A number of studies have reported that extremely low frequency magnetic fields (ELF-MF) can modulate proliferative processes in vitro; however, the transduction mechanisms implicated in such phenomena remain to be identified. The present study was aimed to determine whether a 50 Hz, 100 µT MF can induce cell proliferation in the human neuroblastoma line NB69, and whether the signaling pathway MAPK-ERK1/2 (Mitogen-Activated Protein Kinase - Extracellular-Signal-Regulated Kinase 1 and 2) is involved in that proliferative response. The cultures were exposed intermittently or continuously to the MF for a 63-hour duration. The continuous treatment did not induce significant changes in cell proliferation. In contrast, intermittent exposure caused statistically significant increase in the percent of cells in phase S of the cell cycle, followed by a significant increase in cell number. The intermittent treatment also induced an early, transient and repetitive activation of ERK1/2 that could be involved in the proliferative effects. In fact, both the proliferative response and the repeated activation of ERK1/2 were blocked by PD98059, the specific inhibitor of MEK (ERK kinases 1 and 2). Taken together, the described results indicate that a 50 Hz, 100 µT MF can stimulate proliferation in NB69 cells by triggering MAPK-ERK1/ 2 signaling at each of the “On” periods of an intermittent exposure.
Most of the previous studies on white coat hypertension were performed in hypertension clinics or academic settings and included relatively small series of patients. Consequently, the prevalence of white coat hypertension in primary care settings and the clinical and epidemiologic characteristics of this subgroup of patients are not well known. We performed this study to estimate the frequency of white coat hypertension in a population of mildly to moderately hypertensive subjects attended in a primary care setting and to examine possible epidemiologic and clinical factors that may identify these patients. Patients included in the study underwent clinical interview, measurement of clinic blood pressure (BP) on three visits, determination of serum lipids, glucose, uric acid, and urinary albumin excretion, 24-h ambulatory BP monitoring, and M-mode and Doppler echocardiography. Patients were classified as white coat hypertensives if their daytime ambulatory BP were < 135/85 mm Hg. We studied 345 patients, 136 (39%) of whom were diagnosed with white coat hypertension. The frequency of white coat hypertension was inversely proportional to the severity of clinic BP values. The diagnosis of white coat hypertension was independently associated with female gender and low educational level. Left ventricular mass index and urinary albumin excretion were lower in the white-coat hypertensive group compared with the group with sustained hypertension. Our results show that a high proportion of patients with mild to moderate hypertension attended in a primary care setting have white coat hypertension. Some clinical characteristics may be helpful in the identification of this group of subjects. White coat hypertensives show less target-organ damage than sustained hypertensive patients.
The proliferative response of the neuroblastoma line NB69 to a 100 µT, 50 Hz magnetic field (MF) has been shown mediated by activation of the MAPK-ERK1/2 pathway. This work investigates the MF effect on the cell cycle of NB69, the participation of p38 and c-Jun N-terminal (JNK) kinases in the field-induced proliferative response and the potential involvement of reactive oxygen species (ROS) in the activation of the MAPK-ERK1/2 and -p38 signaling pathways. NB69 cultures were exposed to the 100 µT MF, either intermittently for 24, 42 or 63 h, or continuously for periods of 15 to 120 min, in the presence or absence of p38 or JNK inhibitors: SB203580 and SP600125, respectively. Antioxidant N-acetylcysteine (NAC) was used as ROS scavenger. Field exposure induced transient activation of p38, JNK and ERK1/2. The MF proliferative effect, which was mediated by changes in the cell cycle, was blocked by the p38 inhibitor, but not by the JNK inhibitor. NAC blocked the field effects on cell proliferation and p38 activation, but not those on ERK1/2 activation. The MF-induced proliferative effects are exerted through sequential upregulation of MAPK-p38 and -ERK1/2 activation, and they are likely mediated by a ROS-dependent activation of p38.
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