Objective To investigate the clinical effects and complications of uterine artery embolization (UAE) therapy using different embolic agents in treating uterine adenomyosis. Methods During 2004—2011, a total of 45 female patients with uterine adenomyosis were admmitted to authors’ hospital to receive uterine artery embolization therapy. The embolic agents used in the procedures included domestic iodized oil, sodium alginate microspheres and Embosphere microspheres. The patients were randomly divided into group A (n=15, using domestic iodized oil as embolic agent), Group B (n=13, using sodium alginate microspheres as embolic agent) and group C (n = 17, using Embosphere microspheres as embolic agent). After the treatment, all the patients were followed up for over 2 years, focusing on the observation of the clinical symptoms such dysmenorrheal, changes of MRI signs and severe complications. The results were analyzed and compared among the three groups. Results After UAE, the clinical symptoms such as the degree of dysmenorrhea, menstrual quantity, etc. were improved in all patients. Six months after UAE, the obvious remission rate of dysmenorrheal in group A, B and C was 33.3% (5/15), 30.8% (4/13) and 41.1%(7/17) respectively. Twelve months after UAE, MRI scanning showed that the uterine sizes in group A, B and C were reduced to 49.19%, 48.25% and 50.05% respectively. Follow-up examination at 24 months after UAE showed that recurrence of dysmenorrheal in group A, B and C was seen in 2, 4 and 2 cases respectively, and amenorrhea was seen in 2 cases of group A and one case in group C. Conclusion The use of domestic iodized oil, sodium alginate microspheres or Embosphere microspheres as embolic agents in performing super-selective uterine artery embolization for adenomyosis can effectively relieve the degree of dysmenorrheal, decrease the uterine size. In addition to ovarian dysfunction, the uterine cavity adhesion may be also a possible cause of amenorrhea occurring after UAE may. In order to ensure a similar clinical efficacy, the use of granular solid embolic agent is preferred as its safety is possibly higher than the liquid embolic agents.

Objective: To explore therapeutic effect of modified constraint-induced movement therapy on rehabilitation in patients with stroke hemiplegia.Methods: A total of 136 patients with stroke hemiplegia were selected and divided into routine rehabilitation group and modified rehabilitation group.After 12 weeks, scores of Fugal-Meyer motor assessment (FMA), modified Barthel index (MBI) and Berg balance scale (BBS), 6min walking distance (6MWD), psychological state and quality of life (QOL) were compared between two groups.Results: After 12 weeks, there were significant rise in scores of FMA, MBI and BBS and 6MWD, and significant reductions in scores of self-rating anxiety scale (SAS) and self-rating depression scale (SDS) in two groups, P<0.05 all.Compared with routine rehabilitation group, there were significant rise in scores of FMA [(53.23±5.13) scores vs.(60.67±5.67) scores], MBI [(57.83±6.11) scores vs.(69.93±6.74) scores] and BBS [(41.45±4.12) scores vs.(50.53±4.56) scores] and 6MWD [(179.46±24.62)m vs.(211.34±26.71)m], and significant reductions in scores of SAS [(50.75±2.56) scores vs.(41.11±1.53) scores] and SDS [(51.34±3.35) scores vs.(40.78±2.11) scores] in modified rehabilitation group, P<0.05 all.Compared with before rehabilitation, there were significant rise in physiological, psychological, social and setting dimension scores in both groups after rehabilitation, and those of modified rehabilitation group were significantly higher than those of routine rehabilitation group, P<0.05 all.Conclusion:Modified constraint-induced movement therapy can significantly improve movement, balance function, and anxiety, depression and daily living capacities in patients with stroke hemiplegia.

Renal arterial infusion chemotherapy aided through NT-CRE has been performed in six patients with renal neoplasm. Embolization was followed by nephrectomy within 3-5 days in four cases. The rumor kindeys were easy to be resected and separated from perinephic tissue. Furthermore, the operative this procedure reduced bleeding and increased the killing of cancer cells so as to diminish the spreading, planting and treatment on renal neoplasm to the double treatment of ischemia and chemotherapy, thus improving the life quality and prolonging the patients' life. The embolization principle and its clinical significance were discussed in the essay.

AIM: To purify and refold the inclusion body of a human anti-HBsAg scFv with a 6?His tag, and to determine the affinity constant of the purified recombinant product.METHODS: Solubilizing in buffers containing urea or guanidine hydrochloride (GuHCl), the inclusion body was purified by IMAC, and then refolded by dialysis against urea or GuHCl, at the same time, Ni 2+ charged chelate column was utilized for in situ refolding. The affinity constant of the refolded scFv, polished by immune-affinity chromatography, was determined by non-competitive ELISA. RESULTS: The refolded scFv with highest specific bioactivity was produced by dialysis against GuHCl. Under this condition, the recovery of target protein reached (61.08?1 45)%. The affinity constant of the polished scFv was confirmed to be(2.30?0.32) ?10 7 L/mol. CONCLUSION: The inclusion body studied in this paper can be refolded efficiently under optimal dialysis condition in vitro . The antigen-binding property of this recombinant scFv is not affected by the purification tag fused to the N terminal of the protein.

BACKGROUND:Culture condition,isolation method and efficiency are different in reported human umbilical cord-derived mesenchymal stem cells,which lack of unified identification standards.Therefore,it is necessary to establish a high-efficiency and economical culture system for human umbilical cord-derived mesenchymal stem calls(hUCMSCs).OBJECTIVE:To isolate hUCMSCs and induced differentiate into adipocytes and osteblasts.METHODS:The hUCMSCs were isolated form human umbilical cord by tissue adherence and digested with collagenase.The morphology,proliferation and immunophenotype of the 3rd passage cells were analyzed,and then cells were induced to osteogenic and adipogenic differentiation in vitro.RESULTS AND CONCLUSION:The hUCMSCs isolated from human umbilical cord by tissue adherence and digested with collagenase could be cultured and proliferated in vitro.Flow cytometry analysis revealed that the hUCMSCs were positive for CD29 CD44,CD59,CD105,but were negative for CD40,CD86 and HLA-DR.These calls could be induced to differentiate into adipocytes and osteblasts under proper inducing conditions.The hUCMSCs retained the appearance and phenotype even after being expanded more than 40 passages in vitro.This confirmed that the existence of MSCs in human umbilical cord and they had the capacity of differentiating into adipocytes and osteblasts.

Objective To explore the effect of acute respiratory distress syndrome (ARDS) induced by endotoxin on the right ventricular function in rats. Methods Sixty male Sprague-Dawley (SD) rats were randomly divided into normal saline (NS) control group and lipopolysaccharide (LPS) model group with 30 rats in each group. The rat model of ARDS was reproduced by intratracheal instillation of LPS 10 mg/kg after tracheotomy, and the rats in NS control group was intratracheally given the same volume of NS instead of LPS. The survival of rats in each group was observed. Right ventricular function was evaluated by echocardiography at 6 hours and 12 hours after instillation of LPS or NS respectively. Then the rats were sacrificed by bloodletting, and the right heart and lung tissue were harvested. The lung wet/dry weight (W/D) ratio was assessed. The pathological changes in cardiopulmonary tissue in rats were observed with hematoxylin and eosin (HE) strain, and the pathological score of lung injury was calculated. Results There was no animal death in NS control group. In LPS model group, there were 3 rats dead at 6 hours, and 4 dead at 12 hours. The pathological manifestations of lung injury were found at 6 hours after instillation of LPS, and the marked pathological changes of ARDS, such as atelectasis and hyaline membranes were observed at 12 hours. There was no obvious abnormality in the lung tissue of the NS control group. Compared with the NS control group, the 12-hour lung W/D ratio and the lung injury pathological score in the LPS model group were significantly increased (lung W/D ratio:7.69±1.02 vs. 4.14±0.48, lung injury pathological score: 8.26±2.12 vs. 1.32±0.94, both P < 0.01). Echocardiography showed that the right heart function of rats was significantly abnormal with the prolongation of LPS induction time, which showed that pulmonary arterial diameter (PAD) and right ventricular diastolic diameter (RVDd) were increased, maximum blood flow velocity of pulmonary artery (PAVmax), maximum pulmonary artery pressure gradient (PAmaxPG),pulmonary artery acceleration time (PAAT) and tricuspid annular plane systolic excursion (TAPSE) were decreased, with significant differences at 12 hours as compared with those of NS normal group [PAD (mm): 2.84±0.31 vs. 2.11±0.37, RVDd (mm): 4.18±0.71 vs. 3.17±0.40, PAVmax (mm/s): 704.00±145.13 vs. 809.59±120.48, PAmaxPG (mmHg, 1 mmHg = 0.133 kPa): 2.07±0.88 vs. 2.73±0.76, PAAT (ms): 23.80±4.87 vs. 30.01±3.02, TAPSE (mm): 2.48±0.45 vs. 3.56±0.40, all P < 0.01]. Pathological examination showed that the cardiac tissue in the LPS model group showed disorder of myocardial cells and scattered inflammatory cells at 6 hours, and cardiomyocyte degeneration, structural destruction and inflammatory cells were found at 12 hours. Conclusion ARDS induced by instillation of LPS at 12 hours causes right ventricular dysfunction in rats.

The pathological processes of neurodegeneration and neurodegenerative changes after traumatic brain injury (TBI) are closely related to microglia. The pathophysiological functions of microglia are closely correlated to their different cell subtypes. Disease-related microglia (DAM) are a special subtype of microglia, which recently discover on the lesions of degenerative diseases of the central nervous system. DAM are identified as important cells that induce neurodegeneration. The in-depth discussion of DAM role in pathological mechanism of neurodegeneration after TBI provides new clues for understanding and treating neurodegeneration after TBI; therefore, this article focuses on the above content and summarizes the research progress of DAM and neurodegeneration after TBI.

The pathological process continues to evolve for a long time after acute phase of traumatic brain injury (TBI), often coupling with neurodegeneration and neurodegenerative complications. Microvascular dysfunction and blood-brain barrier (BBB) dysfunction caused by neurovascular unit (NVU) dysfunction are closely related to the pathological process of many neurodegenerative diseases. The study on the pathological mechanism of neurovascular unit dysfunction is a promising research field of TBI-related neurodegeneration, and also provides a new idea for the treatment of neurodegeneration after TBI. Therefore, this article mainly reviews these.

Objective: To investigate the role of endoplasmic reticulum stress (ERS) in rats with acute respiratory distress syndrome (ARDS) related right ventricular dysfunction and the protective effect of sodium 4-phenylbutyrate (4-PBA) on right ventricle. Methods: Sixty male Spragne-Dawley (SD) rats were randomly divided into control group (CON group), lipopolysaccharide (LPS) model group, 4-PBA prevention group and 4-PBA treatment group, with 15 rats in each group. ARDS rat model was established by intratracheal instillation of LPS 10 mg/kg after tracheotomy; CON group was given the same amount of saline. 4-PBA prevention group and 4-PBA treatment group were given 4-PBA 500 mg/kg intragastric administration 2 hours before and after LPS respectively. Echocardiography was performed 12 hours after treatment to evaluate the right ventricular function. Then, the rats were sacrificed by bloodletting, and the serum and right ventricular tissue were harvested. The histopathological changes of myocardial were observed by hematoxylin-eosin (HE) staining, the levels of tumor necrosis factor-α(TNF-α), interleukins (IL-1β and IL-6) in serum and myocardial were detected by enzyme linked immunosorbent assay (ELISA), and Western Blot was used to detect the expression of the marker proteins of ERS in myocardial, including glucose regulatory protein 78 (GRP78), C/EBP cyclic adenosine phosphate reaction primitive binding transcription factor homologous protein (CHOP), caspase-12 and caspase-3. Results: Compared with the CON group, the echocardiography showed pulmonary artery maximum pressure gradient (PAmaxPG), pulmonary artery acceleration time (PAAT), tricuspid annular plane systolic excursion (TAPSE) in LPS model group were significantly decreased, and right ventricular end-diastolic excursion (RVDd) was significantly increased, and the levels of TNF-α, IL-1β and IL-6 in serum and myocardial, as well as the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly increased. Compared with LPS model group, TAPSE of 4-PBA preventive and treatment groups were significantly increased (mm: 3.08±0.65, 2.96±0.61 vs. 2.48±0.45), RVDd were significantly decreased (mm: 3.67±0.58, 3.60±0.61 vs. 4.18±0.71), the levels of TNF-α, IL-1β and IL-6 in serum and myocardial were significantly decreased [TNF-α (ng/L): 187.98±18.98, 176.08±17.98 vs. 332.00±19.90 in serum, 135.06±19.00, 132.78±17.00 vs. 155.00±20.00 in myocardial; IL-1β(ng/L): 12.07±2.98, 11.05±2.41 vs. 24.06±4.01 in serum, 19.89±2.80, 21.06±2.80 vs. 26.00±2.60 in myocardial; IL-6 (ng/L): 42.98±7.90, 34.05±6.09 vs. 89.80±10.07 in serum, 129.45±25.00, 127.08±26.06 vs. 145.77±23.00 in myocardial]; the expressions of GRP78, CHOP, caspase-12 and caspase-3 in myocardial were significantly decreased (GRP78/GAPDH: 0.090±0.070, 0.103±0.060 vs. 0.167±0.090, CHOP/GAPDH: 0.109±0.090, 0.090±0.080 vs. 0.186±0.090, caspase-12/GAPDH: 0.769±0.230, 0.799±0.210 vs. 1.040±0.350, caspase-3/GAPDH: 0.391±0.060, 0.401±0.054 vs. 0.603±0.340), with statistically significant differences (all P < 0.05). There were no significant differences in each indexes between 4-PBA prevention group and 4-PBA treatment group (all P > 0.05). Conclusions ERS is involved in ARDS-related right ventricular dysfunction. 4-PBA can protect the right ventricular function of ARDS rats by inhibiting ERS and alleviating inflammation, and the preventive and therapeutic effects of 4-PBA are similar.