UBVI CCD photometry has been obtained for a region around the Wolf-Rayet star WR 12. We found two young stellar associations in the observed field: the nearer one comprises the field members of Vela OBI association at d = 1.8kpc, while the farther one is the young open cluster Bochum 7 (Bo 7) at d = 4.8kpc. The stars associated with Bo 7 showed no central concentration which suggests that Bo 7 is not a young open cluster but simply a local concentration in the density of young stars belonging to the OB association (Vel OB3). These two associations have similar ages but remarkably different mass function slopes (Γ = -2.1 ± 0.3 for Vel OBI and -1.0 ± 0.3 for Bo 7). The stars in Vel OBI shows an evident age spread (ΔT~ 9Myr). We also found two strong Hα emission stars - WR 12 and #1066 - from narrow band Hα photometry.

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.