Search

Objective: In order to gain a better understanding of the individual and joint impact of testosterone and cortisol on behavior, the present study was developed to test the differences in each hormone alone and conjointly between perpetrators of IPV and non-violent controls. Method: Perpetrators of IPV on probation were compared to a control group of non-aggressive males from Hidalgo County in the Rio Grande Valley on baseline testosterone and cortisol, as well as several relevant questionnaires measuring aggression and trait anger. Differences in cortisol following exposure to a stressful event were also examined. Procedures included two laboratory visits consisting of questionnaires, a number of salivary testosterone and cortisol collections, and exposure to a stressor. Results: Perpetrators had higher basal testosterone and post stressor cortisol levels than non- violent controls as well as a higher T/C ratio. In addition, trait anger moderated the relationship between both testosterone alone, and the testosterone/cortisol ratio and perpetration of IPV. Conclusion: Results are consistent with the hypothesis that testosterone leads to antisocial behavior, including perpetration of violence. The results are also consistent with the dual hormone hypothesis, i.e., that testosterone and cortisol work together to jointly regulate social dominance and aggression. Both the increased freestanding testosterone and the increased cortisol following exposure to stress places these men at risk for perpetrating violence. Clinical implications are discussed. [ABSTRACT FROM AUTHOR]

BackgroundEpidemiological evidence suggests that moderately elevated levels of circulating insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in women. How circulating IGF-I may promote breast cancer incidence is unknown, however, increased IGF-I signaling is linked to trastuzumab resistance in ErbB2 positive breast cancer. Few models have directly examined the effect of moderately high levels of circulating IGF-I on breast cancer initiation and progression. The purpose of this study was to assess the ability of circulating IGF-I to independently initiate mammary tumorigenesis and/or accelerate the progression of ErbB2 mediated mammary tumor growth.MethodsWe crossed heterozygous TTR-IGF-I mice with heterozygous MMTV-ErbB2 mice to generate 4 different genotypes: TTR-IGF-I/MMTV-ErbB2 (bigenic), TTR-IGF-I only, MMTV-ErbB2 only, and wild type (wt). Virgin females were palpated twice a week and harvested when tumors reached 1000 mm(3). For study of normal development, blood and tissue were harvested at 4, 6 and 9 weeks of age in TTR-IGF-I and wt mice.ResultsTTR-IGF-I and TTR-IGF-I/ErbB2 bigenic mice showed a moderate 35% increase in circulating total IGF-I compared to ErbB2 and wt control mice. Elevation of circulating IGF-I had no effect upon pubertal mammary gland development. The transgenic increase in IGF-I alone wasn't sufficient to initiate mammary tumorigenesis. Elevated circulating IGF-I had no effect upon ErbB2-induced mammary tumorigenesis or metastasis, with median time to tumor formation being 30 wks and 33 wks in TTR-IGF-I/ErbB2 bigenic and ErbB2 mice respectively (p = 0.65). Levels of IGF-I in lysates from ErbB2/TTR-IGF-I tumors compared to ErbB2 was elevated in a similar manner to the circulating IGF-I, however, there was no effect on the rate of tumor growth (p = 0.23). There were no morphological differences in tumor type (solid adenocarcinomas) between bigenic and ErbB2 mammary glands.ConclusionUsing the first transgenic animal model to elevate circulating levels of IGF-I to those comparable to women at increased risk of breast cancer, we showed that moderately high levels of systemic IGF-I have no effect on pubertal mammary gland development, initiating mammary tumorigenesis or promoting ErbB2 driven mammary carcinogenesis. Our work suggests that ErbB2-induced mammary tumorigenesis is independent of the normal variation in circulating levels of IGF-I.

Abstract Background Epidemiological evidence suggests that moderately elevated levels of circulating insulin-like growth factor-I (IGF-I) are associated with increased risk of breast cancer in women. How circulating IGF-I may promote breast cancer incidence is unknown, however, increased IGF-I signaling is linked to trastuzumab resistance in ErbB2 positive breast cancer. Few models have directly examined the effect of moderately high levels of circulating IGF-I on breast cancer initiation and progression. The purpose of this study was to assess the ability of circulating IGF-I to independently initiate mammary tumorigenesis and/or accelerate the progression of ErbB2 mediated mammary tumor growth. Methods We crossed heterozygous TTR-IGF-I mice with heterozygous MMTV-ErbB2 mice to generate 4 different genotypes: TTR-IGF-I/MMTV-ErbB2 (bigenic), TTR-IGF-I only, MMTV-ErbB2 only, and wild type (wt). Virgin females were palpated twice a week and harvested when tumors reached 1000 mm3. For study of normal development, blood and tissue were harvested at 4, 6 and 9 weeks of age in TTR-IGF-I and wt mice. Results TTR-IGF-I and TTR-IGF-I/ErbB2 bigenic mice showed a moderate 35% increase in circulating total IGF-I compared to ErbB2 and wt control mice. Elevation of circulating IGF-I had no effect upon pubertal mammary gland development. The transgenic increase in IGF-I alone wasn't sufficient to initiate mammary tumorigenesis. Elevated circulating IGF-I had no effect upon ErbB2-induced mammary tumorigenesis or metastasis, with median time to tumor formation being 30 wks and 33 wks in TTR-IGF-I/ErbB2 bigenic and ErbB2 mice respectively (p = 0.65). Levels of IGF-I in lysates from ErbB2/TTR-IGF-I tumors compared to ErbB2 was elevated in a similar manner to the circulating IGF-I, however, there was no effect on the rate of tumor growth (p = 0.23). There were no morphological differences in tumor type (solid adenocarcinomas) between bigenic and ErbB2 mammary glands. Conclusion Using the first transgenic animal model to elevate circulating levels of IGF-I to those comparable to women at increased risk of breast cancer, we showed that moderately high levels of systemic IGF-I have no effect on pubertal mammary gland development, initiating mammary tumorigenesis or promoting ErbB2 driven mammary carcinogenesis. Our work suggests that ErbB2-induced mammary tumorigenesis is independent of the normal variation in circulating levels of IGF-I.

The cattle tick, Rhipicephalus microplus (Canestrini), is an economically destructive arthropod because of its ability to vector bovine babesiosis. It is known that cattle ticks can spend 80--90% of their lifecycle as questing larvae, yet the effect of climatic factors on their off-host behavior and survival is unclear. The goal of this study was to measure the effects of specific ecological factors on off-host questing larvae in nature. The study was conducted in a south Texas pasture over a two-year period, during which time larval populations were surveyed. Simultaneously, weather variables--precipitation, relative humidity, and ambient temperatures--were recorded. Larval survival rates varied among seasons, with the overall highest populations recorded in the spring and the lowest in the fall by a ratio of 20:1. In the winter, the larger numbers were collected from exposed habitats at a ratio of 6:1. Conversely, canopied habitats in the summer had 10-fold larger larval numbers. In the spring, exposed and canopied habitats showed no difference in tick larval survival rates. The results show that the interaction between season and habitat strongly influence off-host questing tick survival. Relative humidity was a key weather variable. [ABSTRACT FROM AUTHOR]