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.

[EX Q]: Context: Total shoulder arthroplasty (TSA) results in superior clinical outcomes to hemiarthroplasty (HA); however, TSA is a more technical and invasive procedure. This study retrospectively compares perioperative complications after HA and TSA using the National Surgical Quality Improvement Program (NSQIP) database.', 'The NSQIP user file was queried for HA and TSA cases from the years 2005 through 2010. Major complications were defined as life-threatening or debilitating. All complications occurred within 30 days of the initial procedure. We performed multivariate analysis to compare complication rates between the two procedures, controlling for patient comorbidities.', 'The database returned 1,718 patients (HA in 30.4% [n = 523] and TSA in 69.6% [n = 1,195]). The major complication rates in the HA group (5.2%, n = 29) and TSA group (5.1%, n = 61) were similar (P = .706). Rates of blood transfusions for postoperative bleeding in patients undergoing HA (2.3%, n = 12) and TSA (2.9%, n = 35) were indistinguishable (P = .458). Venous thromboembolism was a rare complication, occurring in 0.4% of patients in each group (2 HA patients and 5 TSA patients, P > .999). On multivariate analysis, the operative procedure was not associated with major complications (P = .349); however, emergency case, pulmonary comorbidity, anemia with a hematocrit level lower than 36%, and wound class of III or IV increased the risk of a major complication (P < .05 for all).\Question: Are perioperative complications after hemiarthroplasty and total shoulder arthroplasty equivalent?
[EX A]: Multivariate analysis of patients undergoing TSA or HA in the NSQIP database suggests that patient factors-not the procedure being performed-are significant predictors of major complications. Controlling for patient comorbidities, we found no increased risk of perioperative major complications in patients undergoing TSA compared with HA.

[EX Q]: Context: Besides chronic stress, chronic pain is a prevalent determinant for depression. Changes induced in specific brain regions by sustained pain may alter the processing of affective information, thus resulting in anxiodepressive disorders. Here, we compared the role of the anterior cingulate cortex (ACC) and the posterior insular cortex in the anxiodepressive, sensory, and affective aspects of chronic pain.', 'Neuropathic pain was induced by cuffing the right sciatic nerve of C57BL/6J mice. Lesions were performed by local injection of ibotenic acid and chronic activation of the ACC by optogenetic stimulation. Anxiodepressive-related behaviors were evaluated through the novelty suppressed feeding, marble burying, splash, and forced swimming tests. Mechanical thresholds were determined using von Frey filaments, and the relief of spontaneous pain was determined by using place conditioning.', 'The ACC lesion prevented the anxiodepressive consequences of chronic pain without affecting the sensory mechanical allodynia. Conversely, the tonic or spontaneous pain and the anxiodepressive consequences of pain remained present after posterior insular cortex lesion, even though the mechanical allodynia was suppressed. Furthermore, optogenetic stimulation of the ACC was sufficient to induce anxiety and depressive-like behaviors in naïve animals.\Question: Is the anterior cingulate cortex a critical hub for pain-induced depression?
[EX A]: Our results show that, at cortical level, the sensory component of chronic pain remains functionally segregated from its affective and anxiodepressive components. Spontaneous tonic pain and evoked allodynia can be experimentally dissociated. Furthermore, the ACC appears as a critical hub for mood disorders, including for the anxiodepressive consequences of chronic pain, and thus constitutes an important target for divulging the underlying mechanism.

[EX Q]: Context: We aimed to investigate whether and how the total flavonoid extracts (TFE) from Inula britannica L. block neointimal hyperplasia induced by balloon injury in rats.', 'Rats were administered orally TFE doses of 12.5, 25 and 50 mg/kg/d by gastric gavage from 3 days before balloon injury to 14 days after the injury. The ratio of intima (I) to media (M) thickness (I/M) in carotid arteries was examined by morphological analyses. The MDA content and SOD activity in plasma were measured. The O(2)(-) production in vascular tissues was detected in situ. The expression of p47(phox) in carotid arteries was analyzed by Western blot analysis and immunohistochemistry.', 'The rats treated with TFE 50 mg/kg/d showed a reduction in neointimal hyperplasia, and the ratio of I/M of balloon injured-carotid arteries was significantly reduced by over 70% after TFE treatment, compared with the injured group. The inhibitory effect of TFE on neointimal hyperplasia was almost consistent with that of atorvastatin, a positive control. The plasma SOD activity was obviously increased by TFE treatment (P<0.01), while plasma MDA production was markedly decreased by TFE treatment (P<0.05). On day 14 after balloon injury, the carotid arteries showed an increase in O(2)(-) production that was most evident in the neointimal and medial layer of the vessel. Thus, TFE significantly inhibited injury-induced O(2)(-) production and p47(phox) expression in carotid arteries.\Question: Do flavonoids from Inula britannica L. inhibit injury-induced neointimal formation by suppressing oxidative-stress generation?
[EX A]:
Our results suggest that TFE inhibit the neointimal hyperplasia after balloon injury, at least partly, by suppressing oxidative-stress generation.