Growth pattern and turnover of carbon and nitrogen measured by stable isotope ratios in the hair of sika deer (Cervus nippon).

Rationale: Hair is known to preserve diet history and other physiological information during its growth period and is often used in chemical analyses. However, the growth patterns and turnover of hair vary according to the animal species or habitat, so understanding these patterns in the target animal is necessary for interpreting the results of hair analyses. In this study, we aimed to elucidate the growth pattern and dietary information of winter coat hair in captive sika deer (Cervus nippon).

Endothelin receptor antagonists alleviate blood-brain barrier disruption and cerebral edema in a mouse model of traumatic brain injury: A comparison between bosentan and ambrisentan.

Traumatic brain injury (TBI) is induced by the immediate physical disruption of brain tissue. TBI causes disruption of the blood-brain barrier (BBB) and brain edema. In the cerebrospinal fluid (CSF) of TBI patients, endothelin-1 (ET-1) is increased, suggesting that ET-1 aggravates TBI-induced brain damage.

Angiopoietin-1/Tie-2 signal after focal traumatic brain injury is potentiated by BQ788, an ET receptor antagonist, in the mouse cerebrum: Involvement in recovery of blood-brain barrier function.

Angiopoietin-1, an angiogenic factor, stabilizes brain microvessels through Tie-2 receptor tyrosine kinase. In traumatic brain injury, blood-brain barrier (BBB) disruption is an aggravating factor that induces brain edema and neuroinflammation. We previously showed that BQ788, an endothelin ET receptor antagonist, promoted recovery of BBB function after lateral fluid percussion injury (FPI) in mice.

Importance of mitochondrial dysfunction in oxidative stress response: A comparative study of gene expression profiles.

Mitochondria are considered to play an important role in oxidative stress response since they are a source of reactive oxygen species and are also targeted by these species. This study examined the mitochondrial conditions in cells of epithelial origin that were exposed to H(2)O(2) and found a decline in the membrane potential along with a specific loss of UQCRC1, a sub-unit of complex III, suggesting that mitochondrial dysfunction occurs upon exposure to oxidative stress. This observation led to the hypothesis that certain cellular responses to oxidative stress occurred because of mitochondrial dysfunction.