BACKGROUND:For the treatment of osteoporosis, clinicians general y focus on improving bone mineral density and reducing the incidence of fractures, but often ignore the ease of osteoporotic chronic pain.
OBJECTIVE:To review the research progress in osteoporotic chronic pain from domestic and overseas literature in recent years in order to provide reference for basic and clinical research.
METHODDatabases of PubMed and Wanfang database were retrieved with key words of“osteoporosis;chronic pain;treatment of osteoporotic;vertebral compression fracture”in English and Chinese to search papers published from March 1999 to March 2014. Articles related to characteristics, pathogenesis and drug treatment of osteoporotic chronic pain as wel as surgical treatment of osteoporotic vertebral compression fractures. Final y 49 articles were summarized according to inclusion criteria.
RESULTS AND CONCLUSION:The pathogenesis of osteoporotic chronic pain includes congestion mechanism and mechanisms of cytokines and lactic acid accumulation, but its exact cytological and biochemical mechanisms are not very clear. Commonly used drugs in the treatment of osteoporotic chronic pain include calcitonin and bisphosphonates. Calcitonin plays an analgesic effect by inhibiting bone resorption to indirectly reduce the hydrogen ion concentration, suppress prostaglandin synthesis, improve animal pain threshold, and increase the plasma concentration of beta-endorphin. The main pharmacological action of bisphosphonate is to inhibit osteoclast formation and activity, inhibit bone absorption, improve osteoporotic bone pain, improve bone mineral density, increase bone strength, and prevent osteoporotic fracture. Benign and malignancy tumor of the spine and osteoporotic spinal compression fractures can be treated with percutaneous vertebroplasty or percutaneous kyphoplasty. After treatment, the vertebral height can be restored completely or partial y, the kyphosis is corrected, the vertebral stability is increased and pain is relieved. Combination of various treatments is effective for the treatment of osteoporotic chronic pain, and meanwhile, the prevention and treatment of osteoporotic fractures has a positive role in prevention and treatment of osteoporotic chronic pain.

Objective To observe the impacts of valsartan combined with amlodipine or hydrochlorothiazide regimen on blood pressure variability (BPV) in elderly hypertensive patients.Methods Eighty elderly patients with hypertension were randomized into valsartan and amlodipine (the amlodipine group, n=38) or valsartan and hydrochlorothiazide (the hydro-chlorothiazide group,n=37) group.The 24-hour dynamic blood pressure was monitored at baseline, 6-week and 12-week after treatment for the blood pressure and blood pressure variability. The control rate of blood pressure was calculated at 6-week after treatment, and side effects were observed during the treatment.Results Values of 24 h systolic blood pressure (SBP), daytime SBP, nighttime SBP, morning SBP and 24 h systolic blood pressure variability (SBPV) were significantly low-er at 6-week and 12-week than those of baseline in both two groups(P<0.05). There was an interaction between the group-ing factors and time on 24 h SBP, daytime SBP, nighttime SBP, 24 h SBPV and daytime SBPV (P<0.05). At the 6 and 12-week treatment, 24 h SBP, daytime SBP, nighttime SBP and daytime SBPV were significantly lower in amlodipine group than those in hydrochlorothiazide group (P<0.05). At 12-week treatment, 24 h SBPV was significantly lower in amlodipine group than tjat in hydrochlorothiazide group (P<0.01). There were no significant differences in control rate of blood pressure and side effects between two groups. Conclusion Valsartan in combination with amlodipine or hydrochlorothiazide can both ef-fectively control BPV in elderly hypertensive patients, and valsartan conbined with amlodipine has better effects on lowering blood pressure and BPV.

Cell-cycle deregulation leading to excessive cellproliferation is an important mechanism of human tumorigenesis. CDK6 and CDK4 have been found to be significant regulators of cellcycle, particularly in promoting cell -cycle progress. Moreover, these proteins are usually overly active in most tumors and closely related to tumor development. Recently, research has confirmed CDK4/6 as prospective targets for cancer therapy. However, the mechanism of excessive CDK6 activation leading to tumorigenesis is not completely understood. Therefore, further understanding of the role of CDK4/6 in cell -cycle regulatory pathways and celldifferenti-ation is essential, as well as their overexpression in different types of tumors. This information will elucidate the mechanisms of tumor development and treatment. Therefore, this review intends to discuss the structure and biological function of CDK6, the role and mecha-nism of CDK6 in carcinogenesis, and the clinical application of CDK6 inhibitors.

Background and purpose:Inhibitor of apoptosis-stimulating protein of p53 (iASPP) is one of the ASPP family. It binds to p53 to inhibit the transcriptional activity of p53-target genes and cell apoptosis, which is asso-ciated with tumor formation. Previously, we found a new subtype of iASPP, iASPP splice variant (iASPP-SV), which is a nuclear protein containing 407 amino acid residues and can bind to p53, inhibiting p53 transcriptional activity. However, the relationship of iASPP-SV and breast cancer is still obscure. Therefore, the purpose of this research was to study the role of iASPP-SV on breast cancer tumorigenesis and progression.Methods:5’-rapid ampliifcation of cDNA ends (RACE) was used to identify the 5’-end of iASPP-SV mRNA in MCF-7 cells. HEK 293 cells were transfected with pFLAG-iASPP-SV and pFLAG-iASPP (828). Then Western blot was used to identify whether endogenous iASPP-SV was expressed in HEK 293 cells and 8 types of human tumor cell lines. This study established the stable clones of NIH 3T3 expressing FLAG-iASPP-SV and FLAG-iASPP (828). Cell proliferation assay, colony formation and soft agar colony formation assay were used to identify whether iASPP-SV and iASPP (828) can promote cell proliferation and iASPP-SV is an oncogene. Real-time lfuorescent quantitative polymerase chain reactive (RTFQ-PCR) was used to de-tect the levels of iASPP-SV and iASPP (828) mRNA in primary breast cancers. Luciferase assays were used to identify the relationships between iASPP-SV, iASPP (828), p53 and NF-κB p65.Results:The study identiifed that iASPP-SV was encoded by previously reported NF-κB p65 subunit (RelA)-associated inhibitor (RAI), and endogenously expressed in many human cancer cell lines. Analysis of cell proliferation, colony formation assay and soft agar assay for colony formation identiifed that similarly to iASPP (828), iASPP-SV promoted tumor cell proliferation and acted as an onco-gene. RTFQ-PCR result showed that the median values of iASPP-SV and iASPP (828) in breast cancers with wild-type p53 were more signiifcantly over-expressed than those of mutant p53. Luciferase assays showed that iASPP-SV and iASPP (828) could suppress NF-κB p65 transcriptional activity. Thus iASPP family may participate in the regulation of p53 and NF-κB activity, which imply that iASPP perhaps shows pro- or anti-survival activities when it interacts with different proteins.Conclusion:These ifndings indicate that iASPP-SV may be a potential target for breast cancer thera-py.

Objective:To study the role of FDCs-miR-548m-CDK6 axis on clonogenicity in mantle cell lymphoma. Methods:RT-qPCR and Western blot were used respectively to test the expression of miR-548m and CDK6. Bioinformatics assay was applied to predict the targets of miR-548m, and Western Blot was used to test the expression level of CDK6 after miR-548m overexpression or in-hibition. Luciferase report assay was performed to test whether CDK6 was a direct target of miR-548m. Colony forming assay was used to test the colony forming activity in MCL after overexpression of miR-548m or knockdown of CDK6. Results:Cell adhesion to FDCs induced downregulation of miR-548m and CDK6 expression in MCL. Bioinformatics assay revealed that miR-548m could target the 3'-UTR of CDK6 and that a negative correlation exists between the level of miR-548m and the CDK6 expression. Luciferase report as-say confirmed that miR-548m directly targeted 3'-UTR of CDK6. Colony forming assay showed that overexpression of miR-548m or knockdown of CDK6 significantly suppressed MCL colony formation. Conclusion:This study reveals that FDC-enhanced mantle cell lymphoma clonogenicity is mediated by the miR-548m/CDK6 axis.

Objective To investigate the different distribution of regulatory T cells (Tregs) and CD8+T cells in the local immune microenvironment of mucosal malignant melanoma and cutaneous malignant melanoma, and analyze the relationship between the two indicators and the prognosis of patients. Methods Immunohistochemistry staining was used to assess the ex?pression of Foxp3+Tregs and CD8+T cells in tumor microenvironment of 58 patients with malignant melanoma. The correlation between two factors, clinicopathological characteristics, and prognosis were analyzed. Results There is no correlation be?tween the expression of Foxp3 and CD8. The number of Foxp3+Tregs was significantly higher in mucosa malignant melanoma than that in cutaneous malignant melanoma (t=2.648, P=0.011). The proportion of Foxp3highTregs was significantly higher in pa?tients with tumor diameter≥3 cm, lymph node metastasis and distant metastasis than that in patients with tumor diameter<3 cm, no lymph node metastasis and no distant metastasis (P<0.05). In addition, in patients with ulceration that proportion was significantly higher in CD8high group than that in patients without ulceration (33.3%vs 5.9%, P<0.05). The median progres?sion-free surial (PFS) was 12 months in Foxp3high group, which was significantly longer than that of Foxp3low group (31 months, P<0.05). The median PFS was significantly higher in CD8high group (25 months) than that of CD8low group (12 months, P<0.05). Subgroup analysis showed that the median PFS was 7 months in Foxp3high CD8low group, which was significantly lower than that of Foxp3highCD8high group (25 months) and Foxp3lowCD8low group (18 months, P=0.003). Univariate analysis showed that median PFS was different in patients with different tumor location, different number of Foxp3+Treg, different number of CD8+T cells, and distant metastases. Conclusion The number of Tregs is closely associated with metastasis in patients with malig?nant melanoma. Compared with cutaneous malignant melanoma, our results indicate that the poor prognosis of mucosal malig?nant melanoma may be associated with the infiltration of more Tregs.

Objective To explore the clinico-biological characteristics, treatment and prognosis of salivary duct carcinoma. Methods This study included 12 cases of salivary duct carcinoma treated in our hospital. Clinical data were retrospectively analyzed for patients admitted between April 1995 and October 2006. The clinical characteristics, histological features, imaging, therapy methods and prognosis were analyzed. Results Of 12 salivary duct carcinoma, there were 10 males, 2 females. The age of onset ranged from 53 to 73 year old and the average was 56 year old. Physical examination revealed a firm and unboundary mass accompanied by nerve infiltrating symptom. The histological appearance was characterized by solid cell nests with ductal structures and central comedonecrosis. Extensive resection and radical neck dissection was performed in 11 patients, postoperation radiation done in 10 patients and chemotherapy in 3 patients. One year survival rate was 83. 33% , that of 3 years was 41. 67% , and of 5 years was 25. 00% , the median survival time was 36 months. Conclusion Salivary duct carcinoma is a rare malignant salivary tumor and most patients are men. Regional extensive resection and postoperative radiation or chemotherapy are the mainstay of therapy. Lymph node metastases in level Ⅰ ,Ⅱ , Ⅲ are a common finding in patients with SDC and the prognosis is poor.

Objective To study the single nucleotide polymorphisms (SNPs) in IL-23R gene in Chinese Han population with ankylosing spondylitis (AS). Methods SNPs rs11209026, rs1343151, rs11209032 and another three SNPs near them based on their physical distances were genotyped by PCR-directed sequencing. Hardy-Weinberg equilibrium, genotypes and allele frequency analysis were analyzed by SPSS 13.0. Linkage disequilibrium and haplotype analysis were carried out by SHEsis software. Results The difference of genotypes of rs11209032 and the difference of genotypes and allele frequencies of rs6677188 between patients and controls were statistically significant (P＜O.01) ; The two SNPs rs11209032 and rs6677188 had strong linkage disequlibfium (D'=0.925, r2=0.561 ). Haplotype analysis had shown a higher proportion of GAC haplotype in patients and a higher proportion of GTC haplotype in controls. Conclusion These results suggest that IL-23R polymorphisms is associated with susceptibility to AS in Chinese Han population and IL-23R gene may be a susceptible gene of AS.

OBJECTIVE:To study the inhibitory effects of propolis on growth of transplantation tumor in mice.METHO_ DS:Using different concentrations of propolis to feed the mice for two months,the tumor cells(S 180 )were transplanted into subaxillary tissue of the mice.After8days,the tumor mass was takent off the body of the mice,and weighted,then paraffin sections were observed and the number of karyokinesis of tumor cells was counted under the microscops.RESULTS:The weight of tumor mass were lighter in the propolis group than in the control group(P

Background The data on the prognostic values of high sensitivity C-reactive protein (hsCRP) levels in patients with advanced symp-tomatic heart failure (HF) receiving cardiac resynchronization therapy (CRT) are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP (>3 mg/L) prior to CRT was associated with a significant 2.39-fold increase (P=0.006) in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels (–0.5 ± 4.1 mg/L reduction) compared with non-responders (1.7 ± 6.1 mg/L increase, P=0.018). Com-pared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations (Log-rank P<0.001). The echocardio-graphic improvement was also better among patients in whom 6-month hsCRP levels were reduced or remained low compared to those in whom 6-month hsCRP levels were raised or maintained high. Conclusions Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.