No abstract

Breast cancer is an equal opportunity killer in that as many as 60%-70% of breast cancer patients have no obvious risk factor(s). Thus, the continued reliance on the importance of risk factors to initiate screening programs may inhibit further inquiry into better diagnostic and prognostic indicators. An extensive review of past and recent literature reveals that mammography is not an objective examination. Its use as a screening tool is facilitated among women 40 years old and older whose breast tissue is primarily fatty and provides better visualization. Younger women are not generally advised to use mammography because of its potentially hazardous effects associated with repeated use of radiation. More importantly, regardless of patient age, radiologists interpret mammograms, and different degrees of interpretation error exist for different radiologists as well as for the same radiologist performing the analysis after a period of time. Thus, the use of mammography as the sole screening tool does not provide patients or physicians with a sense of confidence about sensitivity and specificity. Further, recent enthusiasm to promote mammography screening may give women unrealistic expectations, leading them to falsely believe that a negative examination is assurance that cancer is not present in its earliest detectable stage. We propose to supplement the physical examination and mammography with a third screening modality based on thermal detection monitors. This is a noninvasive and nonradiogenic tool and might enable clinicians to provide patients with every opportunity for early diagnosis.

No abstract

Several observations suggest that endothelial cell dysfunction is a central pathophysiologic event of preeclampsia. Endothelin-1 (ET-1) is a vasoconstrictor peptide of the endotheliocyte and is increased in the sera of preeclamptic patients. The aim of this study was to investigate the possible regulatory mechanisms between ET-1 and nitric oxide (NO) production in cultured placental endotheliocytes. We report that endothelial cells of arterial placental blood vessels show a dysfunctional mechanism of negative feedback regulation of ET-1 production by cGMP or insufficient NO release in response to a stimulus in the form of an increasing ET-1 concentration.

No abstract