In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: The aim of this study was to investigate the attitudes and perceptions of staff radiologists regarding the incorporation of a nonanonymous peer review system at an academic hospital.', 'A questionnaire gauging knowledge of, attitudes toward, and perceptions regarding peer review was distributed to all staff radiologists at a large academic hospital. The survey was distributed before the implementation of a nonanonymous peer review system. Data were analyzed using descriptive statistics. Responses were cross-tabulated according to subspecialty and number of years in practice.', 'The majority of respondents agreed that peer review is important for improving patient care (31 of 36 [86%]) and professional development (29 of 36 [81%]), but the vast majority (33 of 36 [92%]) believed that peer review should be anonymous. Twenty-six of 36 respondents (72%) believed that peer review will not be safe from malpractice issues, 24 of 36 (67%) agreed that it has the potential to damage interpersonal relationships within the department, and 15 of 36 (42%) believed that it may influence their job security or rankings within the department. Significant differences were identified between radiologists with more and fewer years of practice experience.\Question: Do survey of radiologist attitudes and perceptions regarding the incorporation of a departmental peer review system?
The incorporation of a nonanonymous peer review system generates anxiety and uncertainty within a radiology department. The investigation of physicians' attitudes toward and perceptions about peer review is important for understanding the potential impact not only on patient care but also on radiologists' relationships and psychology in the workplace.

Context: Glial cell line-derived neurotrophic factor (GDNF) and N-cadherin interact to transduce intracellular signals. However, the specific molecular mechanisms of this interaction are unclear. This study attempted to detect changes in GDNF-induced -catenin phosphorylation and nuclear translocation in C6 glioma cells.', 'C6 glioma cells were treated with GDNF (70 ng/mL) and membrane and cytoplasmic proteins were extracted. A N-cadherin antibody was used for co-immunoprecipitation (co-IP). Western blot analysis using the co-IP protein was completed using antibodies for -catenin, Src and -actin. Immunocytochemistry was conducted with the same antibodies. To determine if Src induced phosphorylation of -catenin Tyr-654, Western blot analysis was also performed on nuclear proteins from C6 cells treated with tyrosine kinase inhibitor PP2 using then p- -catenin antibody.', 'After induced by GDNF, C6 cell membrane -catenin was phosphorylated at Tyr-654 and subsequently separated from the N-cadherin/-catenin complex. Further study confirmed that the induction by GDNF significantly increased cytoplasmic and nuclear expression of phospho--catenin (Tyr-654) in C6 glioma cells. There was also an increase in the binding of non-receptor protein kinase Src with N-cadherin on the inner cell membrane surface. Src induced phosphorylation of -catenin Tyr-654 induced by GDNF decreased significantly.\Question: Does glial cell line-derived neurotrophic factor promote -catenin phosphorylation and nuclear translocation in glioma cells?
The results of our study demonstrate that GDNF increases the intracellular phosphorylation level of -catenin through N-cadherin/Src signaling, which subsequently stimulates the nuclear translocation of -catenin. This study provides a theoretical basis for us to reveal the role of biological mechanisms on glioma cell by GDNF.

Context: Thromboxane A2 (TXA2) activation is involved in several pathophysiological states in producing pulmonary hypertension. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit pulmonary vasoconstriction induced by the TXA2 analogue U 46619 in an isolated lung model.', 'Isolated rat lungs were perfused with physiological saline solution and autologous blood with or without the LA lidocaine, bupivacaine, ropivacaine, or the permanently charged lidocaine analogue QX 314 (all 1 microg/mL) as a pretreatment. Subsequently, pulmonary vasoconstriction was induced by 3 concentrations of U 46619 (25, 50, and 100 ng/mL) and the change in pulmonary artery pressure (Pa) was compared with each LA. In a second experiment, Pa responses to angiotensin II (0.1 microg), hypoxic pulmonary vasoconstriction (HPV, 3% O2 for 10 minutes), or phenylephrine (0.1 microg) were assessed to determine the specificity of ropivacaine effects on TXA2 receptors. Finally, reversibility of pulmonary vasoconstriction was determined by adding ropivacaine to the perfusate after pulmonary vasoconstriction was established with U 46619.', 'Ropivacaine, but not bupivacaine, lidocaine, or QX 314 significantly attenuated pulmonary vasoconstriction induced by 50 ng/mL U 46619 (35.9%, P<.003) or 100 ng/mL U 46619 (45.2%, P<.001). This effect of ropivacaine was likely to be specific for the thromboxane receptor because pulmonary vasoconstriction induced by angiotensin II, HPV, or phenylephrine was not altered. Ropivacaine did not reverse vasoconstriction when it was administered after U 46619.\Question: Does ropivacaine attenuate pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung?
Ropivacaine, but not lidocaine, bupivacaine, or QX 314 at 1 microg/mL, attenuates U 46619-induced pulmonary vasoconstriction in an isolated perfused rat lung model. These results support evidence that the clinically used enantiomer S(-)-ropivacaine may inhibit TXA2 signaling.