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.

Q: Guillotine below-knee amputation (BKA) for wet gangrene is an unfortunate complication of poorly controlled diabetes. We examined risk factors associated with wound complications after amputation formalization in this patient population.', 'Retrospective data over a 4-year period were collected for patients undergoing guillotine BKA for wet gangrene followed by staged formalization. Patients with abnormal distal pulses underwent evaluation before formalization to stratify for peripheral arterial disease (PAD). Those patients with palpable pulses and no known PAD went to formalization without further investigation. Poor operative candidates underwent delayed formalization to allow for preoperative optimization. Patient history, interval between surgeries, pathology, and preformalization laboratories were tested for significance. Primary outcome was postformalization wound complication.', 'Fifty-six amputations in 55 patients met inclusion criteria. Wound complications after formalization occurred in 18 cases, all BKAs (32%). A history of PAD was present in 19 patients (34.5%). On pathology, 23 patients (41%) had small-vessel atherosclerosis or arteriosclerosis. There was no association between wound complications and history of PAD (P = 0.4), preformalization albumin (P = 0.09), glucose (P = 0.9), white blood cell count (P = 0.4), or delayed versus expedited formalization (P = 0.8). Only the presence of microvascular disease on formal pathology was predictive of wound complications (P = 0.03). There was no association between microvascular disease on pathology and a history of PAD (P = 0.07).

A: Is unrecognized arteriosclerosis associated with wound complications after below-knee amputation?
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Q: Intracellular pathogens have developed elaborate strategies for silent infection of preferred host cells. Chlamydia pneumoniae is a common pathogen in acute infections of the respiratory tract (e.g. pneumonia) and associated with chronic lung sequelae in adults and children. Within the lung, alveolar macrophages and polymorph nuclear neutrophils (PMN) are the first line of defense against bacteria, but also preferred host phagocytes of chlamydiae.', 'We could show that C. pneumoniae easily infect and hide inside neutrophil granulocytes until these cells become apoptotic and are subsequently taken up by macrophages. C. pneumoniae infection of macrophages via apoptotic PMN results in enhanced replicative activity of chlamydiae when compared to direct infection of macrophages, which results in persistence of the pathogen. Inhibition of the apoptotic recognition of C. pneumoniae infected PMN using PS- masking Annexin A5 significantly lowered the transmission of chlamydial infection to macrophages. Transfer of apoptotic C. pneumoniae infected PMN to macrophages resulted in an increased TGF-ss production, whereas direct infection of macrophages with chlamydiae was characterized by an enhanced TNF-alpha response.

A: Does chlamydia pneumoniae hide inside apoptotic neutrophils to silently infect and propagate in macrophages?
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Q: We were interested in exploring the molecular mechanisms underlying the observed difference in histamine (H) responsiveness between seasonal allergic rhinitic (SAR) and nonrhinitic (NR) subjects. We hypothesized that SAR subjects express higher nasal mucosal histamine receptor 1 (H1R) and 2 (H2R) levels than do NR subjects. In addition, we examined expression of genes involved in regulating the glandular response, including epidermal growth factor (EGF), EGF receptor (EGFR), and mucins (Muc5Ac and Muc5B).', 'Fourteen subjects, seven SAR and seven NR, were provoked during pollen season with doubling doses of H (0.125-8.0 mg/ml). Nasal airway resistance (NAR) was measured by active posterior rhinomanometry. Provocation was halted when NAR exceeded 150% of baseline. Prior to provocation, nasal scrapings were obtained and mRNA quantified using two-step real-time PCR.', 'The mean PD50 (concentration of H producing a 50% increase in NAR) was significantly lower in the SAR than NR group (0.36 vs 1.32 mg/ml; P < 0.05). The ratio of relative gene copy numbers between the SAR and NR groups were as follows: H1R, 0.85 (P = 0.52); H2R, 0.67 (P = 0.35); EGF, 1.02 (P = 0.93), and EGFR, 103.5 (P < 0.05).

A:
Is epidermal growth factor receptor - but not histamine receptor - upregulated in seasonal allergic rhinitis?
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