 5 more authors.
Molecular Medicine Reports | Year: 2014

Chronic spinal cord compression is the result of mechanical pressure on the spinal cord, which in contrast to traumatic spinal cord injury, leads to slowly progressing nerve degeneration. These two types of spinal cord injuries may trigger similar mechanisms, including motoric nerve cell apoptosis and autophagy, however, depending on differences in the underlying injury severity, nerve reactions may predominantly involve the conservation of function or the initiation of functions for the removal of irreversibly damaged cells. p62 is a multidomain adapter protein, which is involved in apoptosis and cell survival as well as autophagy, and is a common component of protein aggregations in neurodegenerative diseases. In the present study, a rat chronic spinal cord compression model was used, in which the spinal cord was progressively compressed for six weeks and then constantly compressed for another 10 weeks. As a result Basso, Beattie and Bresnahan locomotor scaling revealed a gradual score decrease until the 6th week followed by constant recovery until the 16th week after spinal cord compression was initiated. During the first eight weeks of the experiment, p62 and nuclear factor-κB (NF-κB) were increasingly expressed up to a constant plateau at 12-16 weeks, whereas caspase 3 exhibited a marginally enhanced expression at 8 weeks, however, reached a constant maximum peak 12-16 weeks after the beginning of spinal cord compression. It was hypothesized that, in the initial phase of spinal cord compression, enhanced p62 expression triggered NF-κB activity, directing the cell responses mainly to cell survival and autophagy, whereas following eight weeks of spinal cord compression, caspase 3 was additionally activated indicating cumulative elimination of irreversibly damaged nerve cells with highly activated autophagy.

Li H.-Z.,Shanghai Jiading Central Hospital | Chen Z.,Shanghai University | Hou C.-L.,Shanghai University | Tang Y.-X.,Shanghai University | And 2 more authors.
Journal of Biochemical and Molecular Toxicology | Year: 2015

To investigate the effect of uric acid on the osteogenic and adipogenic differentiation of human bone mesenchymal stem cells (hBMSCs). The hBMSCs were isolated from bone marrow of six healthy donors. Cell morphology was observed by microscopy and cell surface markers (CD44 and CD34) of hBMSCs were analyzed by immunofluorescence. Cell morphology and immunofluorescence analysis showed that hBMSCs were successfully isolated from bone marrow. The number of hBMSCs in uric acid groups was higher than that in the control group on day 3, 4, and 5. Alizarin red staining showed that number of calcium nodules in uric acid groups was more than that of the control group. Oil red-O staining showed that the number of red fat vacuoles decreased with the increased concentration of uric acid. In summary, uric acid could promote the proliferation and osteogenic differentiation of hBMSCs while inhibit adipogenic differentiation of hBMSCs. © 2015 Wiley Periodicals, Inc.

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