The currently proposed factors inducing prostatic hyperplasia are the combined effect of androgen and estrogen and the reawakening of the embryonic growth potential of mature prostatic stroma. This experiment was designed to find out any histological or structural differences occurring after compensating sex hormones on the mature prostate and the implanted fetal urogenital sinus (UGS) tissue which possesses a differentiating potential under the same condition. The ventral lobe of the rat prostate with implanted fetal UGS showed 4.4 fold increase in weight compared to the non-implanted contralateral ventral lobe. After the castration, both ventral lobes showed marked atrophy, and no further progress in differentiation occurred in the implanted UGS. Dihydrotestosterone (DHT) compensation after castration revealed a significant increase in weight in the mature prostate but the ventral lobe with the implanted UGS showed relatively low recovery rate in weight than in non-castrated control group. The compensation of estradiol after the castration showed little difference in mature prostate compared to castrated control group, but the UGS implanted ventral lobe revealed a relative stromal hyperplasia. Unlike the single-hormone compensation, the mature prostate displayed the characteristic hyperplasia of epithelium of each acinar lumen, but the UGS dearly showed the formation of new acini with nodular pattern when compensated with both DHT and estradiol. The level of DHT showed a significant correlation with the height of the prostatic acinar cell which differentiated from the UGS, and an inverse correlation with the stroma/epithelium ratio of implanted group. The serum concentration of estradiol showed a significant correlation with the relative volume of juxta-prostatic tissues, such as the coagulating gland and the adjacent stroma. From the above results, it might be assumed that the estrogen may have an important role in the embryonic stroma-mediated initiation of nodular hyperplastic changes of microacini under the influence of DHT and the determination of histologic pattern after initiation might be controlled by the prostatic DHT concentration.
Acinar Cells ; Adult* ; Animals ; Atrophy ; Castration ; Compensation and Redress ; Dihydrotestosterone ; Epithelium ; Estradiol ; Estrogens ; Gonadal Steroid Hormones ; Humans ; Hyperplasia ; Mice* ; Prostate* ; Prostatic Hyperplasia ; Rats

No abstract available.
Animals* ; Brain* ; Hypothermia* ; Models, Animal*

No abstract available.
Animals* ; Brain* ; Hypothermia* ; In Situ Nick-End Labeling* ; Models, Animal*

Inadequate effectiveness of anticancer drug in treating renal cell carcinoma has been attributed to the overexpression of multidrug resistance gene (MDR1) and its product, membrane-bound P-glycoprotein. P-glycoprotein is known to actively pump out intracellular drug, which results in low intracellular anticancer drug concentration. Progesterone, which has been used in patients with advanced renal cell carcinoma is found to cause a three to four-fold increase in vinblastine accumulation in the P-glycoprotein-expressing murine macrophage-like cell line.We have studied to evaluate the MDR modulating action of medroxyprogesterone acetate (MPA) in renal cell carcinoma cell lines also with tamoxifen and verapamil. A-498 of a high mdrl expressed cell line and Caki-2 of a low mdrl expressed cell line were each placed in 96 multiwell plates. Vinblastine, in concentration from 0.01 ug/ml to 10 ug/ml was added to each well and verapamil, from 0.1 uM to 10 uM, MPA, from 2.5 uM to 25 uM, or tamoxifen, from 0.1 uM to 10 uM was also added. The in vitro chemosensitivity of two renal cell carcinoma cell lines (Caki-2 and A498) to vinblastine was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazol bromide(MTF) colorimetric assay. Growth of Caki-2 cells is inhibited by low doses of vinblastine(IC50: 0.27 ug/ml), but A-498 cells are highly resistant to the drug, with ICs0 value of 0.47 ug/ml. The chemosensitivity of the A-498 cells is increased in response to 5 uM MPA, 1 uM verapamil and 2 uM tamoxifen, which are known to partially reverse the MDR phenotype in other resistant tumors. The effective concentration of MPA for MDR reversal is in clinically achievable concentration but one of verapamil is not. The chemosensitivity of Caki-2 cells does not change according to MDR modulating agents. .MPA is an effective MDR modulating agents to enhance the cytotoxicity of vinblastine in renal cell carcinoma cell line showing P-glycoprotein expression. It suggests that combination therapy of MPA and vinblastine is better than monotherapy with MPA or vinblastine alone.
Carcinoma, Renal Cell* ; Cell Line* ; Drug Resistance, Multiple ; Genes, MDR ; Humans ; Medroxyprogesterone Acetate* ; Medroxyprogesterone* ; P-Glycoprotein ; Phenotype ; Progesterone ; Tamoxifen ; Verapamil ; Vinblastine*

Inadequate effectiveness of anticancer drug in treating renal cell carcinoma has been attributed to the overexpression of multidrug resistance gene (MDR1) and its product, membrane-bound P-glycoprotein. P-glycoprotein is known to actively pump out intracellular drug, which results in low intracellular anticancer drug concentration. Progesterone, which has been used in patients with advanced renal cell carcinoma is found to cause a three to four-fold increase in vinblastine accumulation in the P-glycoprotein-expressing murine macrophage-like cell line.We have studied to evaluate the MDR modulating action of medroxyprogesterone acetate (MPA) in renal cell carcinoma cell lines also with tamoxifen and verapamil. A-498 of a high mdrl expressed cell line and Caki-2 of a low mdrl expressed cell line were each placed in 96 multiwell plates. Vinblastine, in concentration from 0.01 ug/ml to 10 ug/ml was added to each well and verapamil, from 0.1 uM to 10 uM, MPA, from 2.5 uM to 25 uM, or tamoxifen, from 0.1 uM to 10 uM was also added. The in vitro chemosensitivity of two renal cell carcinoma cell lines (Caki-2 and A498) to vinblastine was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazol bromide(MTF) colorimetric assay. Growth of Caki-2 cells is inhibited by low doses of vinblastine(IC50: 0.27 ug/ml), but A-498 cells are highly resistant to the drug, with ICs0 value of 0.47 ug/ml. The chemosensitivity of the A-498 cells is increased in response to 5 uM MPA, 1 uM verapamil and 2 uM tamoxifen, which are known to partially reverse the MDR phenotype in other resistant tumors. The effective concentration of MPA for MDR reversal is in clinically achievable concentration but one of verapamil is not. The chemosensitivity of Caki-2 cells does not change according to MDR modulating agents. .MPA is an effective MDR modulating agents to enhance the cytotoxicity of vinblastine in renal cell carcinoma cell line showing P-glycoprotein expression. It suggests that combination therapy of MPA and vinblastine is better than monotherapy with MPA or vinblastine alone.
Carcinoma, Renal Cell* ; Cell Line* ; Drug Resistance, Multiple ; Genes, MDR ; Humans ; Medroxyprogesterone Acetate* ; Medroxyprogesterone* ; P-Glycoprotein ; Phenotype ; Progesterone ; Tamoxifen ; Verapamil ; Vinblastine*

Surgical tumor resection, most appropriately together with the affected organ, is the sole form of curative therapy in low-staged renal cell carcinoma. But the fact that about 30% of patients show distant metastases or regional lymph node metastases at the time of diagnosis of renal cell carcinoma indicates the urgent need for the development of an effective treatment modalities. Herein we report the preliminary result of chemo-immuno-hormonal(triple) combination therapy which consists of a-interferon, vinblastine and medroxyprogesterone acetate in 17 patients with metastatic renal cell carcinoma from June 1990 to June 1994. The patients received the treatment with the combination of alpha interferon(a-IFN: 6 million units IM three times a week), vinblastine(VBL: 3 mgN2 IV monthly) and medroxyprogesterone acetate(MPA: 600 mg IM twice a month) at least 6 cycles. Although almost all the patients tolerated the treatment a few patients were stopped the treatment when the general condition of the patient became poor in progressive disease The 5 of 17 patients showed partial response and one patient with lung and liver metastasis was resolved completely. The response rate was 35.3% after treatment and the survival rates for 6 month and 1 year were 70.6% and 47.1%, respectively. So the chemo-immuno-hormonal combination therapymight be an alternative safe modality and be able to prolong the survival duration in patients with advanced renal cell carcinoma.
Carcinoma, Renal Cell* ; Diagnosis ; Drug Therapy ; Humans ; Liver ; Lung ; Lymph Nodes ; Medroxyprogesterone ; Medroxyprogesterone Acetate ; Neoplasm Metastasis ; Survival Rate ; Vinblastine

By definition, PSAD is the serum PSA concentration divided volume of the gland, as determined from transrectal ultrasonography. If prostatic volume were the sole determinant of the serum PSA concentration, there would be no correlation between PSAD and age. We examined the relationships between serum PSA concentration, rostatic volume and age. Entry included 318 men over 40 years who have no clinical evidence of prostate cancer. The mean age of this study population was 65.2(range 40-89). The mean PSA was 3.94ng/ml and the mean prostate volume 36.4cc(range 11-120). 85 men(26.7 %) had volumes >20cc and levels >4ng/ml. When all entry included, the serum PSA concentration correlates directly with age (r=0.2, p<0.01). Based on linear regression analysis, the serum PSA concentration would increase approximately 2.7% per year. The prostatic volume correlates directly with age(r=0.3, p<0.01). Based on linear regression analysis, the prostatic volume would increase approximately 2.2% per year. Correlation between the prostatic volume and PSA was also significant(r=0.1, p<0.01). Based on linear regression analysis, an increase in prostatic volume of 1mL will, on the average, produce a corresponding increase of 3.2% in PSA. There was an increasing tendency of PSAD with age but statistically insignificant. The mean PSAD was 0.11 but 47men of 59 had >0.15 in levels 4-10ng/ml. In conclusion, the application of PSAD in clinical field should be taken into consideration seriously and interpretation of PSA should be include the corresponding variables such as age and prostate volume. The PSA velocity or age specific reference range for PSA can aid in the application of PSA.
Aging* ; Humans ; Linear Models ; Male ; Prostate* ; Prostate-Specific Antigen* ; Prostatic Neoplasms ; Reference Values ; Ultrasonography

PURPOSE: The Bard Bladder Tumor Antigen(BTA) test is a latex agglutination assay that qualitatively detects the presence of basement membrane degradation complexes in the urine when the bladder tumor cells invade and destruct an extracellular matrix, called basement membrane. We evaluated the clinical significance of BTA test in the diagnosis and follow-up of patients with bladder cancer by comparing it with bladder washing cytology. MATERIALS AND METHODS: The Bard BTA test was compaired to bladder washing cytology in 26 patients with bladder cancer(group l), 18 undergoing surveillance cystoscopy for previous bladder cancer(group ll), and 10 suffering from other urologic diseases except bladder cancer(group lll). RESULTS: Of the group l patients, 84.6% were correctly diagnosed with the Bard BTA test compared to 69.2% with bladder washing cytology, which is statistically significant(p < 0.05). There was no difference in sensitivity according to tumor grade and stage. There was a high positive rate in group ll and lll patients probably due to the degeneration of basement membrane by other conditions such as intravesical BCG or mitomycin instillation, infection, or prostate cancer. CONCLUSIONS: The Bard BTA test is a non-invasive, simple, rapid, inexpensive adjunct to cystoscopy, and superior to bladder washing cytology in sensitivity, but many false positive results were observed. Further clinical evaluation is warranted to determine whether the false positive results are true or the result of inadequate number of patients studied.
Agglutination ; Basement Membrane ; Cystoscopy ; Diagnosis* ; Extracellular Matrix ; Follow-Up Studies* ; Humans ; Latex ; Mitomycin ; Mycobacterium bovis ; Prostatic Neoplasms ; Urinary Bladder Neoplasms* ; Urinary Bladder* ; Urologic Diseases

No abstract available.
Angioplasty*

To evaluate the diagnostic value of color Doppler ultrasonography in prostatitis and benign prostatic hyperplasia (BPH), we have analysed the patterns of color Doppler image(CDI), expressed prostatic secretion (EPS) findings, quantitative changes of vascular flow and flow velocity parameters (FVP). Of 203 men, there were prostatitis 143 cases, nonprostatitis (prostatodynia) 36 cases, BPH 24 cases (among them 9 cases combined with inflammation). The quantitative criteria of flow were based on 3-point scale (grade 0-3) by Rickards or supplementary doppler spot count. The control group was nonprostatitis. 1) Compared with control group, prostatitis and all BPH had more grade 2-3 (respectively p=0.04, p=0.035) and 2) BPH with inflammation had flow increase to BPH without inflammation (p=0.025), but BPH without inflammation had no flow increase to control group (p =0.976). 3) Using the FVP, no significance was found in maximum flow velocity, mean flow velocity, pulsatility index or resistive index between prostate inflammation and control group. We suggest that CDI rather than FVP is primarily related to the inflammation degree, and BPH alone does not affect CDI grade. So CDI can be applied clinically for the monitoring of treatment response in prostate inflammation.
Humans ; Inflammation ; Male ; Prostate ; Prostatic Hyperplasia* ; Prostatitis* ; Ultrasonography, Doppler, Color