Thevascularendothelialprogenitorcellsareapopulationoffunctionalendothelialprecur sorsincirculatingblood ,whicharederivedfrombonemarroworcordblood .CD34+,Flk - 1+andACl33+ aretheirmolecularmarkers .Inthisreview ,thefunctionalcharacterizationofvascularendothelialprogenitor cellsisintroducedandtherelationshipbetweenvascularendothelialprogenitorcellsandangiogenesisinis chemiccardiovasculardiseasesisdiscussed .Thesedatamayofferafoundationforthedevelopmentofthera peuticangiogenesisforthepreventionandtreatmentofischemiccardiovasculardiseasesbytransplantationof vascularendothelialprogenitorcells .

Controlling serum phosphorus levels is critical in patients with renal failure. Currently phosphate-binding agents are widely used to reduce phosphate absorption in patients with end-stage renal disease. If possible, serum phosphorus level should be reduced without disturbing calcium homeostasis or increasing accumulation of potentially toxic elements. Aluminum hydroxide and traditional calcium-based phosphate binders are commonly used to control serum phosphorus level. Aluminum hydroxide can effectively lower serum phosphorus level, but aluminum can accumulates in the body and results in toxic effect. Traditional calcium-based phosphate binders tend to promote hypercalcemia and calcium overloading, and accelerate cardiovascular calcification. Therefore aluminum-free and calcium-free phosphate-binding agents have become the focus of study; however, agents like sevelamer hydrochloride and lanthanum carbonate are not widely used due to high price, although they are effective in controlling serum phosphorus level. New generation of phosphate binders, such as colestilan, nicotinic acid and magnesium salt, are cheaper than their previous counterparts, but their long-term effect still needs to be observed. This article summarizes the progress of non-calcium phosphate binders in treatment of end-stage renal diseases, hoping to help clinical drug usage.

Adult ; Female ; Gastritis ; therapy ; Humans ; Male ; Massage ; Middle Aged

[Objective]To study the role of nitric oxide on the degeneration of the cartilage endplate(CEP).[Method]Twenty-four New Zealand rabbits were divided into experiment and control groups.In the experiment group,the model of lumbar CEP degeneration was established by resection of all lumbar supraspinous and interspinous ligaments,excision of parts of zygapophysial joints and detachment of the posterior paravertebral muscles from lumbar vertebraes.Mechanical instability of the lumbar spine could induced the process of CEP degeneration.The X-ray examination of lumbar spine was examined by at 12,24 and 36 weeks with or without operation,respectively.Changes of the ultrastructure of CEP were also observed by scanning electron microscope(SEM) during this process,and the content of IL-1?,IL-6,TNF-? in the CEP were also detected during the periods.[Result]X-ray graph showed that the CEP calcified gradually with time increasing,and those of the experiment groups calcified more obviously than those of the control groups.The SEM showed that collagen fibers became thin,irregular and fissured and the content of proteoglycan decreased severely with the elapse of time.The changes in experiment groups were more obvious than those in control groups.The content of IL-1?,IL-6,TNF-? had a significant difference between the experiment groups and the control groups(P0.05).[Conclusion]It implies that inflammatary cytokin may play an important role in the development and progression of the degeneration of cartilage endplate.

Objective To perform PCR site-directed mutagenesis of nine novel PAH gene mutations (Y154H, R157I, Y206C, G247R, D282G, G346R, S349A, A389G, R400K) identified in northern Chinese and construct mutant recombinant plasmids of PAH gene. Methods 1) Every mutant recombinant plasmid was constructed according to the site of the mutation localized in functional domain of PAH gene and the related clinic phenotype of patients with the gene mutation. 2) Using the wild-type PAH expression vector as a templet, the mutant recombinant plasmids were directly amplified by PCR with Platinium Taq DNA polymerase and nine pairs of primers which were designed according to the human PAH cDNA sequence and the requirement for site-directed mutagenesis technology. 3) The positive strains were selected by Amp resistant test, PCR and restriction endonuclease analysis. The Mva Ⅰ, Mva Ⅰ, Hind Ⅲ, Rsa Ⅰ, Rsa Ⅰ sites exist in the sequences near the mutant sites of S349A, D282G, G247R, Y206C, Y154H, respectively, but not in the related sequence of wild-type PAH expression vector. Restriction endonuclease digestion could be directly used in identifying the mutant sites. However, the amplification created restriction site (ACRS) analysis was supplied in the followed identification of R157I, G346R, A389G, R400K. Finally the sequences of mutant recombinant plasmids of PAH gene were confirmed by DNA sequence analysis. Results Every sequence analysis showed that the mutant nucleic acids were introduced at the expected sites of PAH gene, suggesting that the mutant recombinant plasmids of PAH gene were constructed successfully. Conclusion PCR site-directed mutagenesis is accurate and highly efficient. The successfully mutagenized plasmids of PAH gene lay the foundation for the functional analysis of phenylalanine hydroxylase in mammalian cell system.

Objective To study the diagnosis and treatment of coincident vesical transitional cell carcinoma and prostatic cancer. Methods 8 cases of coincident vesical transitional cell carcinoma and prostatic cancer were evaluated clinically. Results All the 8 were diagnosed as vesical transitional cell carcinoma on cystoscopy and biopsy.Whereas on needle biopsy of the prostate,prostatic cancer was diagnosed in 7 and BPH in 1 but turned to be prostatic cancer on pathological study after cystoprostatectomy.4 patients underwent transurethral resection of the bladder cancer and bilateral orchiectomy with bladder instillation of MMC or BCG and oral flutamide for prostatic cancer.1 patient underwent partial cystectomy,bilateral orchiectomy and external radiotherapy for prostatic cancer.3 underwent radical cystoprostatectomy.2 cases were lost to follow up.In the other 6,3 survived less than 1 year because of wide metastasis.The other 3 have been followed up for 1.5 to 4.0 years,remained well and tumor free. Conclusions PSA detection together with rectal palpation,biopsy,transrectal ultrasonography and cystoscopy played the important role in the diagnosis of coincident vesical transitional cell carcinoma and prostatic cancer.Radical cytoprostatectomy yields a better outcome.

0 05) , repectively. Of all dementia, AD and VD accounted for 58 48% and 31 58%, respectively. The AD prevalence in female was higher than that in male( P 0 05). The prevalence of total dementia, AD and VD tended to increase with aging( P 0 05). The prevalence of dementia increased one fold every five year of age increasing. The prevalence of dementia and AD in illiterate group was higher than in educated people with elementary school level and above junior high school level ( P

Objective To evaluate intravesical instillation of mitoxantrone(MTZ) for the prevention of postoperative recurrence of bladder cancer. Methods Intravesical instillation of 12 mg MTZ dissolved in 50 ml normal saline and retained in bladder for 2 hours were given to bladder cancer patients postoperatively once a week for 8 weeks and subsequently once a month for 12 months.Kidney and liver function,blood counting,urinalysis and cystoscopy were taken periodically.The systemic and local reactions were recorded every time after the intravesical instillation. Results All of the 98 cases were followed up for 6 to 24 months with a mean of 13 months.The recurrence rate was 6.2%.There was no generalized side effect. Conclusions Intravesical instillation of MTZ was efficacious for the prevention of postoperative recurrence of superficial bladder cancer with safety and less side effect.So it can be widely used in such patients.

To observe whether there is an interaction between hepatitis virus B (HBV) and tumor suppressor p53, plasmid PCMVp53 was transfected or cotransfected with pCMVHBV a (wild type HBV) or PCMVHBV b (mutation type HBV) into the hepatoma cell line 7721 by phosphate calcium precipitation. Apoptosis cells were labeled by annexin Ⅴ FITC and detected by flow cytometry. Another experiment was performed by cotransfecting the cells with reporter plasmid p21 luc in each group mentioned above, then the luciferase activity was measured. The results showed that the cells transfected by pCMVp53 alone exhibited high luciferase activity and high apoptosis rate. Meanwhile, the luciferase activity and apoptosis rate were further higher in cells cotransfected by pCMVp53 and PCMVHBV a , but remained unchanged in cells cotransfected by PCMVp53 and PCMVHBV b. The results indicated that P53 could induce of 7721 cell apoptosis by activating p21 transcription, and such effect could be enhanced by HBV.

[Objective] To assess the outcomes of lumbar spinal pedicle subtraction osteotomy on single segment for correction of kyphosis in ankylosing spindylitis.[Methods]15 patients were treated with L2 or L3 pedicle subtraction osteotomy and internal fixation by pedicle screw system.All the patients underwent X-ray examinations in standing position before and after the operations.The angles in different part of the sagittal planes were measured and the preoperative and postoperative differences were compared.[Results]All the operations were well complete.The mean time of operations was 3h and the mean bleeding was 840 ml.The lumbar lordosis angle increase from(14.5?15.5)?to(48.4?11.9)?,the total spinal kyphosis angle and the thoracolumbar kyphosis angle improve from(36.1?14.7)?and(30.7?9.3)?to(0.2?14.2)?and(23.7?12.3)? respectively,the sacral slope increase from(12.0?12.7)?to(28.9?8.8)?,whereas thoracic kyphosis angle remained relative stable.[Conclusion]Lumbar spinal pedicle subtraction osteotomy on single segment is a satisfactory and reliable technique for correction of kyphosis in ankylosing spindylitis and the average correction of lumbar lordosis was 33.9?.