We investigated the period variation for 79 eclipsing binary systems using 20 years (1990-2009) of EROS, Macho, and OGLE survey observations. We discovered 9 apsidal motions, 8 mass transfers, 5 period increasing and decreasing systems, 12 light-travel-time effects, 5 eccentric systems and 40 other systems showing no period variations. We select 3 representative eclipsing binary systems; EROS 1052 for apsidal motion, EROS 1056 for mass transfer, and EROS 1037 for the light-travel-time effect. We determine the period variation rate (dP/dt), orbital parameters of the 3rd body (e3, ω3, f(m3), P3, T3), apsidal motion parameters (dω/dt, U, Ps, Pa, e) and apsidal motion period by analyzing the light curves and O-C diagrams.

A stroke is the major cause of death and can cause neurological damage. The striatum serves as an input gate of the basal ganglia in assisting motor behavior. The activity-dependent synaptic plasticity in the dorsal striatum (DS) is known to play a key role for recovery of motor control after brain injury. Exercise supports functional recovery from ischemic brain injury through brain-derived neurotrophic factor (BDNF) -induced synaptic plasticity. Exercise upregulate the levels of BDNF within both the hippocampus and cerebral cortes and might act as a gate that primes the brain to respond to environmental stimulation, while simultaneously increasing the ability of neurons to resist insult. However, little is known about the effects of exercise on neuroprotection in the DS. Therefore, in this study we attempted to investigate the effects of exercise on the neuronal cell population in the DS. Transient focal brain ischemia was induced by middle cerebral artery occlusion (MCAO) on male Sprague-Dawley rats (300±30). Animals were subjected to forced treadmill exercise group and sedentary group after MCAO. Exercise improved neurologic functions measured by modified neurological severity score. Exercise group showed reduced infarct volume measured by vital staining with 2,3,5-triphenyltetrazolium chloride. Immunohistochemical analysis was performed in the DS with antibodies of neuronal nuclei (NeuN) protein, glial fibrillary acidic protein (GFAP), a matured neuronal marker and an astrocyte marker respectively and BDNF. Ischemic injury decreased NeuN+ cell population but exercise attenuated this decrease while increase in GFAP+ cell population induced by MCAO was inhibited by exercise. These findings suggest that the neurological function recovery by exercise after ischemic brain injury may be mediated by alteration of neuronal cell population in the DS.