Association of diet and lifestyle with chronic prostatitis/chronic pelvic pain syndrome and pain severity: a case-control study.

BACKGROUND: Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common problem with unclear etiology. Some diet and lifestyle factors were thought to correlate with CP/CPPS, but studies comprehensively investigate this correlation are rarely available. The current study was conducted to determine the potential lifestyle-related risk factors of CP/CPPS and its pain severity in Chinese population. METHODS: Participants were recruited from seven hospitals in Shanghai from July 2012 to August 2013. Demographics, medical history, diet and lifestyle information, and CP/CPPS symptoms were obtained from each participant using a questionnaire. Univariate and multivariate logistic regression analyses were used to identify potential lifestyle-related risk factors for CP/CPPS and its pain severity. RESULTS: A total of 784 men with CP/CPPS and 785 controls were enrolled in this study. Multivariate regression model indicated that age, nightshift work, stress, smoking status, alcohol consumption, less water intake, imbalanced diet, frequent sexual activity, delaying ejaculation and holding urine were identified as potential risk factors for CP/CPPS, whereas sedentary lifestyle, caffeinated drinks and less water intake were associated with severe pain in CP/CPPS patients. CONCLUSIONS: Several diet and lifestyle factors associated with CP/CPPS and pain severity were determined in this study. These modifiable conditions are potential targets for treatment of CP/CPPS. However, further studies are necessary to determine their role in the pathogenesis of CP/CPPS.

Aesthetic anterior restorations for children and young adults.

Indications for aesthetic anterior restorations include caries, trauma, congenital enamel defects, unaesthetic contour and shape of teeth, tooth discolouration and minor tooth malalignment. Conventional Class III, IV or V cavities can be restored with third and fourth generation composite resins, while glass ionomer cement can be used to restore Class III or V cavities. Laboratory fabricated resin or porcelain veneers enable major shape or colour adjustments of the labial surfaces of anterior teeth. They may be used to treat unaesthetic defects on the tooth surface, moderate to severe tooth discolouration and minor tooth malalignments. The clinical techniques of these restorative treatment modalities have been presented.

Effect of testosterone on gonadotropin response to DBcAMP, cAMP binding, and cAMP production in pituitary cultures.

The role of testosterone (T) in the modulation of pituitary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) sensitivity to DBcAMP was examined in the pituitary monolayer cultures prepared from intact young female rats. Hormone contents in media and cell homogenates were determined by radioimmunoassays. Incubation with 8 and 4 mM DBcAMP for 4 h consistently induced a significant (P less than 0.05) increase in FSH and LH release, respectively. Pretreatment with 10 nM T for 4 days reduced the minimal dose of DBcAMP required to stimulate FSH release (2 vs. 8 mM) but had no effect on the DBcAMP-induced LH release. Data indicate that T treatment for 4 or 7 days stimulated total FSH contents (sum of hormone contents in medium and cells). Similarly, incubation with 10 mM DBcAMP for 4 h significantly increased total FSH content per dish in both the T-treated and non-T-treated cultures. Neither T nor DBcAMP had any effect on LH production under these conditions. Intracellular cAMP was significantly increased to three- to eightfold of control after T treatment for 3 or 6 h, respectively. Furthermore, cAMP-binding activities were significantly increased after T treatment for 1 or 4 days (174 or 422% of control). Our previous data indicate that estrogen increases LH production, cAMP binding, cAMP production, and LH sensitivity to DBcAMP, and these data indicate that T exerts stimulatory effects on FSH in a similar fashion. These results support the concept that the two gonadotropins are regulated independently via different gonadal steroids.

Effect of estrogen and progesterone on the development of endometrial hyperplasia in the Fischer rat.

The effect of changing endocrine status on the uterine endometrium of the female Fischer rat was observed in vivo after neonatal androgenization, after aging, after estrogen (E) implant in ovariectomized (OVX) rats, and in vitro after progesterone (P) addition to monolayer cultures of uterine tumor cells. Neonatal androgenization produced cystic ovarian follicles and persistent vaginal cornification for 10-14 mo, indicative of an anovulatory, persistent E status. The constant estrous (CE) state, induced by androgenization, uniformly produced focal glandular hyperplasia of the endometrium at 9 mo of age. Focal glandular hyperplasia, which was absent in the cycling 6-mo-old estrous endometrium, was also apparent in the 12-mo-old rats which had ceased cycling and entered natural CE. Subcutaneous estradiol-17 beta (E2) implants in 12-mo-old OVX rats induced early cystic and adenomatous changes in the foci of hyperplasia. Acyclic control rats, 21 mo old, in persistent diestrus (PD) exhibited a 3-fold elevation of serum P associated with glandular atrophy of the endometrium. Ten nM P also inhibited proliferation of endometrial cells in cultures prepared from tumors of 21-mo-old rats. On the other hand, adenomatous hyperplasia was observed in 29-mo-old PD rats, despite the presence of low serum E and elevated serum P. These results indicate that either induced or natural constant E status leads to focal glandular hyperplasia in the Fischer rat. E2 implants in the 12-mo-old OVX Fischer rat induced early cystic and adenomatous changes in the focal hyperplasia. Inhibition of these focal hyperplasias was associated with elevated serum P at 21 mo. The development of adenomatous hyperplasia in the aged endometrium, on the other hand, occurred despite elevated serum P at 29 mo.

Luteinizing hormone response to N6, O2'-dibutyryl adenosine 3',5'-cyclic monophosphate in aged, young and androgenized rats: estradiol effect in vitro.

The studies in this report were designed to investigate whether the loss of pituitary luteinizing hormone (LH) responses to N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) in aged noncycling rats was the result of age, endocrine status associated with diestrus, or noncyclic low estrogen status. Pituitary monolayer cultures were prepared from female Fischer 344 rats. Aged (18-month-old) persistent diestrous (PD) rats, young diestrous (D) rats, or noncycling neonatally androgenized-constant estrous (AN-CE) rats were used. Enzymatically dispersed cells were maintained in the same batch of medium supplemented with dextran-coated charcoal adsorbed serums. Total LH contents were 1.75 +/- 0.04, 1.15 +/- 0.03, and 1.71 +/- 0.02 micrograms LH/dish in Day 5 cultures prepared from aged PD, young D, and AN-CE rats, respectively. Incubations with 5 mM DBcAMP for 4 h significantly (P less than 0.05) stimulated LH release in cultures prepared from young D and AN-CE rats but inhibited LH release in cultures prepared from aged PD rats even though a 4-h incubation with 10 nM LH releasing hormone (LHRH) stimulated LH release similarly in cultures of all three types of cells. The loss of DBcAMP-induced LH release in cultures prepared from aged PD rats was reversed by 17 beta-estradiol (E2). This treatment also reduced the basal LH release and increased the cellular LH content. These results indicate that the loss of DBcAMP-induced LH response in the aged rat is not an irreversible aging phenomenon but appears to be associated with the chronically low E2 status of aged PD rats but not young cycling D or noncycling AN-CE rats.

Estradiol stimulation of pituitary cAMP production and cAMP binding.

The role of 17 beta-estradiol (E2) in the modulation of N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP)-induced hormone release was examined in pituitary monolayer cultures prepared from intact and ovariectomized female rats. Incubations with 5 mM DBcAMP for 4 h significantly (P less than 0.05) stimulated both luteinizing hormone (LH) and prolactin (PRL) release in pituitary cultures prepared from rats at diestrus and from cycling rats at random stages of the estrous cycle. However, DBcAMP failed to stimulate the LH or PRL release in cultures prepared from ovariectomized rats in which the basal LH and PRL release was approximately three-fold and one-tenth of that in cycling rats, respectively. Pretreatment with 1 nM E2 augmented or restored the DBcAMP-induced LH release but not the DBcAMP-induced PRL release in cultures prepared from cycling or ovariectomized rats, respectively. Furthermore, E2 treatment alone of cultures prepared from cycling rats significantly increased intracellular cAMP concentrations and cAMP-binding activities by at least twofold over that of the non-E2-treated controls. The E2-induced rise in cellular cAMP concentration preceded the E2-induced rise in cAMP binding. These results indicate that the priming effect of E2 on pituitary LH responsiveness to DBcAMP is associated with increased cAMP production and cAMP binding.

Estradiol stimulation of LH response to LHRH and LHRH binding in pituitary cultures.

The relationship between 17 beta-estradiol (E2) stimulation of luteinizing hormone (LH) response to LH-releasing hormone (LHRH) and E2 effect on LHRH binding was examined in pituitary monolayer cultures prepared from female rats. E2 pretreatment significantly (P less than 0.05) augmented the LHRH-induced LH release to 158-180% of the non-E2-treated controls. The maximal E2-priming effect could be observed after 1 day of treatment. E2 treatment for 3 days stimulated [D-Ala6]luteinizing hormone-releasing hormone (LHRHa) binding to about 1.5-fold that of the non-E2-treated controls without affecting the dissociation constant of LHRH receptor (Kd = 4 X 10(-10) M). The stimulatory effect of E2 on cell proliferation as determined by [3H]thymidine incorporation was also observed 3 days after treatment. However, E2 stimulation of LH accumulation in the cultured cells could be detected as early as 4 h after treatment. These results indicate that E2-priming effect on pituitary LH response to LHRH is initially associated with an increase in cellular LH content and later associated with increases in LHRH binding and in an index of cell proliferation that may include the LH-producing cells.

LH responses to LHRH, DBcAMP, and 17 beta-estradiol in cultures derived from aged rats.

Effects of luteinizing hormone-releasing hormone (LHRH), N6,O2'-dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAmP), and 17 beta-estradiol (E2) on LH responses were compared in 4-day-old pituitary cultures derived from female rats (Fischer 344) of 9 and 31 mo of age. Pituitary LH contents were similar in 5 X 10(5) freshly dispersed cells prepared from the two groups of rats. LH release in response to a 4-h incubation with 10 nM LHRH was virtually the same in cultures derived from 9- and 31-mo-old rats, 140 +/- 2 ng and 138 +/- 18 ng/4 h, respectively. In cultures derived from 9-mo-old rats, incubation with 8 mM DBcAMP for 4 h significantly stimulated LH release (286% of control level), and treatment with 10 nM E2 for 3 days significantly increased both basal LH release and LH accumulation (sum of LH contents in cells and medium) to 162 and 125% of control level, respectively. Neither DBcAMP nor E2 affected cultures derived from the 31-mo-old rats. These results indicate that there is a difference in the LH response to DBcAMP and E2 between cultures derived from 9- and 31-mo-old rats. The loss of pituitary responsiveness to DBcAMP and E2 and the loss of pituitary cyclicity in the aged female rat may be causally related.

Effect of 17 beta-estradiol on pituitary cAMP binding and responses to DBcAMP.

Effects of 17 beta-estradiol (E2) on adenosine 3',5'-cyclic monophosphate (cAMP) binding and luteinizing hormone (LH) and prolactin (PRL) responses to N6-O-2'-dibutyryl cAMP (DBcAMP) were examined in pituitary monolayer cultures prepared from female rats. Incubation with 8 mM DBcAMP for 4 h significantly (P less than 0.05) increased both LH and PRL release into medium by two- to threefold. E2 pretreatment augmented the DBcAMP-induced LH release but not PRL release to 160% of the non-E2-treated controls. However, the cellular and total accumulation of both LH and PRL were significantly increased in cultures pretreated with E2. The effect of E2 was time dependent, and the maximal effect was observed after 3 days of treatment. Furthermore, E2 treatment significantly increased cAMP-binding activities to 254% of the non-E2-treated controls. The time course of the E2 effect on cAMP-binding activities closely resembled the time course of the E2 effect on LH and PRL accumulation as well as the DBcAMP-induced LH release. These results suggest that the priming effect of E2 on pituitary LH and PRL responses to DBcAMP is associated with increased hormone synthesis and cAMP binding stimulated by E2 pretreatment.

Effect of serum sex steroids on pituitary LH response to LHRH and LH synthesis.

To determine the factors responsible for the sex difference in luteinizing hormone (LH) response to luteinizing hormone-releasing hormone (LHRH) observed earlier in pituitary cultures, we examined the effects of serum, 17 beta-estradiol, and testosterone on pituitary LHRH-responsiveness and LH synthesis. Cultures prepared from female rats were maintained in medium supplemented with serums. Dextran-coated charcoal (DCC) adsorption of female rat serum reduced, whereas DCC adsorption of male rat serum increased the pituitary LHRH-responsiveness, indicating the existence of stimulatory factor(s) in female rat serum and inhibitory factor(s) in male rat serum. Readdition of testosterone to DCC female rat serum significantly reduced LH release in response to LHRH (78-32% of the control) without affecting total LH content. Readdition of 17 beta-estradiol to DCC female rat serum significantly increased the LH release in response to LHRH, cellular LH content, and 3H-labeled precursor uptake and incorporation into immunoprecipitable LH. These results indicate that the sex difference in LHRH responsiveness may be attributed to the stimulatory effect of 17 beta-estradiol and the inhibitory effect of testosterone on the LH cells.

Sex difference in LH response to LHRH and DBcAMP and effect of testosterone.

Because luteinizing hormone-releasing hormone (LHRH) stimulates both pituitary cAMP production and LH release, cAMP has been implicated in the action of LHRH on LH release. The effects of LHRH and DBcAMP on LH release were tested in 4-h incubations with pituitary cultures prepared from male or female rats. LH contents in medium and cells were separately determined by radioimmunoassays. LH release in response to 10 nM LHRH was significantly greater in cultures prepared from female rats (female-RPC) than in cultures prepared from male rats (male-RPC), 1,070 and 418% of control, respectively. Addition of DBcAMP (3, 5, or 10 mM) significantly stimulated LH release by female-RPC (212, 206, or 286% of control, respectively) but did not affect LH release in male-RPC. Furthermore, DBcAMP significantly increased the cellular LH content in female- but not in male-RPC. Testosterone pretreatment of female-RPC significantly lowered the LHRH-induced LH release but did not affect the DBcAMP-induced LH release. These data indicate that testosterone may contribute to the sex difference in pituitary LH response to LHRH but not to DBcAMP.

Effects of hypothalamic-releasing hormones on LH, FSH, and prolactin in pituitary monolayer cultures.

Four-day-old pituitary monolayer cultures were incubated with various hypothalamic releasing hormones. Rat hypothalamic extract stimulated the release of LH, FSH, and PRL by these cultures in a dose-related fashion. Synthetic LH-RH stimulated the release of LH and FSH but not of PRL. Synthetic TRH increased the release of PRL but had no effect on LH or FSH. At 10(-8) M, somatostatin did not affect any of the three adenohypophyseal hormones. Incubation with DBcAMP or theophylline also stimulated PRL release without any detectable effect on LH and FSH release. These data suggest the involvement of cyclic AMP--adenylate cyclase system in the mechanism of PRL release, but their involvement in gonadotropin release requires further studies.

Effects of gonadal steroids on the basal and LRF-induced gonadotropin secretion by cultures of rat pituitary.

The effects of 17beta-estradiol (E2), progesterone (P4), 20alpha-hydroxypregn-4-en-3-one (20alpha-OHP4), and testosterone (T) on the basal and LRF-induced secretion of LH and FSH were studies in monolayer cultures prepared from the pituitaries of adult female rats. Day 4 cultures were used and all steroids were tested at 10-8M concentration for 4 hr. E2 (2.72 ng/ml) alone caused a nonsignificant increase in basal secretion of both LH and FSH; however, the same dose of E2 significantly (p less than 0.001) inhibited the LRF-induced secretion of LH but not of FSH (74% and 88% of 10-8M LRF-treated level, respectively), Testosterone (2.88 ng/ml) alone significantly increased the basal secretion of LH (136% of control level, p less than 0.05) and augmented the effect of LRF on FSH secretion to 130% of the LRF-treated level (p less than 0.05). Contrary to its negative feedback action on the basal secretion of FSH (46% of control level, P less than 0.05), 20ALPHA-OPH4 (3.15 ng/ml) augmented the effect of LRF on LH secretion (130% of LRF-treated level, P less than 0.05). On the other hand, P4 (3.14 ng/ml) did not cause any significant inhibition in the basal and LRF-induced secretion of either LH or FSH. These data indicate that both of the LH- and FSH-LRF; however, their secretory activities are modulated differently by various steroids.