Association between non-alcoholic hepatic steatosis and hyper reactive blood pressure response on the exercise treadmill test.

AIMS: Non-alcoholic hepatic steatosis (HS) is associated with hypertension and increased cardiovascular risk. While Blood pressure hyper-reactive response (HRR) during peak exercise indicates an increased risk of incident hypertension and increased cardiovascular risk, no data on the association of non-alcoholic HS and HRR exists. In this study, we have evaluated the association of HS with HRR. METHODS: We included 13 410 consecutive individuals with a mean age: 42.4 ± 8.9 years, 3561 (26.6%) female with normal resting blood pressure and without a previous diagnosis of hypertension, who underwent symptom limited exercise treadmill test, abdominal ultrasonography and clinical and laboratory evaluation. HS was detected by abdominal ultrasonography. HRR was defined by a peak exercise systolic blood pressure >220 mmHg and/or elevation of 15 mmHg or more in diastolic blood pressure from rest to peak exercise. RESULTS: The prevalence of HS was 29.5% (n = 3956). Overall, 4.6% (n = 619) of the study population presented a HRR. Subjects with HS had a higher prevalence of HRR (8.1 vs. 3.1%, odds ratio 2.8, 95% CI 2.4-3.3, P < 0.001). After adjustment for body mass index, waist circumference, fasting plasma glucose and low density lipoprotein cholesterol, HS (odds ratio 1.4, 95% CI 1.1-1.6, P = 0.002) remained independently associated with HRR. HS was additive to obesity markers in predicting exercise HRR. CONCLUSIONS: Non-alcoholic HS is independently associated with hyper-reactive exercise blood pressure response.

Cytotoxicity of receptor-mediated 16 alpha-[125I]iodoestradiol in cultured MCF-7 human breast cancer cells.

Therapeutic strategies using 125I-labeled steroid hormones are attractive in light of the estrogen dependence of many human breast cancers and the favorable microdosimetry resulting from 125I decay. We determined the uptake, specific estrogen receptor (ER) binding, and cytotoxicity of 16 alpha-[125I]iodoestradiol in cultured MCF-7 human breast cancer cells. The cytotoxicity of receptor-mediated 125I appears to be sufficient in MCF-7 cells to warrant in vivo experimentation. Furthermore, cytotoxicity not specific to ERs is minimal within the dose range necessary for ER saturation and specific cell killing. Competitive toxicity studies using nonradioactive 17 beta-estradiol demonstrate an unequivocal relationship between ER binding and clonogenic viability.