Human- or object-like? Cognitive anthropomorphism of humanoid robots.

Across three experiments (N = 302), we explored whether people cognitively elaborate humanoid robots as human- or object-like. In doing so, we relied on the inversion paradigm, which is an experimental procedure extensively used by cognitive research to investigate the elaboration of social (vs. non-social) stimuli. Overall, mixed-model analyses revealed that full-bodies of humanoid robots were subjected to the inversion effect (body-inversion effect) and, thus, followed a configural processing similar to that activated for human beings. Such a pattern of finding emerged regardless of the similarity of the considered humanoid robots to human beings. That is, it occurred when considering bodies of humanoid robots with medium (Experiment 1), high and low (Experiment 2) levels of human likeness. Instead, Experiment 3 revealed that only faces of humanoid robots with high (vs. low) levels of human likeness were subjected to the inversion effects and, thus, cognitively anthropomorphized. Theoretical and practical implications of these findings for robotic and psychological research are discussed.

Grain free diets for utility dogs during training work: Evaluation of the nutrient digestibility and faecal characteristics.

Two different diets characterized by the absence of cereals or by the presence of conventional cereals were evaluated on the nutrient digestibility and faecal characteristics and faecal fermentative end-product concentrations of 8 neutered adult Labrador retrievers housed at the Regional Centre Helen Keller (Messina, Italy) during the training work for the service guide for the blind. Dogs (age = 17 ± 1 months, initial body weight [BW] = 26.3 ± 1 kg, and body condition score [BCS] = 4.5 ± 0.11) were divided into 2 homogeneous groups for sex (half males and half females). Dogs in the grain free (GF) group were fed a commercial diet characterized by the absence of grain cereals, and dogs in the control (CTR) group were fed a super-premium pet food characterized by conventional grains as the carbohydrate source. The trial lasted 84 d, preceded by a 7-d of adaption period. Physical examination, digestibility, and faecal characteristics were studied. The statistical model included the effects of diet (GF vs. CTR), time (from d 0 to 84, end of the trial) and the interaction (diet × time). The high-protein, low-carbohydrate dry diet (GF) offered higher apparent nutrient digestibility of protein (+10%; P = 0.002) and fat (+7%; P < 0.001) and more stable large intestinal fermentation of carbohydrate compared to the commercial high-carbohydrate dry diet, enabling dogs to use nutrients from the diet more efficiently and thus requiring less food (-13%) to satisfy their nutrient requirements, producing less excrement (-33%; P = 0.033), and reaching a higher final BW (+8%; P < 0.0001) and a higher final BCS (+15%; P = 0.003). Therefore, the GF diet appears the nutritional plan most suitable for these animals taking due account not only of the training work done by animals with their increased nutrient and energy needs, but also of the gastrointestinal disorders consequent to stress coming from work and life in kennels, which cause in the Labrador retrievers an unusual weight loss.

Motivational enhancement therapy in obese patients: A promising application.

A pilot uncontrolled study aimed at investigating the efficacy of a motivational enhancement therapy adapted for obesity was conducted on 71 obese patients (59 females). Treatment consisted of 5 weekly group sessions and 3 weekly individual sessions. Outcome measures included Treatment, Motivation and Readiness test (TREMORE) and anthropometric measures. Patients showed a significant reduction of all anthropometric parameters (with exception of waist circumference), and a significant improvement of TREMORE scores at the end of the treatment. The motivational interviewing program applied in the current study appears to be effective and consistent with both patient recommendations and health care clinic demands.

Male sexuality and cardiovascular risk. A cohort study in patients with erectile dysfunction.

INTRODUCTION: Although penile blood flow (PBF) has been recommended as an additional diagnostic test in identifying erectile dysfunction (ED) patients at risk for latent cardiovascular disease, no study has ever assessed the possible association of PBF and the relational component of sexual function with incident major cardiovascular events (MACE). AIM: The aim of this study is to investigate whether severity of ED, PBF, and other factors related to a couple's relationship predict incident MACE. METHODS: A consecutive series of 1,687 patients was studied. Different clinical, biochemical, and instrumental (penile flow at color Doppler ultrasound) parameters were evaluated. MAIN OUTCOME MEASURES: Information on MACE was obtained through the City of Florence Registry Office. RESULTS: During a mean follow-up of 4.3 +/- 2.6 years, 139 MACE, 15 of which were fatal, were observed. Cox regression analysis, after adjustment for age and Chronic Disease Score, showed that severe ED predicted MACE (hazard ratio [HR] 1.75; 95% confidence interval 1.10-2.78; P < 0.05). In addition, lower PBF, evaluated both in flaccid (before) and dynamic (after prostaglandin-E1 stimulation) conditions, was associated with an increased risk of MACE (HR = 2.67 [1.42-5.04] and 1.57 [1.01-2.47], respectively, for flaccid [<13 cm/second] and dynamic [<25 cm/second] peak systolic velocity; both P < 0.05). Reported high sexual interest in the partner and low sexual interest in the patient proved to have a protective effect against MACE. CONCLUSIONS: The investigation of male sexuality, and in particular PBF, and sexual desire, could provide insights not only into present cardiovascular status but also into prospective risk.

The effect of statin therapy on testosterone levels in subjects consulting for erectile dysfunction.

INTRODUCTION: Previous clinical studies on effect of statins treatment on testosterone (T) levels have produced mixed results. AIM: The aim of the present study is to evaluate the association between statin therapy and hormonal parameters in a large series of subjects seeking medical care at our unit for erectile dysfunction (ED). METHODS: A consecutive series of 3,484 (mean age 51.6 + or - 13.1 years) patients with ED was studied. MAIN OUTCOME MEASURES: Several hormonal and biochemical parameters were investigated, along with ANDROTEST structured interview measuring hypogonadism-related symptoms. RESULTS: Among the patients studied, 244 (7%) patients were being treated with statins. After adjustment for confounding factors (including body mass index and Progetto Cuore cardiovascular (CV) risk engine score), both total and calculated free testosterone levels were significantly lower in subjects taking statins, when compared to the rest of the sample (hazard ratio [HR] = 0.93 [0.90; 0.96] and 0.26 [0.01; 0.18] for each decrement of total T and calculated free T, respectively; both P < 0.0001). The use of statins was also associated with a reduced testis volume and a higher prevalence of hypogonadism-related symptoms and signs, as assessed by higher ANDROTEST score (HR = 1.12 [1.03; 1.21]; P < 0.01 after adjustment for confounders). Follicle-stimulating hormone levels were significantly higher in subjects treated with statins when compared to the rest of the sample, while there was a trend toward higher luteinizing hormone levels, but this did not reach statistical significance. The lower levels of total and calculated free T observed in subjects treated with statins were also confirmed comparing them with age-waist circumference and CV risk score matched controls. Finally, subjects being treated with statins showed lower prolactin levels when compared to the rest of the sample. CONCLUSIONS: Our data demonstrated that statin therapy might induce an overt primary hypogonadism and should be considered as a possible confounding factor for the evaluation of testosterone levels in patients with ED.

Low testosterone is associated with an increased risk of MACE lethality in subjects with erectile dysfunction.

INTRODUCTION: Although testosterone (T) has been suggested to play a protective role against the development of atherosclerosis, studies demonstrating an association between low T and incident major adverse cardiovascular events (MACE) are scanty in the general population and absent in subjects with erectile dysfunction (ED). AIM: To investigate whether low T in subjects with ED predict incident fatal or nonfatal MACE. METHODS: This is an observational prospective cohort study evaluating a consecutive series of 1687 patients attending our andrological unit for ED. Patients were interviewed using the structured interview on erectile dysfunction (SIEDY) and ANDROTEST structured interviews measuring components relative to ED and hypogonadal-related symptoms, respectively. MAIN OUTCOME MEASURES: Total T was evaluated at baseline. Information on MACE was obtained through the City of Florence Registry Office. RESULTS: Among the patients studied, 5.2, 13.8, and 22.4% were hypogonadal according to different thresholds (T < 8, 10.4 and 12 nmol/L or 230, 300 and 350 ng/dL, respectively). During a mean follow-up of 4.3 + or - 2.6 years, 139 MACE, 15 of which were fatal, were observed. Unadjusted incidence of MACE was not associated with T levels. Conversely, the proportion of lethal events among MACE was significantly higher in hypogonadal patients, using either 10.4 nmol/L (300 ng/dL) or 8 nmol/L (230 ng/dL) thresholds. However, after adjustment for age and Chronic Diseases Score in a Cox regression model, only the association between incident fatal MACE and T < 8 nmol/L (230 ng/dL) was confirmed (HR = 7.1 [1.8-28.6]; P < 0.001). Interestingly, measuring hypogonadal-related symptoms and signs through ANDROTEST, only fatal MACE were also associated with a higher score (HR = 1.2 [1.0-1.5] for each ANDROTEST score increment; P = 0.05 after adjustment for age and Chronic Diseases Score). CONCLUSIONS: T levels are associated with a higher mortality of MACE. The identification of low T levels should alert the clinician thus identifying subjects with an increased cardiovascular risk.

The relationship of testosterone to prostate-specific antigen in men with sexual dysfunction.

INTRODUCTION: Concern about a testosterone (T)-induced prostate-specific antigen (PSA) increase is often perceived as one of the main limitations in treating hypogonadism even when it is symptomatic, such as in subjects with sexual dysfunction (SD). AIM: The aim of this study was to evaluate the relationship between T and PSA levels in subjects with SD. Methods. We retrospectively evaluated the relationship between T and PSA in 2,291 subjects seeking medical care at our outpatient clinic for SD (sample A). The analysis was then repeated in a selected subpopulation of 1,421 subjects apparently free from prostatic diseases (sample B). MAIN OUTCOME MEASURES: The specific association between PSA levels, circulating androgens, and different clinical signs and symptoms of hypogonadism, as assessed by ANDROTEST structured interview, was evaluated. RESULTS: In both samples A and B, subjects with higher PSA levels reported a lower prevalence of hypogonadism-related symptoms and signs, as well as higher total testosterone (TT), and analogue and calculated free T. However, when the association between PSA and T was evaluated as a function of T deciles, the upper nine groups had similar PSA values, with the lowest demonstrated a significantly reduced PSA (the lowest vs. the rest of the sample: 0.61[0.38-1.23] ng/mL vs. 0.86[0.57-1.44] ng/mL, and 0.51[0.30-0.94] ng/mL vs. 0.73[0.52-1.10] ng/mL, respectively, for samples A and B; both P < 0.0001). Furthermore, when the relationship between hypogonadism (TT < 8 nmol/L) and PSA levels was evaluated according to age, it was significant only in younger subjects, but not in the older ones. CONCLUSIONS: Our data demonstrated that PSA is unrelated to T concentration across most of the T range, except for the most severely T deficient, and that a significant relationship between T and PSA is seen in younger but not in older men.

Characterization of phosphodiesterase type 5 expression and functional activity in the human male lower urinary tract.

INTRODUCTION: Phosphodiesterase type 5 (PDE5) inhibitors ameliorate low urinary tract (LUT) symptoms in men with ED and symptomatic benign prostatic hyperplasia (BPH). PDE5 is highly expressed in rat and human bladder, where it regulates cyclic guanosine monophosphate (cGMP) degradation, muscle tone, and proliferation. AIM: To investigate PDE5 tissue distribution and activity in human LUT tissues (urethra, prostate, and bladder). MAIN OUTCOME MEASURES: PDE5 expression and activity were analyzed and compared within the same BPH patient in LUT tissues and in smooth muscle cells (SMCs) cultured from urethra, prostate, and bladder. METHODS: In LUT tissues, PDE5 was localized by immunohistochemistry and mRNA expression by quantitative real-time polymerase chain reaction. Proliferation assay was used as readout of PDE5 activity, evaluated as ability of vardenafil to increase the antiproliferative effect of different nitric oxide (NO)/cGMP pathway activators [the PDE5-resistant cGMP analog Sp-8-Br-PET-cGMPS, the NO donor sodium nitroprusside (SNP), and the soluble guanylate cyclase (sGC) stimulator BAY 41-8543]. RESULTS: In all the LUT tissues, PDE5 was immunolocalized in blood vessels and in muscular fibres, but not in epithelium. PDE5 mRNA expression was higher in urethra and bladder than in prostate SMC. The antiproliferative effect of Sp-8-Br-PET-cGMPS was similar in all LUT SMC. In prostatic SMC, SNP and BAY 41-8543 show a dose-dependent antiproliferative effect that resulted marginally enhanced by vardenafil. Conversely, in urethra and bladder SMC the antiproliferative effect of SNP and BAY 41-8543 was lower than in prostatic SMC, but it was significantly enhanced by vardenafil. In urethral and bladder cells vardenafil half-maximal response inhibiting concentration was in the subnanomolar range, whereas in prostate cells it resulted significantly higher. CONCLUSIONS: The highest expression and biological activity of PDE5 was found in bladder. However, a consistent PDE5 expression and activity was also found in prostatic urethra. In contrast, the prostate gland showed the lowest PDE5 abundance and cultures derived from this tissue were less sensitive to vardenafil.

Estrogens regulate humans and rabbit epididymal contractility through the RhoA/Rho-kinase pathway.

INTRODUCTION: We have previously demonstrated that oxytocin (OT) and endothelin-1 (ET-1) peripherally regulate epididymal motility in an estrogen-dependent way. Because RhoA/Rho-kinase (ROCK) pathway is a contractile effector downstream to both OT and ET-1 receptors, we hypothesized an estrogenic modulation of OT- and ET-1-induced contraction through the up-regulation of RhoA/ROCK signaling. AIM: To evaluate the effect of changing endocrine milieu on RhoA/ROCK pathway in the epididymis. METHODS: We induced a pharmacological hypogonadotropic hypogonadism in rabbits and replaced hypogonadal animals with different sex steroids (testosterone, T, or estradiol valerate, [E(2v)]). Effects of estrogen deprivation were also evaluated in rabbits chronically treated with the P450-aromatase inhibitor letrozole. An "in vitro" model of human epididymal smooth muscle cells was established and stimulated with sex hormones (72 hours). Protein and mRNA expression and functional activity of RhoA/ROCK signaling were studied by quantitative reverse transcriptase-polymerase chain reaction, immunohistochemistry, western blot analysis, cell migration and by "in vitro" contractility studies using the ROCK inhibitor Y-27632. MAIN OUTCOME MEASURES: Effects of sex steroids on expression and functional activation of RhoA/ROCK signaling in rabbit epididymis and human epididymal smooth muscle cells. RESULTS: The relaxant effect of Y-27632 on ET-1-pre-contracted epididymal strips was significantly reduced in hypogonadal rabbits, as well as in letrozole-treated animals. T supplementation normalized T plasma levels, but not Y-27632 epididymal strip sensitivity. E(2)v not only completely restored Y-27632 responsiveness but even amplified it, indicating an estrogenic up-regulation of RhoA/ROCK pathway. Accordingly, ROCK1 protein and gene expressions were strongly induced by E(2)v but not by T. The estrogen-induced up-regulation of RhoA/ROCK signaling was confirmed in human epididymal smooth muscle cells. CONCLUSIONS: Our results suggest that estrogens regulate epididymal motility by increasing RhoA/ROCK signaling, and therefore calcium sensitivity, which tunes up responsiveness to contractile factors.

Dihydrotestosterone and leptin regulate gonadotropin-releasing hormone (GnRH) expression and secretion in human GnRH-secreting neuroblasts.

INTRODUCTION: The reversal of hypogonadotropic hypogonadism (HH), occurring after discontinuation of testosterone therapy in adolescents with delayed puberty and in a small percentage of adults with congenital HH, suggests a role for androgens in favoring a spontaneous recovery of reproductive function. AIM: We investigated the effect of androgens and leptin on gonadotropin-releasing hormone (GnRH) expression and secretion in human GnRH-secreting neuroblasts (FNC-B4). METHODS: Quantitative real-time polymerase chain reaction RT-PCR for mRNA expression and radioimmunoassay for GnRH secretion were used. Immunohistochemical studies assessed GnRH protein expression. FNC-B4 migration was analyzed with multiwell Boyden chamber technique. MAIN OUTCOME MEASURES: Effects of the non-aromatizable androgen dihydrotestosterone (DHT) and leptin in FNC-B4 were tested after 24 and 48 hours. RESULTS: Exposure to increasing concentrations of DHT after 24 hours significantly stimulated GnRH mRNA in FNC-B4. This effect was still present after prolonged exposure (48 hours). Similarly, treatment with leptin significantly induced GnRH mRNA after 24 hours, but not at 48 hours. Interestingly, mRNA for leptin receptors (LEPR) was significantly reduced after 48 hours of leptin, while, at this time point, it was stimulated by DHT. Coincubation for 48 hours with leptin and DHT maintained the stimulatory effect on both GnRH and LEPR mRNA, suggesting that DHT could stabilize the leptin effect by preventing downregulation of LEPR. Similar results were obtained for GnRH protein expression analysis. Moreover, both DHT and leptin increased GnRH release into the culture medium. We also found that DHT or leptin treatment significantly increased FNC-B4 basal migration. As we previously found that GnRH stimulates FNC-B4 migration, we hypothesized that this effect could be mediated by DHT- and leptin-induced GnRH release. Accordingly, the GnRH antagonist cetrorelix inhibited DHT- and leptin-induced migration. CONCLUSION: Our results suggest that androgens (adequate hormonal status) could have a positive effect on GnRH neuronal activity by synergizing with leptin (adequate energy status) in the regulatory mechanisms required for reproductive and sexual fitness.