Objective To investigate the expression level and clinical significance of T‐cadherin protein and gene in the mixed cell type of hybrid hodgkin lymphoma .Methods The lymph nodetissue samples were obtained from 45 hybrid Hodgkin lymphoma patients and 20 reactive hyperplasia lymphoid patients .The expression level of T‐cadherin of these samples were detected by immu‐nohistochemical staining and RT‐PCR .The relationship of clinic pathological features and prognosis in hybrid Hodgkin lymphoma patients were analyzed by the expression level of T‐cadherin .Results The positive expression rates of T‐cadherin in protein hybrid hodgkin lymphoma and reactive hyperplasia lymphoid tissue specimens were 31 .1% (14/45) and 90 .0% (18/20)(P< 0 .05) .T‐cad‐herin mRNA relative expression in hybrid Hodgkin lymphoma was significantly lower than reactive hyperplasia lymphoid tis ‐suespecimens(P< 0 .05) .The expression of T‐cadherin was significantly correlated with TNM and lymph node involvement (all P< 0 .05) ,but not significantly correlated with age ,gender ,WBC ,PLT and Hb count ,LDH and IPS grade (all P> 0 .05) .Multiva‐riate logistic regression analysis demonstrated TNM stage and T‐cadherin negative expression were independent factors of lymph node involvement .Log‐rank test revealed the two‐year survival rate in hybrid Hodgkin lymphoma patients of T‐cadherin negative and positive expressionwere 83 .9% and 92 .9% (P> 0 .05) ,three‐year survival rate were 71 .0% and 85 .7% (P> 0 .05) ,five‐year survival rate were 41 .9% and 78 .6% (P< 0 .05) .Kaplan‐Meier survival analysis showed the five‐year survival in T‐cadherin nega‐tive expressionwas lowersignificantly than T‐cadherin positive expression (P< 0 .05) .Conclusion T‐cadherin was low expression in hybrid Hodgkin lymphoma and correlated with TNM and lymph node involvement .T‐cadherin may be a new molecular marker to evaluate the prognosis of hybrid hodgkin lymphoma .

Objective To investigate the expressions and clinical significance of Id1 in diffuse large B‐cell Lymphomas (DL‐BCL) tissue and Id1 gene in bone warrow cell .Methods Forty cases of DLBCL(observation group) and 25 cases of reactive lymph‐oid hyperplasia (control group) were included in this study which were admitted by our hospital from October 2011 to October 2014 .The expression of Id1 proteins in DLBCL and reactive lymphoid hyperplasia were detected by imunohistochemical technique . The expression of Id1 genes in all patients′marrow cells was detected by reverse‐transcriptase polymerase chain reaction .The data were collected and analyzed by designed person .Results In 40 DLBCLs ,the positive rate of Id1 were 75 .00% (30/40) ,which was higher than in RHs 32 .00% (8/25) ,with statistic difference(P= 0 .001) .Id1 protein was not correlated with sex and age(P>0 .05) ,but was correlated with clinical stage ,LDH level and extranodal infiltration(P<0 .05) .The expression of Id1 genes in mar‐row cells in DLBCL was higher than in RH (Id1mRNA level 2 .80 ± 0 .87 vs .1 .37 ± 0 .51 ,P<0 .05) ,and also correlated with clini‐cal stage ,LDH level and extranodal infiltration(P<0 .05) .Conclusion The expression of Id1 proteins and genes are much higher in DLBCL tissue and marrow and probably related to the prognosis of DLBCL .This discovery would contribute to predicting prognosis of DLBCL ,w hich also could be a therapeutic target of DLBCL in the future .

Traditional Tibetan medicine nature theory was the core of Tibetan medicine. This study was aimed to understand the scientific values of Tibetan medicine correctly and catch its unique advantages accurately. The history origin, nature and taste, target, effect, the relationship between diseases and Tibetan medicine and other aspects of traditional Tibetan medicine nature theory were discussed in this paper. Several points were put forward, which included the research of Tibetan medicine nature theory was the premise to maintain and develop Tibetan medicine; it was necessary to carry out literature research, definite and improve the nature theory; the data mining technology and systems biology should be applied to the theory research to elucidate the rules and scientific connotation of Tibetan medicine nature; building the model of experimental study with clinical research to determine its clinical values forward during the development of Tibetan medicine nature theory research.

Meridians in human body were classified as white meridian and black meridian according to Tibetan medicine.Season and environment,improper diet,toxic heat and trauma were recognized as main reasons damaging the white meridian in Tibetan Medicine,leading to the emerge of white meridian disease induced by Long (one of the three factors) and blood disorder.White meridian disease in Tibetan medicine involved a series diseases,such as many clinical diseases,due to the damage of white meridian system caused by pathogenic factors.Stroke also belonged to white meridian disease.Drugs and treatments were selected based on the nature of disease such as cold and heat,onset,thelocation of disease and the three factors (Chi Ba,Long and Pei Gen).It was the fundamental principle of the treatment rules of white meridian disease in Tibetan medicine,namely,prescribing medication with the rule of diagnosis and treatment,comprehensive analysis of the causes of diseases and mastering the change law of diseases and syndromes in clinic.

Diffuse large B-cell lymphoma(DLBCL)is more common in the elderly,who often exhibit a poor treatment response,more ad-verse reactions to chemotherapy,and significant inter-individual differences.There is currently no optimal treatment regimen,and the over-all prognosis for elderly patients with DLBCL is poor.The R-CHOP regimen(consisting of rituximab,cyclophosphamide,vincristine,doxorubi-cin,and prednisone)is the standard first-line therapy for DLBCL;however,some elderly patients find it difficult to tolerate.Various treat-ment plans to date have been explored for this specific group,including reducing R-CHOP use,combining R-CHOP with novel drugs,or utiliz-ing new drug combinations.These approaches have achieved varying degrees of success.As the number of treatment options increases,in-dividualized therapy is chosen according to patient age,general physical condition,and comorbidities as well as pathological characteristics of the disease.The key to improving prognosis lies in the early selection of an appropriate treatment plan to enhance remission and reduce recurrence rates.

OBJECTIVETo explore the effect and mechanism of rosuvastatin on tumor necrosis factor-α induced human mesenchymal stem cells (MSCs) apoptosis.

METHODHuman MSCs were treated as follows: (1) culture medium; (2) TNF-α (20 µg/ml) for 6 h; (3) rosuvastatin (20 µmol/L) for 24 h; (4) rosuvastatin (20 µmol/L) for 24 h followed by TNF-α (20 µg/ml) for 6 h; (5) TNF-α+rosuvastatin+50 nmol/L antago-miRNA; (6) TNF-α+rosuvastatin+100 nmol/L antago-miRNA. Cell survival and apoptosis were determined by MTT, TUNEL and caspase-3 activity assay. The changes of miRNA-210 in each group were detected with quantitative PCR.

RESULTTNF-α significantly induced human MSCs apoptosis in a concentration-dependent manner, and pretreatment with rosuvastatin significantly reduced MSCs apoptosis (caspase-3 assay: TNF-α+Statin group vs. TNF-α group: (1.63 ± 0.25) vs. (2.05 ± 0.36), P < 0.05). Meanwhile, TNF-α progressively reduced the expression of miRNA-210 in human MSCs in a dose-dependent manner, while the miRNA-210 expression was significantly upregulated in TNF-α+Statin group (P < 0.05). The protective effect of rosuvastatin on TNF-α induced MSCs apoptosis was largely abolished by co-treatment with 100 nmol/L antago-miRNA (TUNEL:TNF-α + Statin + antago-miR group vs. TNF-α + Statin group: (42.58 ± 6.71) % vs. (16.87 ± 9.27) %, P < 0.05).

CONCLUSIONPretreatment with rosuvastatin can significantly improve the viability of human MSCs after TNF-α injury, the protective mechanism of rosuvastatin is partly mediated through miRNA-210 up-regulation.

Apoptosis ; drug effects ; Caspase 3 ; Cell Survival ; Fluorobenzenes ; pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Mesenchymal Stromal Cells ; drug effects ; MicroRNAs ; pharmacology ; Pyrimidines ; pharmacology ; Rosuvastatin Calcium ; Sulfonamides ; pharmacology ; Tumor Necrosis Factor-alpha ; drug effects ; Up-Regulation

Unlike healthy, non-transformed cells, the proteostasis network of cancer cells is taxed to produce proteins involved in tumor development. Cancer cells have a higher dependency on molecular chaperones to maintain proteostasis. The chaperonin T-complex protein ring complex (TRiC) contains eight paralogous subunits (CCT1-8), and assists the folding of as many as 10% of cytosolic proteome. TRiC is essential for the progression of some cancers, but the roles of TRiC subunits in osteosarcoma remain to be explored. Here, we show that CCT4/TRiC is significantly correlated in human osteosarcoma, and plays a critical role in osteosarcoma cell survival. We identify a compound anticarin-β that can specifically bind to and inhibit CCT4. Anticarin-β shows higher selectivity in cancer cells than in normal cells. Mechanistically, anticarin-β potently impedes CCT4-mediated STAT3 maturation. Anticarin-β displays remarkable antitumor efficacy in orthotopic and patient-derived xenograft models of osteosarcoma. Collectively, our data uncover a key role of CCT4 in osteosarcoma, and propose a promising treatment strategy for osteosarcoma by disrupting CCT4 and proteostasis.