; 3. therapy with A&A (A&A); 4. Astragali alone (A); 5. Astragali polysac-charide Ⅰ (APⅠ); 6. AP Ⅱ ; 7. Astragali glucoside (AG), Results The level of serum albumin,albumin mRNA and albumin gene transcription were measured by biochemistry, Northern blot hybridization, nuclear run-on assay and quantity in laser density screening. The level of serum albumin in N was significantly lower than C. The serum albumin concentration in each therapy group was higher than N group. The transcription of the albumin gene was higher in N than in C and highest in A&A. The alterations of northern blot hybridization were same as the transcription results. But both the level of albumin mRNA and the transcription of albumin gene in A, AP I , AP I and AG were no change compared with N. Conclusion A&A increases albumin mRNA expression at least in part by improving the rate of gene transcription, which participate the protection of the decrease of serum albumin in NS. But the effect of A, AP 1 , AP I and AG may mediated by other unknown mechanisms.

Objective To assess the efficacy of a long-pulsed 1064 nm Nd :YAG laser system in treating pediatric cutaneous hemangiomas. Methods 207 patients (20 days-10 years old,164 cases in pro-liferative phase and 43 in stationary phase) with cutaneous hemangiomas were divided into 2 groups ac-cording lesions. Group A contained 142 patients with lesions located in skin completely. Group B con-tained 65 patients, in which the lesions involved in subcutaneous portion. All patients were treated with single pulse shots by a long-pulsed 1 064 nm Nd :YAG laser, with 2 mm and 6 mm spot size in diameter, and with related energies from 50 to 90 J/cm~2 and pulse lengths of 10, 40 and 60 ms, respectively. All treatments were given at 1-month interval. Results After 1-6 times of treatment, there was no statistic significance of effective rate between group A and group B. Both general effective rates were 100%. The rate of side effects was 11.6 %, all of which recovered gradually. Conclusions The long-pulsed 1064 nm Nd : YAG laser offers efficient treatment of pediatric superficial cutaneous hemangiomas and side effects are minimal and transient.

ING1 family is a candidate for tumor suppressor,which has three splicing isoforms named p47ING1a,p33ING1b,and p24ING1c. Study of the effect of different isoforms of ING1 on HeLa cells proliferation and its molecular mechanism would help further identifying the functional relationship of ING1 isoforms,and finding important genes regulated by ING1. Cell growth curve and cell cycle analysis were used to observe the effect of ING1a,ING1b,and ING1c on HeLa cells growth,and the result indicated that they could all inhibit HeLa cells growth by arresting cell cycle at G0/G1 phase. PCR method was used to construct the PHD domain deletions of ING1a and ING1b. ING1a,ING1b,ING1c and the PHD domain deletions 1a?C and 1b?C were then overexpressed in HeLa cells. p16INK4a,PTEN/p27Kip1 and p53/p21Waf1 protein levels were detected by Western blot. The result showed that ING1a,ING1b,ING1c,and 1a?C except for 1b?C induced p16INK4a protein expression,in which ING1c had the most powerful effect. Luciferase assay identified that overexpression of pcDNA3.1(+)-1a?C facilitated p16INK4a transcription through enhancing p16INK4a promoter activity,while pcDNA3.1(+)-1b?C repressed the p16INK4a promoter activity . In a word,it was found for the first time that except for the p53/p21Waf1 pathway,three splicing isoforms of ING1 family could also inhibit HeLa cells proliferation though upregulation of p16INK4a and PTEN,and the PHD domain deletion of ING1a enhanced p16INK4a transcription. These findings provide new clews to further study on the mechanisms of ING1 family suppressing cancer cells growth.

Objective To investigate the effects of ?-2-macroglobulin on the aging process of human diploid fibroblasts. Methods pIRES-A2M sense and antisense vectors were constructed and transferred into 2BS cells mediated by lipofectamine.2BS/A2Ms and 2BS/A2Ma cell lines were verified by Southern and Northern blot analysis respectively.Cell growth curve,the population doublings,cell cycle analysis,staining of senescent-associated-?-galactosidase and expression of p16 and p21 in transfected cells were measured. Results Southern and Northern blot analysis verified that the exogenous cDNAs were integrated into genomic DNA in the transfected cells.The ultmost population doublings of 2BS/A2Ms cells were slightly higher than normal 2BS cells.Cell growth curve,cell cycle analysis,staining of senescent-associated-?-galactosidase and the population doublings all revealed that 2BS/A2Ms cells demonstrated obvious difference compared with 2BS/A2Ma cells((P0.05). Conclusions The aging process of 2BS cells is influenced slightly by expression of A2M.

OBJECTIVETo reveal the role of Phosphatidylinositol 3-kinases (PI3Ks) in regulating human diploid fibroblast (2BS cell) senescence as well as the possible mechanisms involved.

METHODSUsing a PI3Ks specific inhibitor, LY294002, cell cycle, apoptosis, proliferation, senescence association beta-galactosidase staining as well as senescence association CKIs, p16(INK4) and p21(Cip1) protein expressions were all measured in the low passages of 2BS cells.

RESULTSBoth 25 micro mol/L and 50 micro mol/L concentrations of LY294002 could cause a significant decrease in cells entering into S phase, and this cell cycle of G(1) phase arrest was dose-dependent. Meanwhile, LY294002 contributed to apoptosis, caused 2BS cell growth arrest, and activated senescence association beta-galactosidase (P < 0.05). In addition, LY294002 could induce time-course expressions of p16(INK4) and p21(Cip1) in 2BS cell lines.

CONCLUSIONSPI3Ks inhibitor LY294002 could induce senescence-like changes in 2BS cell lines. Two senescence associated CKIs, p16(INK4) and p21(Cip1), might be involved in this senescence phenotype proceeding in 2BS cell lines.

Cells, Cultured ; Cellular Senescence ; drug effects ; Chromones ; pharmacology ; Cyclin-Dependent Kinase Inhibitor p16 ; analysis ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins ; analysis ; Dose-Response Relationship, Drug ; Enzyme Inhibitors ; pharmacology ; Fibroblasts ; drug effects ; physiology ; G1 Phase ; drug effects ; Humans ; Morpholines ; pharmacology ; Phosphatidylinositol 3-Kinases ; antagonists & inhibitors