Seminal Vesicle Enlargement Research Articles

A Prospective Study to Evaluate Sexual Dysfunction and Enlargement of Seminal Vesicles in Sexually Active Men Treated for Benign Prostatic Hyperplasia by Alpha-blockers

To evaluate sexual dysfunction and enlargement of seminal vesicles in sexually active men who were treated by α1-blockers for benign prostatic hyperplasia and its possible clinical application. This is a prospective cohort study from January 2015 to December 2016. We enrolled sexually active men above the age of 40 years having moderate to severe lower urinary tract symptoms (LUTS). We excluded patients with a history of prostate surgery, suspicious digital rectal examination findings, a serum prostate-specific antigen of >4 ng/dL, and a history of medication with anticholinergic, cholinergic, and diuretic agents. Patients were divided into groups A, B, and C based on the prescription of silodosin 8 mg, tamsulosin 0.4 mg, or alfuzosin 10 mg orally once for LUTS and at 4 and 12 weeks. The mean age was 54.8 years (41-68 years). Twelve weeks of treatment with silodosin, tamsulosin, and alfuzosin resulted in a significant improvement in the total International Prostate Symptom Score and the quality of life score (P <.001). The baseline erectile function scores were 26.4, 27.6, and 28.1, and the baseline overall satisfaction (OS) (International Index of Erectile Function [IIEF]-OS) scores were 7.1, 8.3, and 8.6 among groups A, B, and C, respectively. After 12 weeks of α1-blockers, the IIEF-erectile function scores were 24.0, 24.7, and 26.2, and the IIEF-OS scores were 6.4, 7.8, and 7.9. All 3 groups demonstrated a statistically significant enlargement of seminal vesicles after 12 weeks' treatment, most significant in group A patients (7.65-14.11 cc, P <.001). Alpha-blockers as silodosin, tamsulosin, and alfuzosin are a safe and effective tool in benign prostatic hyperplasia for improving LUTS and the quality of life. Loss of seminal emission with alpha-blockers appears as the cause of seminal vesicle enlargement. The exact mechanism of these findings needs further clinical and experimental research.

Silodosin Causes Impaired Ejaculation and Enlargement of Seminal Vesicles in Sexually Active Men Treated for Lower Urinary Tract Symptoms Suggestive of Benign Prostatic Hyperplasia

To evaluate the sexual side effects including ejaculation after silodosin treatment in potent men with regular sexual activity, as well as possible alterations in seminal vesicle volume. Sexually active patients aged ≥ 40 years with moderate to severe lower urinary tract symptoms were enrolled prospectively. International Prostate Symptom Score (IPSS) and Quality of Life (QoL), International Index of Erectile Function (IIEF) questionnaire, ejaculation frequency, and seminal vesicle volumes measured by transrectal ultrasonography were determined at study entry, and silodosin 8 mg/d was prescribed for 4 weeks. Alterations in IPSS-QoL, all domains of IIEF, ejaculation frequency, seminal vesicle volumes, and patient-reported side effects were evaluated after silodosin treatment. Thirty patients were included, and mean age was 56.7 ± 6.9 years (44-70 years). IPSS-total, IPSS-storage, and IPSS-voiding subscores and QoL were significantly improved after treatment. Despite a slight decrease in erectile function domain of IIEF (26.7 ± 1.9 vs 22.9 ± 7.5; P <.05), no significant change was determined for orgasmic functions, sexual desire, intercourse satisfaction, and overall satisfaction. Ninety percent of patients (27 of 30) had impaired ejaculation, and seminal vesicles were significantly enlarged at the end of treatment (8.1 ± 6.4 vs 16.4 ± 8.2 cc; P <.001). Impaired ejaculation is a common problem for sexually active men treated with silodosin, and this may result in the slight decrease in erectile functions. Enlargement of seminal vesicles may represent for the loss of seminal emission and accumulation of seminal vesicle secretion. Further studies are required for better clarifying the effects of silodosin on sexual functions including ejaculatory functions.

Evidence of Late-Summer Mating Readiness and Early Sexual Maturation in Migratory Tree-Roosting Bats Found Dead at Wind Turbines

Understanding animal mating systems is an important component of their conservation, yet the precise mating times for many species of bats are unknown. The aim of this study was to better understand the details and timing of reproductive events in species of bats that die most frequently at wind turbines in North America, because such information can help inform conservation strategies. We examined the reproductive anatomy of hoary bats (Lasiurus cinereus), eastern red bats (L. borealis), and silver-haired bats (Lasionycteris noctivagans) found dead beneath industrial-scale wind turbines to learn more about when they mate. We evaluated 103 L. cinereus, 18 L. borealis, and 47 Ln. noctivagans from wind energy facilities in the United States and Canada. Histological analysis revealed that most male L. cinereus and L. borealis, as well as over half the Ln. noctivagans examined had sperm in the caudae epididymides by late August, indicating readiness to mate. Testes regression in male hoary bats coincided with enlargement of seminal vesicles and apparent growth of keratinized spines on the glans penis. Seasonality of these processes also suggests that mating could occur during August in L. cinereus. Spermatozoa were found in the uterus of an adult female hoary bat collected in September, but not in any other females. Ovaries of all females sampled had growing secondary or tertiary follicles, indicating sexual maturity even in first-year females. Lasiurus cinereus, L. borealis, and Ln. noctivagans are the only North American temperate bats in which most first-year young of both sexes are known to sexually mature in their first autumn. Our findings provide the first detailed information published on the seasonal timing of mating readiness in these species most affected by wind turbines.

Suppressive effects of the antiandrogen agent, chlormadinone acetate and the 5α-reductase inhibitor, dutasteride on prostate weight and intraprostatic androgen levels in rats

The objectives of this study were to investigate whether chlormadinone acetate (CMA, Prostal, CAS 302-22-7) more markedly decreased ventral prostate and seminal vesicle weights and exerted more beneficial effects on intraprostatic androgen levels than dutasteride (DUT, CAS 164656-23-9) in rats. Dose-dependent inhibiting effects on prostate and seminal vesicle enlargement were observed after the 14-day administration of CMA (30, 100 mg/kg/day) and DUT (0.3, 1 mg/kg/day). The prostate atrophy rates calculated as the percentages relative to the vehicle-treated group were 50.5 and 67.9% with 30 and 100 mg/kg CMA and 34.9 and 37.0% with 0.3 and 1 mg/kg DUT, respectively, and the atrophying effect of CMA was significantly greater than that of DUT (p < 0.05). The results of 7-day administration were similar to those of 14-day administration. While CMA dose-dependently and significantly (p < 0.05) reduced the testosterone (T) and dihydrotestosterone (DHT) concentrations in prostate, DUT reduced the DHT concentration but markedly increased the T concentration (20-40 times). Even though it was carried out in rats, this study revealed for the first time that the antiandrogen CMA showed a stronger atrophying effect than the 5alpha-reductase inhibitor DUT on direct comparison. The difference between the atrophying effects of CMA and DUT is considered to be attributed to the present results that CMA reduced the concentrations of both androgens (T and DHT) in prostate but DUT did not, and the fact that CMA has a potent androgen receptor-blocking action but DUT does not.

Systemic SIRT1 insufficiency results in disruption of energy homeostasis and steroid hormone metabolism upon high‐fat‐diet feeding

SIRT1 is a highly-conserved NAD(+)-dependent protein deacetylase that plays essential roles in the regulation of energy metabolism, genomic stability, and stress response. Although the functions of SIRT1 in many organs have been extensively studied in tissue-specific knockout mouse models, the systemic role of SIRT1 is still largely unknown as a result of severe developmental defects that result from whole-body knockout in mice. Here, we investigated the systemic functions of SIRT1 in metabolic homeostasis by utilizing a whole-body SIRT1 heterozygous mouse model. These mice are phenotypically normal under standard feeding conditions. However, when chronically challenged with a 40% fat diet, they become obese and insulin resistant, display increased serum cytokine levels, and develop hepatomegaly. Hepatic metabolomic analyses revealed that SIRT1 heterozygous mice have elevated gluconeogenesis and oxidative stress. Surprisingly, they are depleted of glycerolipid metabolites and free fatty acids, yet accumulate lysolipids. Moreover, high-fat feeding induces elevation of serum testosterone levels and enlargement of seminal vesicles in SIRT1 heterozygous males. Microarray analysis of liver mRNA indicates that they have altered expression of genes involved in steroid metabolism and glycerolipid metabolism. Taken together, our findings indicate that SIRT1 plays a vital role in the regulation of systemic energy and steroid hormone homeostasis.

Case Report: Endoscopic Laser Lithotripsy of Seminal-Vesicle Stones

A 25-year-old man presented with painful ejaculation, an ejaculate volume of 0.75, and complaints of passing "granules" in the semen. Transrectal ultrasonography showed bilateral seminal vesicle enlargement. The patient underwent transurethral resection of the ejaculatory duct. The entry point of duct was resected using pure cutting current, resulting in the passage of multiple proteinaceous-appearing stones. Approximately 10 months later, the patient reported recurrent painful ejaculation and passage of granules in his semen. At cystoscopy, the ejaculatory duct openings were intubated with a cone-tipped catheter to perform bilateral seminal vesiculograms, which showed numerous mobile filling defects and a Steinstrasse appearance at the ejaculatory ducts. A 7F semirigid ureteroscope entered the lumen without difficulty over a guidewire, and the stones were fragmented with a 270-microm holmium laser fiber. The ejaculatory ducts were balloon dilated to 18F. To our knowledge, this is the first reported case where a ureteroscope was utilized to treat seminal-vesicle stones. The seminal vesiculogram proved to be extremely valuable in the diagnosis.

Amiloidosis localizada de vesículas seminales

Amyloidosis of the seminal vesicles is a common finding in autopsies, with increased incidence in older population. It is usually asymptomatic. We report a case of symptomatic localized amyloidosis of the seminal vesicles, with hemospermia and suprapubic pain. Diagnosis was achieved through ultrasound-guided transrectal biopsy. Systemic amyloidosis must be ruled out through proper evaluation. Seminal vesicle enlargement secondary to amyloid deposit may be misdiagnosed as carcinomatous invasion.

Is transrectal ultrasonography a reliable diagnostic approach in ejaculatory duct sub-obstruction?

We studied the diagnostic predictive power of transrectal ultrasonography (TRUS) coupled with semen volume in cases of distal seminal tract sub-obstruction. As a gold standard for diagnosis we used seminal tract washout (STW). Non-azoospermic subjects (n = 112) were submitted to transrectal ultrasonography because of suspected excretory infertility or other andrological pathologies, before performing STW. STW indicated ejaculatory duct sub-obstruction in 36.6% of the patients. Seminal vesicle enlargement (anterior-posterior diameter > or = 15 mm) and seminal vesicle roundish anechoic areas (stasis) were the ultrasonographic anomalies more often associated with ejaculatory duct sub-obstruction. Stepwise logistic regression (SLR) analysis revealed that the ultrasonographic evidence of stasis was highly diagnostic only in the presence of a low semen volume (< or = 1.5 ml) and that ejaculatory duct sub-obstructions may be present but with no evidence of ultrasonographic anomalies. Therefore, TRUS is a useful approach for the treatment of suspected ejaculatory duct sub-obstruction, but is not a reliable diagnostic tool and, before performing transurethral surgery, STW should be mandatory.

Isopropanol vapor inhalation oncogenicity study in Fischer 344 rats and CD-1 mice.

The potential oncogenic effects of isopropanol, a widely used solvent, were investigated. Four groups of animals, each consisting of 75 CD-1 mice/sex and 75 Fischer 344 rats/sex, were exposed to isopropanol vapor (CAS No. 67-63-0) at target concentrations of 0 (filtered air control), 500, 2500, or 5000 ppm. Animals assigned to the core group (55 mice/sex/group and 65 rats/sex/group) were exposed for 6 hr/day, 5 consecutive days/week for at least 78 weeks for the mice or 104 weeks for the rats. Ten mice/sex/group and 10 rats/sex/group were assigned to an interim euthanasia group and were terminated during Weeks 54 and 73, respectively. In addition, 10 mice/sex/group were assigned to a recovery group and did not receive any further exposure following Week 53 but were retained until the core group of animals was euthanized. Transient signs of narcosis were observed for both mice and rats during exposure to 2500 and 5000 ppm and following exposure for mice from the 5000-ppm group. Increased mortality (100% versus 82% for controls) and a decreased mean survival time (577 days versus 631 days for controls) were noted for male rats from the 5000-ppm group. Increases in body weight and/or body weight gain were typically observed for both sexes of mice and rats from the 2500- and 5000-ppm groups throughout the study. Urinalysis and urine chemistry changes indicative of impaired kidney function (i.e., decreased osmolality and increased total protein, volume, and glucose) were noted for male rats from the 2500-ppm group as well as for male and female rats from the 5000-ppm group. At the interim euthanasia, a concentration-related increase in testes weight (absolute and relative as a percentage of body and brain weight) was observed for male rats. Concentration-related increases in absolute and relative liver weight (as a percentage of body weight) were observed for male and female mice. In addition, increased absolute and/or relative (as a percentage of body and brain weight) liver and kidney weights were observed for male and/or female rats from the 2500- and 5000-ppm groups. At necropsy, an increased incidence of seminal vesicle enlargement was observed grossly for male mice from the 2500- and 5000-ppm groups. Microscopically, some of the nonneoplastic lesions noted for mice included an increased incidence of ectasia of the seminal vesicles for male mice from the 2500- and 5000-ppm groups, minimal renal tubular proteinosis for male and female mice from all isopropanol groups, and renal tubular dilation for female mice from the 5000-ppm group. A number of nonneoplastic lesions were observed for male and female rats from the 2500- and 5000-ppm groups, with the most significant lesions being observed in the kidney and associated with chronic renal disease. The lesions noted with increased severity and/or frequency included mineralization, tubular dilation, glomerulosclerosis, interstitial nephritis, interstitial fibrosis, hydronephrosis, and transitional cell hyperplasia. The only tumor type increased in incidence during the study was interstitial cell adenomas of the testes in male rats. However, the increase in these adenomas was not believed to be exposure-related due to an unusually low incidence observed for the control group. There were no increased frequencies of neoplastic lesions noted for male or female mice or for female rats from any isopropanol exposure group. Chronic renal disease was attributed to be the main cause of death for male and female rats from the 5000-ppm group and was also considered to account for much of the mortality observed for male rats from the 2500-ppm group. In conclusion, the no-observed-effect level (NOEL) for toxic effects for both rats and mice was 500 ppm. The NOEL for oncogenicity effects for both mice and rats was determined to be greater than 5000 ppm.

Isopropanol Vapor Inhalation Oncogenicity Study in Fischer 344 Rats and CD-1 Mice

The potential oncogenic effects of isopropanol, a widely used solvent, were investigated. Four groups of animals, each consisting of 75 CD-1 mice/sex and 75 Fischer 344 rats/sex, were exposed to isopropanol vapor (CAS No. 67-63-0) at target concentrations of 0 (filtered air control), 500, 2500, or 5000 ppm. Animals assigned to the core group (55 mice/sex/group and 65 rats/sex/group) were exposed for 6 hr/day, 5 consecutive days/week for at least 78 weeks for the mice or 104 weeks for the rats. Ten mice/sex/group and 10 rats/sex/group were assigned to an interim euthanasia group and were terminated during Weeks 54 and 73, respectively. In addition, 10 mice/sex/group were assigned to a recovery group and did not receive any further exposure following Week 53 but were retained until the core group of animals was euthanized. Transient signs of narcosis were observed for both mice and rats during exposure to 2500 and 5000 ppm and following exposure for mice from the 5000-ppm group. Increased mortality (100% versus 82% for controls) and a decreased mean survival time (577 days versus 631 days for controls) were noted for male rats from the 5000-ppm group. Increases in body weight and/or body weight gain were typically observed for both sexes of mice and rats from the 2500- and 5000-ppm groups throughout the study. Urinalysis and urine chemistry changes indicative of impaired kidney function (i.e., decreased osmolality and increased total protein, volume, and glucose) were noted for male rats from the 2500-ppm group as well as for male and female rats from the 5000-ppm group. At the interim euthanasia, a concentration-related increase in testes weight (absolute and relative as a percentage of body and brain weight) was observed for male rats. Concentration-related increases in absolute and relative liver weight (as a percentage of body weight) were observed for male and female mice. In addition, increased absolute and/or relative (as a percentage of body and brain weight) liver and kidney weights were observed for male and/or female rats from the 2500- and 5000-ppm groups. At necropsy, an increased incidence of seminal vesicle enlargement was observed grossly for male mice from the 2500- and 5000-ppm groups. Microscopically, some of the nonneoplastic lesions noted for mice included an increased incidence of ectasia of the seminal vesicles for male mice from the 2500- and 5000-ppm groups, minimal renal tubular proteinosis for male and female mice from all isopropanol groups, and renal tubular dilation for female mice from the 5000-ppm group. A number of nonneoplastic lesions were observed for male and female rats from the 2500- and 5000-ppm groups, with the most significant lesions being observed in the kidney and associated with chronic renal disease. The lesions noted with increased severity and/or frequency included mineralization, tubular dilation, glomerulosclerosis, interstitial nephritis, interstitial fibrosis, hydronephrosis, and transitional cell hyperplasia. The only tumor type increased in incidence during the study was interstitial cell adenomas of the testes in male rats. However, the increase in these adenomas was not believed to be exposure-related due to an unusually low incidence observed for the control group. There were no increased frequencies of neoplastic lesions noted for male or female mice or for female rats from any isopropanol exposure group. Chronic renal disease was attributed to be the main cause of death for male and female rats from the 5000-ppm group and was also considered to account for much of the mortality observed for male rats from the 2500-ppm group. In conclusion, the no-observed-effect level (NOEL) for toxic effects for both rats and mice was 500 ppm. The NOEL for oncogenicity effects for both mice and rats was determined to be greater than 5000 ppm.

Establishment and Characterization of Testicular Cell Lines from MT-PVLT-10 Transgenic Mice

Males of the MT-PVLT-10 transgenic mouse line, which expresses the polyomavirus large T-antigen under the control of the metallothionein promoter, develop testicular adenomas and display seminal vesicle enlargement. Histological analysis of adenomatous testis indicates a predominance of Leydig cells, with few normal Sertoli cells or seminiferous tubules remaining. Primary cell cultures established from the testes of control nontransgenic animals (all ages) and young MT-PVLT-10 animals (before the appearance of any phenotype) quickly entered crisis and died. In contrast, permanent cell lines could be derived from pre- and postadenomatous testes from older MT-PVLT-10 mice. All primary cultures and cell lines expressed large T-antigen. A primary culture (D-37) derived from an MT-PVLT-10 male with normal testes but enlarged seminal vesicles has been maintained for over 2 years and experiments indicate that the D-37 culture is unable to form tumors in nude mice. In contrast, a primary culture (D-4) derived from adenomatous testes of an MT-PVLT-10 mouse is also immortal, but injection of this culture into nude mice consistently resulted in tumor formation. Cloning of the D-4 culture resulted in pure Sertoli or Leydig cell clones, neither of which could form tumor upon injection into nude mice. Injection of a mixture of both cell types did result in tumor formation, suggesting a dynamic interaction between these cell types in MT-PVLT-10-induced tumorigenesis.

Significance of ct-scan-detected seminal vesicle enlargement in prostate cancer A pilot study

The significance of CT-scan-detected seminal vesicle enlagement was investigated by correlating preoperative CT scans and pathologic findings for 25 patients undergoing radical prostatectomy. Seminal vesicle size was found to be a poor predictor of pathologic involvement when compared with tumor differentiation and obliteration of seminal vesicle angle.

精嚢炎におけるとう痛に関する実験的検討

Enlargement of the seminal vesicles (SV) and subjective pain are very important factors for the diagnosis of seminal vesiculitis. The relationship between enlargement of SV and pain was studied experimentally.A total of 25 male Wistar rats weighing between 300 and 400 g were divided into 5 groups: control; saline injection; and 3 saline injection after pretreatment groups, consisting of intraluminal HCl washing of SV (chemical stimulation), compression with forceps of SV (physical stimulation) and intraperitoneal Aspirin DL-lysine injection, as the pretreatments. For the saline injection groups physiological saline was injected into SV at the speed of 1 and 2 ml/min through a tube placed in SV through a subcutaneous tunnel. Expression of pain was judged by an original criteria including twisting and turning of trunk and so on. No pain was observed in control group and group with analgesia. Pain was expressed in other 3 groups and was specially exaggerated in chemical and physical stimulation groups.Thus the relationship between enlargement of SV and pain was proved.

Growth response and androgen receptor expression in seminal vesicles from aging transgenic mice expressing human or bovine growth hormone genes.

Previous work has shown that expression of human (h) GH in transgenic mice is associated with significant age-related enlargement of seminal vesicles. To further explore this aberrant growth activity, we have characterized seminal vesicles from various GH transgenic lines and examined their androgen receptor (AR) content and distribution. Six groups of animals were initially studied: young adult (3-5 months) control mice, old (greater than 12 months) control mice, young adult hGH transgenic mice, old hGH transgenics, young adult bovine (b) GH transgenics, and old bGH transgenic mice. Young transgenic mice (hGH and bGH) possessed seminal vesicles with similar relative weights, DNA and protein contents, and AR levels as nontransgenic littermates. Histologically, the glands appeared similar. With aging, the hGH transgenic seminal vesicles exhibited massive stromal hyperplasia, whereas the glands from controls and bGH transgenic mice did not show this response. Seminal vesicles from old hGH mice presented with a marked increase in cell number (DNA content) and a marked decrease in cell size and/or glandular secretions (protein/DNA ratio) compared to those from old controls and young hGH transgenic mice. Tissue AR content was markedly reduced in old hyperplastic hGH seminal vesicles compared to that in seminal vesicles from young hGH transgenics, old controls, and old bGH transgenic mice. Immunohistochemistry indicated the absence of AR in the proliferating stromal cells, whereas acinar epithelial cells showed similar or moderately reduced AR staining intensity compared to control seminal vesicles. To examine whether the above results may be due to insertional mutagenesis rather than hGH itself, two additional GH transgenic lines were examined. Aged transgenic mice expressing bGH with an alternate promoter possessed seminal vesicle weights that were not different from those of old controls, whereas aged transgenic mice expressing an hGH. V gene (variant gene, placental origin) possessed significantly larger vesicles than the controls, which further suggests that vesicular hyperplasia is specifically related to hGH. To assess androgen responsiveness, aged control and hGH transgenic mice were castrated and examined after 15 days. While control seminal vesicles significantly decreased in size, glands from transgenic mice did not. Regressive changes were observed in the remaining epithelium of hGH transgenic mice; however, stromal tissue exhibited no response to androgen withdrawal. The present results suggest that the aging-associated seminal vesicle hyperplasia in hGH transgenic mice is a result of a massive increase in stromal tissue that is low or devoid of AR, suggesting a loss of direct androgen regulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Growth response and androgen receptor expression in seminal vesicles from aging transgenic mice expressing human or bovine growth hormone genes

Previous work has shown that expression of human (h) GH in transgenic mice is associated with significant age-related enlargement of seminal vesicles. To further explore this aberrant growth activity, we have characterized seminal vesicles from various GH transgenic lines and examined their androgen receptor (AR) content and distribution. Six groups of animals were initially studied: young adult (3-5 months) control mice, old (greater than 12 months) control mice, young adult hGH transgenic mice, old hGH transgenics, young adult bovine (b) GH transgenics, and old bGH transgenic mice. Young transgenic mice (hGH and bGH) possessed seminal vesicles with similar relative weights, DNA and protein contents, and AR levels as nontransgenic littermates. Histologically, the glands appeared similar. With aging, the hGH transgenic seminal vesicles exhibited massive stromal hyperplasia, whereas the glands from controls and bGH transgenic mice did not show this response. Seminal vesicles from old hGH mice presented with a marked increase in cell number (DNA content) and a marked decrease in cell size and/or glandular secretions (protein/DNA ratio) compared to those from old controls and young hGH transgenic mice. Tissue AR content was markedly reduced in old hyperplastic hGH seminal vesicles compared to that in seminal vesicles from young hGH transgenics, old controls, and old bGH transgenic mice. Immunohistochemistry indicated the absence of AR in the proliferating stromal cells, whereas acinar epithelial cells showed similar or moderately reduced AR staining intensity compared to control seminal vesicles. To examine whether the above results may be due to insertional mutagenesis rather than hGH itself, two additional GH transgenic lines were examined. Aged transgenic mice expressing bGH with an alternate promoter possessed seminal vesicle weights that were not different from those of old controls, whereas aged transgenic mice expressing an hGH. V gene (variant gene, placental origin) possessed significantly larger vesicles than the controls, which further suggests that vesicular hyperplasia is specifically related to hGH. To assess androgen responsiveness, aged control and hGH transgenic mice were castrated and examined after 15 days. While control seminal vesicles significantly decreased in size, glands from transgenic mice did not. Regressive changes were observed in the remaining epithelium of hGH transgenic mice; however, stromal tissue exhibited no response to androgen withdrawal. The present results suggest that the aging-associated seminal vesicle hyperplasia in hGH transgenic mice is a result of a massive increase in stromal tissue that is low or devoid of AR, suggesting a loss of direct androgen regulation.

Influence of low protein diet on the life span of male and female C57B1 mice

The feeding of a diet lower in protein (LP: 13.7 per cent) than the normal higher protein stock diet (HP:22.6 per cent) but of equivalent caloric concentration to C57B1 mice led to significant life span prolongation of the males but not of the females. Male mice which started LP diet feeding at 3 months of age, showed a longer life span than males starting at 3 weeks of age. Both in LP fed males as well as in females the number of lymphoid tumours nearly doubled. This indicates that tumour incidence is probably independent of life span prolongation. Enlargement of seminal vesicles was found in 21 per cent of the LP in comparison with 54 per cent of the HP males.

Hyperlipermia and atherosclerosis: A preliminary note on the mechanism of action

1. 1. Increasing dietary levels of lipid leads to an enlargement of seminal vesicles of male mice, indicating an increased production of male sex hormone. 2. 2. No changes are noted in the target organ when either the gonad or hypophysis is removed, indicating that an intact pituitary-gonadal axis is required. 3. 3. Present experimental evidence indicates that an increase in male sex hormone secretion may result from increased dietary lipid levels, and since the incidence of athetosclerosis/cardiovascular accidents is markedly greater in the male than female, this may be the mechanism whereby the high incidence of atherosclerosis/cardiovascular accidents are elicited in the male.