Adenosine protects mitochondria from oxidant damage through a pathway involving A(2) receptors, eNOS, NO, PI3-kinase/Akt, and Src tyrosine kinase.

Previously, the authors cloned and characterized murine brain-specific angiogenesis inhibitor 1 (mBAI1). In this study, the authors cloned mBAI2 and analyzed its functional characteristics. Northern and Western blot analyses demonstrated a unique developmental expression pattern of mBAI2 in the brain. The expression level of mBAI2 appeared to increase as the development of the brain progressed. Reverse transcription-polymerase chain reaction (RT-PCR) analyses demonstrated the existence of alternative splice variants of mBAI2, which were defective in parts of type I repeat of thrombospondin or the third cytoplasmic loop of the seven-span transmembrane domain that were considered essential to the functions of mBAI2. The expressions of spliced variants in the brain were differently regulated compared with wild-type mBAI2 during development and ischemic conditions. In situ hybridization analyses of the brain showed the same localization of BAI2 as BAI1, such as in most neurons of cerebral cortex. In the in vivo focal cerebral ischemia model and the in vitro hypoxic cell culture model with cobalt, BAI2 expression decreased after hypoxia and preceded the increased expression of vascular endothelial growth factor (VEGF). RT-PCR analysis of antisense BAI2 cDNA-transfected SHSY5Y cells showed an increased VEGF expression as well as a decreased BAI2 expression. Immunohistochemical study of focal ischemic cortex showed that the regional localization of decreased BAI2 was related to the formation of new vessels. These results suggest that the brain-specific developmental expression pattern of angiostatic BAI2 is correlated with the decreased neovascularization in the adult brain, and that angiostatic BAI2 participates in the ischemia-induced brain angiogenesis in concert with angiogenic VEGF.

BackgroundPostoperative nausea and vomiting (PONV) is the major complication related to general anesthesia, occurring in 60–80% of patients after thyroidectomy. The objective of this study was to compare the effects of an intraoperative dexmedetomidine infusion with remifentanil, as anesthetic adjuvants of balanced anesthesia, on PONV in patients undergoing thyroidectomy.MethodsEighty patients scheduled for thyroidectomy were randomized into the following two groups: 1) The dexmedetomidine group (Group D), who received an initial loading dose of dexmedetomidine (1 µg/kg over 10 min) during the induction of anesthesia, followed by a continuous infusion at a rate of 0.3–0.5 µg/kg/h; 2) the remifentanil group (group R), who received remifentanil at an initial target effect site concentration of 4 ng/ml during the induction of anesthesia, followed by a target effect site concentration of 2–3 ng/ml. PONV was assessed during the first 24 hours in 2 time periods (0–2 h and 2–24 h). The pain intensity, sedation score, extubation time, and hemodynamics were also assessed.ResultsDuring the 2 time periods, the incidence and severity of PONV in group D were significantly lower than in group R. In addition, the need for rescue antiemetics was significantly lower in group D than in group R. The effect of dexmedetomidine on postoperative pain relief (2–24 h) was superior to that of remifentanil. The hemodynamics were similar in both groups, whereas eye opening and extubation time were delayed in group D.ConclusionsAdjuvant use of intraoperative dexmedetomidine infusion may be effective for the prevention of PONV.

We studied the variations in the ventral rami of 152 brachial plexuses in 77 Korean adults. Brachial plexus were composed mostly of the fifth, sixth, seventh and eighth cervical nerves and the first thoracic nerve (77.0%). In 21.7% of the cases examined, the fourth, fifth, sixth, seventh and eighth cervical and the first thoracic nerves contributed to the plexus. A plexus composed of the fourth, fifth, sixth, seventh and eighth cervical and the first and second thoracic nerves, and a plexus composed of the fifth, sixth, seventh eighth cervical nerves were also observed. The plexuses were classified into three groups according to cephalic limitation, and the plexus of group 2 in which the whole fifth cervical nerve enters the plexus, were observed the most frequent. The average diameter of the sixth and the seventh cervical ventral rami of the plexus was greatest and that of the fifth cervical was smallest. The largest nerve entering the plexus was the sixth or the seventh cervical nerve in about 79% of cases. The dorsal scapular nerve originated from the fifth cervical ventral ramus in 110 cases (75.8%). The long thoracic nerve was formed by joining of roots from the fifth, sixth, and seventh cervical nerves in 76.0% of cases. Also, a branch to the phrenic nerve, the suprascapular nerve, a nerve to the pectoralis major muscle and a nerve to the subscapular muscle arising from the ventral rami of the plexus were observed.

During the prostate cancer (PCa) development and its progression into hormone independency, androgen receptor (AR) signals play a central role by triggering the regulation of target genes, including prostate-specific antigen. However, the regulation of these AR-mediated target genes is not fully understood. We have previously demonstrated a unique role of HOXB13 homeodomain protein as an AR repressor. Expression of HOXB13 was highly restricted to the prostate and its suppression dramatically increased hormone-activated AR transactivation, suggesting that prostate-specific HOXB13 was a highly potent transcriptional regulator. In this report, we demonstrated the action mechanism of HOXB13 as an AR repressor. HOXB13 suppressed androgen-stimulated AR activity by interacting with AR. HOXB13 did neither bind to AR responsive elements nor disturb nuclear translocation of AR in response to androgen. In PCa specimen, we also observed mutual expression pattern of HOXB13 and AR. These results suggest that HOXB13 not only serve as a DNA-bound transcription factor but play an important role as an AR-interacting repressor to modulate hormone-activated androgen receptor signals. Further extensive studies will uncover a novel mechanism for regulating AR-signaling pathway to lead to expose new role of HOXB13 as a non-DNA-binding transcriptional repressor.