The effects of flexibility training on exercise-induced muscle damage in young men with limited hamstrings flexibility.

Adaptations to 6 weeks of supervised hamstring stretching training and its potential impact on symptoms of eccentric exercise-induced muscle damage (EIMD) were studied in 10 young, untrained men with limited hamstrings flexibility. Participants performed unilateral flexibility training (experimental leg; EL) on an isokinetic dynamometer, while the contralateral limb acted as control (CL). Hip range of motion (ROM), passive, isometric, and concentric torques, active optimum angle, and biceps femoris and semitendinosus muscle thickness and ultrasound echo intensity were assessed both before and after the training. Additionally, muscle soreness was assessed before and after an acute eccentric exercise bout in both legs (EL and CL) at post-training only. Hip ROM increased (P < .001) only in EL after the training (EL = 10.6° vs CL = 1.6°), but no changes (P > .05) in other criterion measurements were observed. After a bout of eccentric exercise at the end of the program, isometric and dynamic peak torques and muscle soreness ratings were significantly altered at all time points equally in EL and CL. Also, active optimum angle was reduced immediately, 48 and 72 hours post-exercise, and hip ROM was reduced at 48 and 72 hours equally in EL and CL. Finally, biceps femoris muscle thickness was significantly increased at all time points, and semitendinosus thickness and echo intensity significantly increased at 72 hours, with no significant differences between legs. The stretching training protocol significantly increased hip ROM; however, it did not induce a protective effect on EIMD in men with tight hamstrings.

Proliferative indices and oncoprotein expression in benign and malignant breast biopsies.

BACKGROUND: Prognostic factors are used routinely in the management of breast cancer. However, their potential for identifying precursor malignant lesions has not been assessed. METHODS: We have examined 285 breast biopsy specimens (140 benign, 145 malignant) for DNA ploidy, S-phase fraction, Ki-67 nuclear antigen proliferative indices, and HER-2/neu and epidermal growth factor receptor oncoproteins. RESULTS: When proliferative indices were compared between the benign and malignant groups, differences were noted for DNA ploidy, S-phase fraction, and cell cycling index (p < 0.0005). When the benign nonproliferative specimens were compared with the atypical/proliferative benign specimens, proliferative indices failed to show any differences. When the specific subset of proliferative/atypical benign breast tissue was compared with the malignant specimens, DNA index, S-phase fraction, and cell cycling index showed significant differences. The mean for epidermal growth factor receptor was greater in the non-proliferative group but not statistically significant (p < 0.1). HER-2/neu oncoprotein failed to show any differences between the benign and malignant groups. Within the atypical benign group, Ki-67 correlated strongly with S-phase fraction and HER-2/neu (p < 0.01). CONCLUSIONS: We have demonstrated that proliferative indices can differentiate between benign and malignant breast tissues but not among specific subgroups. In addition, epidermal growth factor may differentiate between nonproliferative and proliferative/atypical benign biopsy results. Oncoprotein determination, ploidy, and DNA proliferative indices may be useful in defining malignant and benign breast disease but are not useful in distinguishing between benign and malignant breast disease with an increased likelihood for malignant transformation.

Cytokine secretion induced by superantigens in peripheral blood mononuclear cells, lamina propria lymphocytes, and intraepithelial lymphocytes.

Superantigens are potent inducers of T-cell proliferation and induce a broad range of cytokines, including tumor necrosis factor (TNF), gamma interferon, and interleukin 2 (IL-2). In the present study, we compared the abilities of different staphylococcal superantigens (staphylococcal enterotoxin B [SEB], staphylococcal enterotoxin E [SEE], and toxic shock syndrome toxin 1 [TSST-1]) to stimulate distinct cytokine profiles in peripheral blood mononuclear cells (PBMC), lamina propria lymphocytes (LPL), and intraepithelial lymphocytes (IEL). One million PBMC, LPL, and IEL were stimulated with various concentrations of superantigen (10 to 0.001 ng/ml) for 24, 48, and 72 h. Maximum cytokine production by PBMC, LPL, and IEL was observed for all three superantigens at 48 h at a concentration of 1 ng/ml. In PBMC, SEE and TSST-1 stimulated more IL-2 and gamma interferon than SEB. SEE and TSST-1 also stimulated more TNF and IL-4 production than SEB. In contrast, SEB stimulated more IL-6 than either SEE or TSST-1. In LPL, there was no SEE-induced IL-2 or IL-4 production, but IL-6, TNF, and gamma interferon were induced. SEB similarly induced no IL-2 or gamma interferon from the LPL, but IL-4, IL-6, and TNF were detected. TSST-1 stimulation of LPL resulted in IL-2 and TNF production but no IL-4, IL-6, or gamma interferon. In IEL, SEE induced no IL-2, IL-4, or gamma interferon but produced IL-6 and TNF, while SEB stimulation resulted in no IL-2 or gamma interferon but did result in detectable IL-4, IL-6, and TNF. Taken together, these data indicate that there are significant differences in the cytokine profiles induced by superantigens in LPL and IEL compared with those in PBMC, and these differences may relate to differences in activation requirements.

Ethnic differences in risk and prognostic factors for breast cancer.

BACKGROUND: Poor survival among African American patients with breast cancer has been attributed to low socioeconomic status and lack of access to health care. However, Hispanics of equivalent socioeconomic status and health care access exhibit much higher survival rates, almost comparable to whites. This suggests that biologic differences play a role in differences in breast cancer survival in addition to socioeconomic and health care access factors. METHODS: The authors studied clinical and molecular differences between patients with breast cancer of different ethnicity to determine biologic explanations for the observed differences in survival. Consecutive patients scheduled for breast biopsies were identified preoperatively and were interviewed. Blood was withdrawn for serum marker measurements, and tumor specimens collected at frozen section diagnosis were analyzed by flow cytometry, hormone receptor concentration, tumor grade, and Ki-67 nuclear antigen, HER-2/neu, and epidermal growth factor oncoprotein expression. RESULTS: Age, age at menarche, number of lymph nodes with metastasis, estrogen and progesterone receptor levels, ploidy status, S-phase, Ki-67, HER-2/neu expression, tumor grade, epidermal growth factor receptor expression, lipid-associated sialic acid (LASA), and carcinoembryonic antigen level were not significantly related to ethnicity. African Americans presented at a significantly more advanced stage and with significantly larger tumors. They were significantly heavier and had a significantly higher mean Quetelet's index and a significantly higher number of pregnancies and number of live births. Whites and Hispanics were significantly older at menopause. CONCLUSIONS: The molecular indices associated with breast cancer prognosis do not differ significantly among whites, African Americans, and Hispanics, suggesting that the reported differences in survival among these groups are not due to biologic differences in breast cancer among ethnic groups.