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.
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Question: Context: Stem cell factor (SCF) has well-known proliferative effects on hematopoietic cells. SCF also has effects on differentiation and proliferation in other cell types. Interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha have proliferative effects in the liver. Recent studies in our laboratory have linked SCF's hepatoproliferative actions to those of IL-6, demonstrating that IL-6-induced hepatocyte proliferation depends, at least in part, on SCF. We now hypothesize that TNF-alpha's hepatoproliferative effects are also dependent on SCF.", 'In vitro studies using primary mouse hepatocytes show that SCF is induced by TNF-alpha; anti-SCF antibody treatment in this system inhibits TNF-alpha-induced hepatocyte proliferation, suggesting that TNF-alpha-induced hepatocyte proliferation is also SCF dependent. Additional in vivo experiments were performed in which wild type and/or TNF-alpha receptor-1 knockout mice (TNFR1(-/-)) were subjected to 70% hepatectomy or sham laparotomy. TNFR1(-/-) mice are known to have delayed hepatic regeneration after partial hepatectomy. Initial experiments demonstrated that the SCF receptor, c-kit, is upregulated after partial hepatectomy in wild-type mice, further emphasizing the importance of this system in the restoration of hepatic mass. SCF administration to TNFR1(-/-) mice in the context of partial hepatectomy restores hepatocyte proliferation to normal. Further, SCF administration to TNFR1(-/-) mice before hepatectomy increases phosphotyrosine signal transducer and activator (p-stat-3) levels, suggesting that SCF-induced increases in hepatocyte proliferation may also be stat-3 mediated.\Question: Are stem cell factor and its receptor , c-kit , important for hepatocyte proliferation in wild-type and tumor necrosis factor receptor-1 knockout mice after 70 % hepatectomy?

Answer: These data suggest that TNF-alpha-induced hepatocyte proliferation depends, at least in part, on SCF and that SCF and its receptor, c-kit, are important for the liver's regenerative processes.


Question: Context: "Virtual fracture clinics" have been reported as a safe and effective alternative to the traditional fracture clinic. Robust protocols are used to identify cases that do not require further review, with the remainder triaged to the most appropriate subspecialist at the optimum time for review. The objective of this study was to perform a "top-down" analysis of the cost effectiveness of this virtual fracture clinic pathway.', 'National Health Service financial returns relating to our institution were examined for the time period 2009 to 2014 which spanned the service redesign.', 'The total staffing costs rose by 4% over the time period (from £1 744 933 to £1 811 301) compared with a national increase of 16%. The total outpatient department rate of attendance fell by 15% compared with a national fall of 5%. Had our local costs increased in line with the national average, an excess expenditure of £212 705 would have been required for staffing costs.\Question: Does fracture clinic redesign reduce the cost of outpatient orthopaedic trauma care?

Answer: The virtual fracture clinic system was associated with less overall use of staff resources in comparison to national cost data. Adoption of this system nationally may have the potential to achieve significant cost savings.Cite this article: P. J. Jenkins. Fracture clinic redesign reduces the cost of outpatient orthopaedic trauma care. Bone Joint Res 2016;5:33-36. doi: 10.1302/2046-3758.52.2000506.


Question: Context: Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H(2)O. Both lungs inflated at 20 cm H(2)O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H(2)O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes.\Question: Does localized airway anesthesia with lidocaine partially suppress cardiovascular responses To lung inflation?

Answer:
Localized airway anesthesia with lidocaine is unlikely to suppress the cardiovascular responses to lung inflation. This suggests that a limited number of neurogenic mechanisms are involved in the cardiovascular responses to lung inflation in anesthetized humans.