Objective To investigate the clinical efficacy of acupoint application plus massotherapy for scapulohumeral periarthritis (periarthritis of shoulder). Method One hundred and two patients with scapulohumeral periarthritis were randomly allocated to treatment and control groups, 51 cases each. The treatment group received acupoint application plus massotherapy and the control group, massotherapy. Both groups were treated for three courses. The VAS score and the Neer shoulder function score were recorded in the two groups before and after treatment. Result The VAS score and the Neer shoulder function score improved in the two groups after treatment compared with before (P<0.05) and improved more in the treatment group than in the control group (P<0.05). Conclusion Clinically acupoint application plus massotherapy has a satisfactory therapeutic effect on scapulohumeral periarthritis with a certain effect on pains in the affected shoulder.

Obesity is an independent risk factor for acute pancreatitis (AP),and the morbidity risk and severity of AP in obese patients were significantly increased than those in non-obese patients.However,the exact mechanism has not been fully elucidated.In recent years,the researches on the role of adipose tissue (AT) in AP have gradually attracted wide attention of scholars both at home and abroad.To better understand the pathogenesis and new therapeutic targets of AP,in this paper,we overviewed the recent research progress on the role of AT in AP.

Objective To assess the therapeutic effect of human adipose-derived mesenchymal stem cells on radiation-induced vascular injury in the small intestine of rat. Methods A total of 34 male Sprague-Dawley rats were enrolled in this study. To establish a model of radiation-induced intestinal injury, each rat was irradiated with 15 Gy in whole abdomen. 17 rats were randomly selected and infused intraperitoneally with passage 6 ( P6 ) Ad-MSCs, and the other 17 rats that received PBS were set as control. 10 days post-irradiation, the number of CD31+ endothelial cells in the small intestine villus was measured by flow-cytometry, the expressions of CD31, CD105 and isolectin-B4 in the na?ve endothelial cells with detected by IHC-staining, and the vascular integrity was evaluated by measuring VE-Cadherin. The origination of na?ve endothelial cells within injured intestine was also analyzed. In addition, total mRNA were extracted from irradiated small intestine to assay the expressions of VEGF, bFGF, Flk-1 and SDF-1 using quantitative Real-time PCR. Results Compared to the control, the amount of CD31-postive endothelial cells within irradiated intestine was significantly increased after Ad-MSCs infusion ( t=12?15, P<0?05). The microvascular density in the injured sites was also significantly increased by the infusion of Ad-MSCs (20 d:t=10?33, P<0. 05;30 d:t=32?85, P<0?05). Moreover, the expressions of VEGF, bFGF, Flk-1 and SDF-1 were significantly up-regulated after delivery of Ad-MSCs ( VEGF:t =10?34, bFGF:t=11?25,Flk-1:t=6?73, SDF-1:t=6?73, all P<0?05), which was beneficial in maintaining the integrity of intra-villus blood-vessels as well as promoting neovascularization in the injured sites. Conclusion Ad-MSCs had potentials in healing radiation-induced vascular injury in rat small intestine.

Objective To evaluate the therapeutic effect of adipose-derived mesenchymal stem cells on radiation enteritis.Methods A total of 52 male Sprague-Dawley rats were used in the present study.Herein,46 rats were randomly selected and irradiated with a dose of 15 Gy at their abdomens.Two hours post-irradiation,23 rats were randomly selected and infused intraperitoneally with adipose-derived mesenchymal stem cells in passage 6 from young-female donor.The other 23 rats were intraperitoneally infused with PBS.The rest 6 rats were set as normal control.During the first 10 days post-irradiation,peripheral blood-samples from irradiated rats were harvested for testing the levels of IL-10 in serum using ELISA assay.Additionally,after isolating the thymic cells and peripheral blood mononuclear cells,the percentages of CD4/CD25/Foxp(3)-positive regulatory T cells in thymus and peripheral blood were tested by flow-cytometry.Finally,infiltration of inflammatory cells and deposition of collagens within irradiated small intestine were analyzed by H&E staining and Masson Trichrome staining,respectively.Based on the MPO-immunohistochemistry staining,the type of infiltrated cells was identified.The Kaplan-Meier method was used for analyzing the survival rate of irradiated rats.Results During a period of 30 days post-irradiation,the irradiated rats receiving adipose-derived mesenchymal stem cells survived longer than those receiving PBS (t =4.53,P ＜ 0.05).Compared to the irradiated rats with PBS-treatment,adipose-derived mesenchymal stem cells could elevate the level of IL-10 in serum (7 d:t =13.93,P ＜ 0.05) and increase the percentages of CD4/CD25/Foxp(3)-positive regulatory T cells in both peripheral blood (3.5 d:t =7.72,7 d:t=11.11,10 d:t =6.99,P ＜0.05) and thymus (7 d:t =16.17,10 d:t =12.12,P＜ 0.05).Moreover,infiltration of inflammatory cells and deposition of collagens within irradiated small intestine were mitigated by adipose-derived mesenchymal stem cells.Conclusions Adipose-derived mesenchymal stem cells were capable of curing radiation enteritis.

Objective To study the efficacy and toxicity of gensenoside-Rg3 (Rg3) combined with radiotherapy on non-small cell lung cancer ( NSCLC ) at advanced stages (Ⅲ and Ⅴ ).Methods Sixty-three patients with stage Ⅲ or Ⅳ NSCLC were divided randomly into two groups:treatment group ( n =35 ) treated with Rg3 combined with radiotherapy and control group ( n =28 ) treated with radiotherapy alone.The efficacy and side effects were compared after the treatment.Results The response rate ( CR + PR) of the treatment group was 57.14％,significantly higher than that of the control group (32.14％,x2 =3.91,P ＜ 0.05).The median survival time of the treatment group was 14.2 months,significantly longer than that of the control group ( 11.2 months,x2 =2.07,P ＜ 0.05 ).The one-year survival rate of the treatment group was 62.86％,significantly higher than that of the control group (39.29％,x2 =4.40,P ＜0.05).The incidence rates of side effects of the treatment group were all lower than those of the control group,but there were not significant difference. Conclusions Gensenoside-Rg3 combined with radiotherapy is effective for advanced stage NSCLC,with attenuation and synergistic effects.

BACKGROUND: The protein kinase C (PKC) family consists of 3 groups of PKCs, namely the conventional PKC (cPKC), atypical PKC and novel PKC.Accumulating studies conducted in recent years have suggested that PKCs may play important roles in the development of cerebral ischemic/hypoxic preconditioning ( I / HPC ).OBJECTIVE: To observe membrane translocation of hypoxia-activated cPKC isoforms(α, βⅠ, βⅡ and γ) at cellular levels in a cell hypoxia model.DESIGN: Randomized block design.SETTING: Department of Neurobiology, College of Basic Medical Sciences,Capital University of Medical Sciences.MATERIALS: The experiment was completed at the Neurobiological Cell Culture Laboratory of Capital University of Medical Sciences in May 2004.Human neuroblastoma cells with the properties of neurons were maintained and passaged in this laboratory.METHODS: The activation of cPKC isoforms under hypoxic condition and changes of cPKCα, βⅠ, βⅡ and γ membrane translocation(an indicator of PKCs activation) in SH-SY5Y neuroblastoma cells in response to hypoxia (1% 02, 5% CO2 and 94% N2) for 0 to 24 hours were observed using SDS-PAGE, Western blotting and immunocytochemistry.MAIN OUTCOME MEASURES: Effect of sustained hypoxia on cPKC membrane translocation in human neuroblastoma cells was observed with SDS-PAGE, cPKC Western blotting, and immunocytochemistry.RESULTS: cPKCα, βⅠ and βⅡ membrane translocation were increased significantly ( P ＜ 0.05 ) in a time-dependent manner in response to hypoxic exposure, and the increase of cPKCβⅠ was more evident( P ＜ 0. 001 ) after 4hours of hypoxic exposure, whereas no cPKCγ was detected in SH-SY5Y neuroblastoma cells either under normoxic or hypoxic condition. The results suggested that all cPKC isoforms, epically cPKCβⅠ, could be activated by sustained hypoxia, and the absence of cPKCγ in SH-SY5Y neuroblastoma cells may be relevant to the loss of specific biological features of the cultured cells.CONCLUSION: Sustained hypoxia activates the isoforms of cPKCα, βⅠ and βⅡ in human neuroblastoma cells and induces their membrane translocation.cPKCγ isoform may not exist in human neuroblastoma cells, or the cells has lost certain biological characteristics.

BACKGROUND:cAMP response element binding protein (CREB) is a key protein of memory, which is closely related to long-term memory. It wil provide a new way for the treatment of hypoxic ischemic brain damage (HIBD) to study the effects of dental pulp stem cel s transplantation on the long-term behavior and CREB protein via the lateral ventricle in neonatal HIBD rats. OBJECTIVE:To observe the changes in long-term behavior and CREB protein expression in neonatal HIBD rats after human dental pulp stem cel transplantation, thereby providing scientific evidence for clinical treatment of neonatal HIBD. METHODS:Thirty-six healthy 7-day-old Sprague-Dawley rats were randomly divided into normal, HIBD and cel transplantation group. The hypoxic ischemic brain damage models were established in the brain damage and cel transplantation groups. Twenty-four hours after HIBD, human dental pulp stem cel s were injected into the left lateral cerebral ventricle of rats in the cel transplantation group, total y 3×106 living cel s. Equal volume of normal saline was injected into the left lateral cerebral ventricle of rats in the normal control and HIBD groups. RESULTS AND CONCLUSION:The average time to seek water, the average escape latency and escape distance of the human dental pulp stem cel s group were significantly shorter than those of hypoxic ischemic brain injury group (P<0.01), but longer than those in the normal group (P<0.01). Nissl staining showed that the cel s in the hippocampal CA1 region in human dental pulp stem cel s group were more regular, the number of cel s was significantly higher than that of hypoxic ischemic brain injury group, but stil significantly less than that in the normal group (P<0.05). Immunohistochemical staining results showed that the number of CREB positive cel s in human dental pulp stem cel s group was significantly higher than those in HIBD group, but stil significantly less than those in the normal group (P<0.01). It is suggested that human dental pulp stem cel s transplantation could promote the expression of CREB protein in the hippocampal CA1 region, to improve the long-term learning and memory ability of hypoxic ischemic neonatal rats, and thus repair HIBD.

Insufficient remyelination due to impaired oligodendrocyte precursor cell (OPC) differentiation and maturation is strongly associated with irreversible white matter injury (WMI) and neurological deficits. We analyzed whole transcriptome expression to elucidate the potential role and underlying mechanism of action of lipocalin-2 (LCN2) in OPC differentiation and WMI and identified the receptor SCL22A17 and downstream transcription factor early growth response protein 1 (EGR1) as the key signals contributing to LCN2-mediated insufficient OPC remyelination. In LCN-knockdown and OPC EGR1 conditional-knockout mice, we discovered enhanced OPC differentiation in developing and injured white matter (WM); consistent with this, the specific inactivation of LCN2/SCl22A17/EGR1 signaling promoted remyelination and neurological recovery in both atypical, acute WMI due to subarachnoid hemorrhage and typical, chronic WMI due to multiple sclerosis. This potentially represents a novel strategy to enhance differentiation and remyelination in patients with white matter injury.
Mice ; Animals ; Remyelination/physiology* ; Oligodendrocyte Precursor Cells/metabolism* ; White Matter ; Subarachnoid Hemorrhage/metabolism* ; Lipocalin-2/metabolism* ; Early Growth Response Protein 1/metabolism* ; Oligodendroglia/metabolism* ; Mice, Knockout ; Cell Differentiation/physiology* ; Brain Injuries/metabolism*