instruction:
Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
question:
To describe the epidemiology of acute hand injuries and hand infections and to describe the factors associated with the transfer of these patients to a level 1 trauma center. In addition, we sought to understand management before transfer.', 'Retrospective review of patients with hand trauma or hand infection transferred to our level 1 trauma center from May 2009 to August 2011. We also identified hospitals with emergency departments (EDs) in our region and surveyed ED providers in these hospitals with regard to acute hand care.', 'A level 1 trauma center in the United States.', 'Four hundred sixty consecutive transfers for acute hand care.', 'The average patient age was 38. Most were male (84%), uninsured (51%), and from another county (59%). The average distance of transfer was 51 miles, and 80% were transferred by ground ambulance. The most common reasons for transfer were amputations (24%), infections (21%), lacerations (17%), and fractures/dislocations (16%). Of the 345 hospitals with an ED surveyed, 71% never had hand surgery coverage.
answer:
Do lack of Acute Hand Care in the Southwest United States?


question:
Mitochondrial permeability transition pore (mPTP) opening is a terminal event leading to mitochondrial dysfunction and cell death under conditions of oxidative stress (OS). However, mPTP blockade with cyclosporine A (CsA) has shown variable efficacy in limiting post-ischemic dysfunction and arrhythmias. We hypothesized that strong feedback between energy dissipating (mPTP) and cardioprotective (mKATP) channels determine vulnerability to OS.', 'Guinea pig hearts (N = 61) were challenged with H2O2 (200 μM) to elicit mitochondrial membrane potential (ΔΨm) depolarization. High-resolution optical mapping was used to measure ΔΨm or action potentials (AP) across the intact heart. Hearts were treated with CsA (0.1 μM) under conditions that altered the activity of mKATP channels either directly or indirectly via its regulation by protein kinase C. mPTP blockade with CsA markedly blunted (P < 0.01) OS-induced ΔΨm depolarization and delayed loss of LV pressure (LVP), but did not affect arrhythmia propensity. Surprisingly, prevention of mKATP activation with the chemical phosphatase BDM reversed the protective effect of CsA, paradoxically exacerbating OS-induced ΔΨm depolarization and accelerating arrhythmia onset in CsA treated compared to untreated hearts (P < 0.05). To elucidate the putative molecular mechanisms, mPTP inhibition by CsA was tested during conditions of selective PKC inhibition or direct mKATP channel activation or blockade. Similar to BDM, the specific PKC inhibitor, CHE (10 μM) did not alter OS-induced ΔΨm depolarization directly. However, it completely abrogated CsA-mediated protection against OS. Direct pharmacological blockade of mKATP, a mitochondrial target of PKC signaling, equally abolished the protective effect of CsA on ΔΨm depolarization, whereas channel activation with 30 μM Diazoxide protected against ΔΨm depolarization (P < 0.0001). Conditions that prevented mKATP activation either directly or indirectly via PKC inhibition led to accelerated ΔΨm depolarization and early onset of VF in response to OS. Investigation of the electrophysiological substrate revealed accelerated APD shortening in response to OS in arrhythmia-prone hearts.
answer:
Do functional crosstalk between the mitochondrial PTP and KATP channels determine arrhythmic vulnerability to oxidative stress?


question:
Morphine and other opioids are routinely used systemically and as wound infusions in the postoperative period. Their effect on wound and fracture healing remains unclear.', 'The primary outcome was to assess the potential cytotoxicity of clinically relevant concentrations of morphine on human fibroblasts.', 'Laboratory in-vitro study.', 'Institute of Physiology, Zurich Center for Integrative Human Physiology, University of Zurich.', 'Monolayers of human fibroblasts.', 'Exposure of human fibroblast monolayers to several concentrations of morphine, for different periods of time, with and without an artificially induced inflammatory process.', 'Cell count, cell viability, cell proliferation and apoptosis.', 'A concentration, time and exposure-dependent cytotoxic effect of morphine-mediated apoptosis was observed. Simulated inflammatory conditions seemed to lessen toxic effects.
answer:

Are clinical concentrations of morphine cytotoxic on proliferating human fibroblasts in vitro?