AIMTo study the characteristic pattern of the age-related growth of the human prostate gland.

METHODSThe volume (weight) of the prostate in 1,601 males, aged from newborn to 92 years, was determined by B-ultrasonography.

RESULTSProstatic volume determination by B-ultrasonography in 1601 males (1301 normal subjects and 300 BPH patients) pointed out that the age-stratified growth of human prostate could be categorized into 4 life stages: (1) the first slow growing phase (from newborn to 9 years): the prostate grows slowly at a rate of 0.14 g per year; (2) the first rapid growing phase (from 10 to 30 years): the prostate grows at a rate of 0.84 g per year; (3) the second slow growing phase (from 30 to 50 years), the prostate grows at a rate of 0.21 g per year; (4) the second rapid growing phase (from 50 to 90 years): the prostate grows at one of the following rates: in one group the growth rate is of 0.50 g per year and in the other 1.20 g per year, leading to benign prostatic hyperplasia (BPH).

CONCLUSIONThe volumes of the prostate are different in different age groups and it grows with age at different rates in four life phases. The prostate growth in phases can be expressed by the following equation: Y=19.36+1.36X'-0.58X'(2+0.33X'3), where Y = prostate volume, X = age (up to 70 years), X'=(X-35.5)/10.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Aging ; Child ; Child, Preschool ; Humans ; Infant ; Infant, Newborn ; Male ; Middle Aged ; Organ Size ; Prostate ; anatomy & histology ; diagnostic imaging ; growth & development ; Ultrasonography

Objective To study the efficacy and safety of T-614 in treating rheumatoid arthritis(RA). Methods Two hundred and eighty patients with active RA were randomly allocated to 3 groups:T-614 50 mg each day,25 mg each day or placebo.Clinical and laboratory parameters were analyzed at baseline,2,4,6,12, 18 and 24 weeks.Results The ACR response rate was significantly higher in the T-614 treatment group com- pared with the placebo group during the first 6 weeks.After 24 weeks,25 mg/d,50 mg/d dosage group and the placebo group showed 39.1%,61.3% and 24.2% in ACR20,23.9%,31.2% and 7.4% in ACR50 respectively.A time-response in ACR response after 24 weeks was observed,with clear superiority of the 25 mg/d and 50 mg/d dosage groups compared to the placebo,and 50 mg/d dosage group compared to 25 mg/d dosage group(P

OBJECTIVEThis paper is to investigate the effects of steroid or IFN alpha-2b on apoptosis and cell pathway of fibroblasts from keloids, hypertrophic scars and normal skins and different responses of different fibroblasts.

METHODS6 samples from keloid, hypertrophic scar and normal skin were collected respectively and fibroblasts from different sources were cultured in vitro. After different fibroblasts were treated with dexamethasone (0.1 mg/ml) or IFN alpha-2b (1000 U/ml), Bax and Bcl-2 protein expressions were detected in situ by immunohistochemical staining; DNA ladders of different fibroblasts were observed by gel electrophoresis; and relative activated (phospho-) ERK1/2 and JNK pathways were detected by method of FACE ELISA.

RESULTSDexamethasone could induce apoptosis of fibroblasts from keloids, hypertrophic scars and normal skins through activating (phospho-) ERK1/2 and JNK pathways; IFN alpha-2b could not induce apoptosis of fibroblasts from different sources. IFN alpha-2b could inhibit (phospho-) ERK1/2 pathway and could not affect (phospho-) JNK pathways of fibroblasts from keloid and hypertrophic scar. IFN alpha-2b could affect neither (phospho-) ERK1/2 pathway nor (phospho-) JNK pathways of fibroblasts from normal skin.

CONCLUSIONSThe responses of different fibroblasts to steroid or IFN alpha-2b were different.

Adult ; Apoptosis ; drug effects ; Cells, Cultured ; Cicatrix, Hypertrophic ; chemically induced ; metabolism ; pathology ; Female ; Fibroblasts ; metabolism ; pathology ; Hormones ; pharmacology ; Humans ; Interferon-alpha ; pharmacology ; Keloid ; chemically induced ; metabolism ; pathology ; Male ; Middle Aged ; Recombinant Proteins ; Signal Transduction

OBJECTIVETo evaluate the effect of capsaicin on nude mice xenografted with colorectal carcinoma cells, and to explore its mechanism of action.

METHODSA nude mouse model of colorectal cancer was established by subcutaneous inoculation of human colorectal carcinoma HT-29 cells. Terminal deoxynucleotidyl transferase-mediated nicked labeling assay (TUNEL) was undertaken to detect the cell proliferation and apoptosis in the xenograft tissue in nude mice. Immunohistochemical (IHC) staining and Western blot were used to detect the expression of HSP27, Cyt-C and active caspase-3.

RESULTSThe tumor growth of the groups C10 and C20 was significantly slower than that of the group NS. The integrated optical density (IOD) of both the group C5 (2532.14 ± 578.11) and group C10 (6364.03 ± 1137.98) was significantly higher than that of the group NS (760.12 ± 238.05), (P < 0.05). The integrated optical density (IOD) of the group C20 was (15743.96 ± 1855.95), significantly higher than that of the groups C10, C5 and NS (all were P < 0.01). Immunohistochemistry showed that the cytoplasmic expression of HSP27 was strongly positive in the group NS, and significantly reduced with the increasing dose of capsaicin in the treated groups. The expression of active caspase-3 and Cyt-C in the group NS was weakly positive, and was significantly increased with the increasing dose of capsaicin in the groups C5 and C10 (P < 0.05), and the expression of active caspase-3 and Cyt-C of the group C20 was significantly higher than that of the groups C5, C10 and NS (P < 0.01). Western blot analysis showed that both the expressions of HSP27 of the group C5 (0.73 ± 0.05) and the group C10 (0.41 ± 0.03) were significantly lower than that of the group NS (P < 0.05). The expression of HSP27 of the group C20 (0.22 ± 0.06) was significantly lower than that of the groups C5, C10 and NS (P < 0.01). The expressions of active-caspase-3 and Cyt-C in the group C5 were (2.57 ± 0.34) and (2.03 ± 0.38), significantly higher than those of the group NS (P < 0.05). The expressions of active-caspase-3 and Cyt-C in the group C10 were (4.23 ± 0.45) and (3.13 ± 0.44), also significantly higher than those of the group NS (P < 0.05). The expressions of active-caspase-3 and Cyt-C in the group C20 were (5.78 ± 0.48) and (4.92 ± 0.52), significantly higher than those of the group C5, C10 and NS (P < 0.01). TUNEL analysis showed that there was a significant difference of cell apoptosis in comparison of each two groups. The higher dose of capsaicin was used, the more apoptosis was observed.

CONCLUSIONSCapsaicin can significantly inhibit the tumor growth and induce cell apoptosis in the colorectal carcinoma xenograft in nude mice. Its mechanism of action is possibly related with the down-regulation of HSP27 expression and up-regulation of expression of active caspase-3 and Cyt-C in the colorectal carcinoma xenograft in nude mice.

Animals ; Antineoplastic Agents, Phytogenic ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Capsaicin ; administration & dosage ; pharmacology ; Caspase 3 ; metabolism ; Cell Proliferation ; drug effects ; Cytochrome c Group ; metabolism ; Dose-Response Relationship, Drug ; Female ; HSP27 Heat-Shock Proteins ; metabolism ; HT29 Cells ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Random Allocation ; Tumor Burden ; Xenograft Model Antitumor Assays

Objective:Study on the mechanism of Tongfengning in promoting uric acid excretion from the perspective of urate transporter and mRNA in renal of hyperuricemia （HUA） model rats. Method:The 80 sprague-dawley rats were randomly divided into two groups， the blank group with 20 rats and the model group with 60 rats. Rats in model group were established as hyperuricemia （HUA） models by intraperitoneal injection of oxonic acid potassium salt （OAPS） and intragastric administration ethambutol hydrochloride （EMB） once a day for 21 days. After successful modeling， rats in the model group were divided into the model group， Tongfengning group and benzbromarone group， with 20 rats per group. Tongfengning solution （15.3 g·kg^-1·d^-1） was administered to the Tongfengning group by gavage feeding. Rats in benzbromarone group were administered 5.2 mg·kg^-1·d^-1 benzbromarone suspension， whereas those in the blank group and the model group were administered the equivalent amount of normal saline for 21 days. On days 14^th and 21^st following intervention， urine， blood， and kidney were collected from rats， serum uric acid （SUA） and urinary uric acid （UUA） levels， blood urea nitrogenand（BUN） and creatinine（CRE） levels and the expression of urate transporter proteins and their mRNAs of all rats were detected by enzyme-colorimetric method， urease method， sarcosine oxidase method， Western blot and Real-time quantitative PCR（Real-time PCR）， respectively. Result:On days 14^th and 21^th following intervention， compared with blank group， SUA， CRE and BUN levels， and urate transporter 1（URAT1），glucose transporter 9（GLUT9） expression increased（P<0.05，P<0.01）， whereas UUA level， and adenosine triphosphate-binding cassette transporter protein G2（ABCG2）， organic anion 1（OAT1）， organic anion 3（OAT3） expression decreased in the model group（P<0.05，P<0.01）. Compared with model group， SUA， CRE and BUN levels， and URAT1， GLUT9 expression decreased in Tongfengning group and the benzbromarone group（P<0.05）， whereas UUA level， and ABCG2， OAT1， OAT3 expression increased（P<0.05）. Creatinine and BUN levels decreased in the Tongfengning group（P<0.05，P<0.01）， with the trend much better than the benzbromarone group（P<0.05）. On day 21^st， except for the BUN level did not change much compared with day 14^th， all the rest indicators got improved obviously. Conclusion:Intraperitoneal injection of OAPS and intragastric administration of EMB can cause HUA models with renal dysfunction. Tongfengning reduced URAT1， GLUT9 mRNA and protein expression， and upregulated ABCG2， OAT1， OAT3 mRNA and protein expression in the rat kidney， which may be one of the mechanisms of promoting uric acid excretion. Tongfengning has a certain protective effect on renal function.