In order to study of etiology, pathogenesis, and therapy of endometriosis(EM) through animal models, we review the literature on rodent and primate models of endometriosis, including establishment of models and their applications.We hope that animal models provide useful tools for the studies of endometriosis.

Objective To detect osteoprotegerin (OPG) protein levels in synovial tissues from ankylosing spondylitis (AS) patients and compare the expression level and distribution of OPG protein in AS, rheumatoid arthritis (RA), osteoarthritis (OA) and normal synovial tissues. By studying the correlation of OPG expressions with pathological changes of inflammatory joints to explore the role of OPG in the pathogenesis of bone destruction in AS. Methods Immunohistochemical analysis was performed using OPG monoclonal antibody to detect OPG expression in 13 AS, 16 RA,17 OA patients and 6 healthy controls. The labeled synovial tissue sections were quantified by digital image analysis and semiquantitively analyzed to compare the expression of OPG positve cells in different patient groups and normal subjects. In addition, the correlation of OPG expression with certain inflammatory indices (including ESR, CRP, blood platelet count) and radiological stage of involved joints was analyzed respectively. Results Positive staining of OPG was seen in all 13 AS patients. OPG expression was predominantly seen in the synovial lining layer and sublining areas. Positive staining of OPG was also found in the synovial tissues of 2 normal subjects, but the OPG level was significantly lower. No positive staining of OPG was found in synovial tissues from all patients with RA and OA. Conclusions {1}Higher levels of OPG are expressed in synovial tissues from AS patients than in tissues from normal subjects (P

30 mm Hg) was diagnosed with Doppler echocardiography in 28 patients with SSc.Twenty patients have isolated PHT,while 8 patients were of secondary PHT which was due to severe pulmonary fibrosis.The levels of albumin, ? globulin ,IgA,IgG and CRP in serum of patients with PHT were significantly higher than those without PHT ( P

Objective To compare expression and distribution of CD68 protein and TRAP positive protein in ankylosing spondylitis (AS), rheumatoid arthritis (RA), osteoarthritis (OA), and normal synovial tissues to study the differentiation of osteoclast in synovial tissues obtained from AS patients and its role in the pathogenesis of bone destruction in AS. Methods Immunohistochemical analysis was performed using CD68 monoclonal antibody to detect CD68 expression, and the distribution of TRAP positive cells in the synovial tissues was examined by enzyme histochemistry in 13 AS, 16 RA, 17 OA patients and 6 healthy controls. The above two variables were quantified in the labeled sections by digital image analysis and semiquantitative analysis to compare the expression of CD68 positive cells in different patient groups and normal subjects. Results Positive CD68 staining was seen in synovial cells from all the patients with AS, RA, OA and normal subjects, and the expression levels of CD68 from patients with AS and RA were higher than those from OA patients and healthy subjects. The CD68 positive cells were abundant mainly in lining layer. In areas where elevated RANKL expression levels were present, the number of TRAP positive cells was found significantly increased in AS and RA synovium. TRAP positive cells were rarely observed in synovium from OA patients and normal controls. There was positive correlation between the number of TRAP positive cells and the RANKL expression (r=0.442, P=0.043) in RA patients. Conclusions An obvious increase in the number of CD68 positive cells and TRAP positive cells in synovium may provide a main source of osteoclastogenesis in AS patients. The up-regulation of activity and quantity of osteoclast may have an important role in peripheral articular destruction in patients with AS.

Objective To determine the protein levels of receptor activator of NF ?B ligand (RANKL) in synovial tissues obtained from ankylosing spondylitis (AS) patients, and compare the expression level and distribution of RANKL protein in AS with that in rheumatoid arthritis (RA), osteoarthritis (OA) and normal synovial tissues, in order to define the role of RANKL expressions in the pathogenesis of arthritis and bone destruction in AS. Methods Immunohistochemical analysis was performed using monoclonal antibodies to determine RANKL expression in 13 AS, 16 RA, 17 OA patients and 6 healthy controls. The protein levels of RANKL in labeled synovial tissue sections were quantified by digital image analysis and semiquantitative analysis to compare the expression of RANKL in positve cells among different patient groups and normal subjects. In addition, RANKL expression was correlated with certain inflammatory indices (including ESR, CRP, blood platelet count) and radiological stage of involved joints, respectively. Results Positive staining of RANKL was seen respectively in all 13 AS patients and 16 patients with RA, and the positive expression was distributed predominantly in the synovial lining layer and at synovium cartilage junctions. There was no significant difference between levels of RANKL expression in tissues from patients with AS and in tissues from RA. No positive staining of RANKL was observed in 6 normal subjects and all OA patients. Positive correlation was found between RANKL protein expression and X ray stage of bone destruction of involved joints in the patients with AS and RA ( r =0 73,0 41, P =0 003,0 021 respectively). Conclusions RANKL plays an important role in the pathogenesis of bone destruction in patients with AS, and its elevated expression level may reflect the degree of bone destruction of peripheral joints in AS patients. Since similar patterns of RANKL expression are found in synovial tissues from AS and RA patients, therefore, we conclude that the pathogenesis of bone destruction in AS may be similar to that in RA

Objective To investigate the influential factors of cognitive impairment after lacunar brain infarction(LBI).Methods The neuropsychological tests including mini-mental state examination(MMSE) scale,clock-drawing test(CDT),execute function(EF)in ADAS-cog were applied in 136 LBI patients(LBI group) and 60 gender,age and concomitant chronic diseases matched controls(control group).Those results were compared between the two groups.The influence of the LBI patients's age,the number of cerebral lesion and concomitant disease(hypertension,diabetes,hyperlipidemia) on the scores of the above tests were analyzed.Results(1)The incidence of cognitive impairment in LBI group(55.8%) was distinctly higher than that in control group(15%);the scores of total MMSE and CDT in LBI group were significantly lower than those in control group;while the EF score was higher(all P

Objective To evaluate the effect of miR‐335 regulate cell proliferation by targeting survivin in breast cancer cells MCF‐7 .Methods (1)Chose breast cancer tissue and para‐carcinoma tissue ,and used RT‐PCR or Western blot to detect the expres‐sion of miR‐335 and survivin protein .(2)Chose breast cancer cells MCF‐7 ,respectively transfected miR‐335 mimic and mimic con‐trol .The expression of miR‐335 and survivin protein were detected by RT‐PCR or Western blot .(3)Chose breast cancer cells MCF‐7 ,respectively co‐transfection wild type survivin 3′‐UTR(survivin‐wt)or mutant type urvivin 3′‐UTR(survivin‐Mut)and miR‐335 mimic or negative control(NC)to breast cancer cells MCF‐7 .The cell luciferase activity were detected by dual‐luciferase report gene experiment .(4)Chose breast cancer cells MCF‐7 ,respectively transfected mimic control ,miR‐335 mimic and miR‐335 mimic+ sur‐vivin .The cell proliferation activity of each group were detected by MTT method .Results (1)Compared with para‐carcinoma tis‐sue ,the miR‐335 expression of breast cancer tissue significantly decreased(P<0 .05) ,and the survivin protein expression of breast cancer tissue significantly increased(P<0 .05) .(2)Compared with transfection mimic control ,transfection miR‐335 mimic can made the miR‐335 expression of MCF‐7 increased(P<0 .05) ,and made the survivin protein expression of MCF‐7 decreased(P<0 .05) . (3)Compared with transfection NC ,co‐transfection miR‐335 mimic and survivin‐wt can made luciferase activity of MCF‐7 signifi‐cantly decreased(P<0 .05) ,but the luciferase activity of MCF‐7 was not significantly changes after co‐transfection miR‐335 mimic and survivin‐Mut (P>0 .05) .(4)Compared with transfection mimic control ,the MCF‐7 proliferative activity significantly decreased after transfection miR‐335mimic(P<0 .05) .Compared with transfection miR‐335 mimic ,the MCF‐7 proliferative activity signifi‐cantly increased after transfection miR‐335 mimic+survivin(P<0 .05) ,but still lower than transfection mimic control(P<0 .05) . Conclusion In breast cancer tissue ,the miR‐335 show low expression ,and survivin show high expression .miR‐335 can target sur‐vivin to inhibit the proliferation activity of breast cancer cells MCF‐7 .

CD4+ ..CDS+ -.CD4+ /CDS+ was decreased more significantly in those patients who were older, severe, demential and depressive. Conclusion:Severe natural kill cell and T lymphocyte immune functional decline and disbalance were observed in PD patients. The significant decline of the levels of CD3+ ,CD4+ .CD8+ ,CD4+ /CD8+ in PD patients might be closely related to it's pathogenesis. The levels of CD3+ ,CD4+ ,CD8+ CD4+/CD8+ was even significantly lower in older, severe,dementia and depressive patients, so the levels of natural kill cell and T lymphocyte subsets can provide basis for evaluating severity .progression and prognosis of disease in PD. It was a new connotation for the study of PD on prevention and therapy in the future.

Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Azacitidine ; administration & dosage ; analogs & derivatives ; Female ; Humans ; Leukemia, Myeloid, Acute ; drug therapy ; etiology ; Male ; Myelodysplastic Syndromes ; complications ; pathology ; Treatment Outcome

Objective To determine the monokine levels of serum and synovial fluid (SF) in patients with JSpAs and estimate the correlation between monokines and inflammatory indices.Methods Serum and SF monokines (IL 1?,IL 1?,IL 6,IL 8,IL 12 and TNF ?) were measured by sandwich ELISA in patients with JSpAs ( n =28) and healthy controls ( n =10).The correlation between serum monokines and inflammatory indeces and between both serum and SF monokine levels was analysed.Results Elevated serum level of IL 6 was found in patients with JSpAs as compared to healthy controls ( P