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INTRODUCTION: Non-iatrogenic trauma to the airway is rare and presents a significant challenge to the anaesthetist. Although guidelines for the management of the unanticipated difficult airway have been published, these do not make provision for the 'anticipated' difficult airway. This systematic review aims to inform best practice and suggest management options for different injury patterns. METHODS: A literature search was conducted using Embase, Medline, and Google Scholar for papers after the year 2000 reporting on the acute airway management of adult patients who suffered airway trauma. Our protocol and search strategy are registered with and published by PROSPERO (http://www.crd.york.ac.uk/PROSPERO, ID: CRD42016032763). RESULTS: A systematic literature search yielded 578 articles, of which a total of 148 full-text papers were reviewed. We present our results categorized by mechanism of injury: blunt, penetrating, blast, and burns. CONCLUSIONS: The hallmark of airway management with trauma to the airway is the maintenance of spontaneous ventilation, intubation under direct vision to avoid the creation of a false passage, and the avoidance of both intermittent positive pressure ventilation and cricoid pressure (the latter for laryngotracheal trauma only) during a rapid sequence induction. Management depends on available resources and time to perform airway assessment, investigations, and intervention (patients will be classified into one of three categories: no time, some time, or adequate time). Human factors, particularly the development of a shared mental model amongst the trauma team, are vital to mitigate risk and improve patient safety.

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This mixed method paper explored the effect of family structure on children's physical activities and sedentary pursuits. It furthers the limited understanding of how family structure impacts on children's time in, and reasons behind engaging in, certain physical activities. Children from three inner city comprehensive schools in the Midlands, United Kingdom, participated through questionnaires (n = 381) and semi-structured interviews (n = 62). The results indicated that boys and girls from single parent families spent more time in sedentary activities during the week and at the weekend (P < 0.01) when compared with their intact couple family counterparts. It was identified that children in single-parent families received less parental support due to a lack of time, transport and additional parental responsibilities that created a family environment that encouraged sedentary pursuits. Moreover, the barriers that encouraged sedentary activities also prevented children in single parent families from engaging in lifetime activities during the week. Children from intact couple families recorded more time in lifetime activities than those in single parent families (P < 0.01). Finally, children in two-parent families had more opportunities to engage not only in these activities individually but also in joint activities with their parents, further reinforcing these behaviours.

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Exercise studies have suggested that the presence of carbohydrate in the human mouth activates regions of the brain that can enhance exercise performance but direct evidence of such a mechanism is limited. The first aim of the present study was to observe how rinsing the mouth with solutions containing glucose and maltodextrin, disguised with artificial sweetener, would affect exercise performance. The second aim was to use functional magnetic resonance imaging (fMRI) to identify the brain regions activated by these substances. In Study 1A, eight endurance-trained cyclists (VO2max 60.8 +/- 4.1 ml kg(-1) min(-1)) completed a cycle time trial (total work = 914 +/- 29 kJ) significantly faster when rinsing their mouths with a 6.4% glucose solution compared with a placebo containing saccharin (60.4 +/- 3.7 and 61.6 +/- 3.8 min, respectively, P = 0.007). The corresponding fMRI study (Study 1B) revealed that oral exposure to glucose activated reward-related brain regions, including the anterior cingulate cortex and striatum, which were unresponsive to saccharin. In Study 2A, eight endurance-trained cyclists (VO2max 57.8 +/- 3.2 ml kg(-1) min(-1)) tested the effect of rinsing with a 6.4% maltodextrin solution on exercise performance, showing it to significantly reduce the time to complete the cycle time trial (total work = 837 +/- 68 kJ) compared to an artificially sweetened placebo (62.6 +/- 4.7 and 64.6 +/- 4.9 min, respectively, P = 0.012). The second neuroimaging study (Study 2B) compared the cortical response to oral maltodextrin and glucose, revealing a similar pattern of brain activation in response to the two carbohydrate solutions, including areas of the insula/frontal operculum, orbitofrontal cortex and striatum. The results suggest that the improvement in exercise performance that is observed when carbohydrate is present in the mouth may be due to the activation of brain regions believed to be involved in reward and motor control. The findings also suggest that there may be a class of so far unidentified oral receptors that respond to carbohydrate independently of those for sweetness.

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The present study investigated the effects of head cooling during endurance cycling on performance and the serotonergic neuroendocrine response to exercise in the heat. Subjects exercised at 75 % VO(2max) to volitional fatigue on a cycle ergometer at an ambient temperature of 29+/-1.0 degrees C, with a relative humidity of approximately 50 %. Head cooling resulted in a 51 % (p<0.01) improvement in exercise time to fatigue and Borg Scale ratings of perceived exertion were significantly lower throughout the exercise period with cooling (p<0.01). There were no indications of peripheral mechanisms of fatigue either with, or without, head cooling, indicating the importance of central mechanisms. Exercise in the heat caused the release of prolactin in response to the rise in rectal temperature. Head cooling largely abolished the prolactin response while having no effect on rectal temperature. Tympanic temperature and sinus skin temperature were reduced by head cooling and remained low throughout the exercise. It is suggested that there is a co-ordinated response to exercise involving thermoregulation, neuroendocrine secretion and behavioural adaptations that may originate in the hypothalamus or associated areas of the brain. Our results are consistent with the effects of head cooling being mediated by both direct cooling of the brain and modified cerebral artery blood flow, but an action of peripheral thermoreceptors cannot be excluded.

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Pituitary hormones have an important role during exercise yet relatively little is known about the stimulus for their release. Body temperature progressively increases during prolonged steady-state exercise in the heat and we have investigated the role that this may play in the release of prolactin, growth hormone and cortisol (as an indicator of adrenocorticotropic hormone) into the circulation. Fit young male subjects exercised at 73% V(O2,max) until volitional fatigue at 20 degrees C and at 35 degrees C (30% relative humidity at both temperatures). Rectal temperature and mean skin temperature were monitored and blood samples analysed for lactate, glucose, cortisol, growth hormone and prolactin concentrations. During the first 20 min, core temperature rose continuously and to a similar extent at both temperatures, while mean skin temperature was approximately 4 degrees C lower during exercise in the cool. Blood glucose concentration was essentially constant throughout the period of exercise while lactate concentration increased in the first 10 min and then remained constant with very similar changes in the two exercise conditions. Prolactin and growth hormone concentrations both increased during the exercise period while the concentration of cortisol declined slightly before rising slightly over the 40 min period. Prolactin release was significantly greater when exercise was carried out in the heat while there was no difference in the release of growth hormone or cortisol in the two conditions. When plotted as a function of rectal temperature, growth hormone concentration showed a linear relationship which was the same at ambient temperatures of 35 degrees C and 20 degrees C. Prolactin concentration had a curvilinear relationship with rectal temperature and this differed markedly at the two ambient temperatures. Cortisol concentration showed no dependence on any measure of body temperature. Our results are consistent with some aspect of body temperature being a stimulus for growth hormone and prolactin secretion; however, the precise mechanism clearly differs between the two hormones and we suggest that skin temperature modulates prolactin release, but does not affect the release of growth hormone.

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RATIONALE: Buspirone is used as a neuroendocrine challenge in which the increase of circulating prolactin is taken as a measure of the sensitivity of central serotonergic (5-HT(1A)) pathways. Interpretation of the test is complicated, however, by the fact that buspirone possesses D(2) antagonist and 5-HT(1A) agonist activity, both of which will result in the release of prolactin. To understand the significance of prolactin secretion in response to buspirone, it is important to measure the differential actions of the two controlling pathways. OBJECTIVE: To characterise the dual action of buspirone in stimulating the secretion of prolactin by blocking the 5-HT(1A) action with the 5-HT1A antagonist action of pindolol. METHODS: Healthy male subjects (n=35) received buspirone (0.5 mg x kg bw(-1) orally) with and without pre-treatment with the 5-HT(1A) receptor antagonist pindolol (40 mg over 2 days, 0.5 mg x kg bw(-1) on test day). Nine subjects underwent two additional trials in which they received a placebo with and without pre-treatment with pindolol. RESULTS: Pindolol alone caused a small but significant reduction (18%) in the tonic release of prolactin. Buspirone alone produced a robust prolactin response which was reduced to approximately half by pindolol pre-treatment. Pindolol pre-treatment also, on average, delayed the onset and peak of the prolactin response. There was wide variation among individuals both in the absolute response to buspirone and in the proportion that could be attributed to the non-serotonergic agonist action of buspirone (22-82% IQ range). CONCLUSIONS: Our results indicate that while serotonergic pathways play a minor role in the tonic release of prolactin, the response to a buspirone challenge alone cannot be used as a simple index of central serotonergic activity. However, if two challenges are carried out, one with buspirone and the other with buspirone plus pindolol, quantitative measures can be made of the sensitivity of both the 5-HT(1A) and the putative D(2) pathways controlling prolactin release.

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An inverse relationship appears to exist between cigarette smoking and the risk of Parkinson's and Alzheimer's diseases. Since both diseases are characterized by enhanced oxidative stress, we investigated the antioxidant potential of nicotine, a primary component of cigarette smoke. Initial chromatographic studies suggest that nicotine can affect the formation of the neurotoxin 6-hydroxydopamine resulting from the addition of dopamine to Fenton's reagent (i.e., Fe2+ and H2O2). Thus, under certain circumstances, nicotine can strongly affect the course of the Fenton reaction. In in vivo studies, adult male rats being treated with nicotine showed greater memory retention than controls in a water maze task. However, neurochemical analysis of neocortex, hippocampus, and neostriatum from these same animals revealed that nicotine treatment had no effect on the formation of reactive oxygen species or on lipid peroxidation for any brain region studied. In an in vitro study, addition of various concentrations of nicotine to rat neocortical homogenates had no effect on lipid peroxidation compared to saline controls. The results of these studies suggest that the beneficial/protective effects of nicotine in both Parkinson's disease and Alzheimer's disease may be, at least partly, due to antioxidant mechanisms.

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This abstract presents a model project aimed to train community lay health workers about genetics, increase cultural competency of genetic services providers, and provide local access to genetic services in primarily Hispanic communities in the state of Arizona. Health Start, a community-based prenatal outreach program, served as the basis for providing genetic education and services. A genetics training curriculum was developed and training of community lay health workers was provided. Cultural and Spanish language training was provided for all genetic services providers. Pediatric genetics outreach clinics were established in eight communities. Community-based lay health workers eagerly incorporate genetic information into their public health knowledge base, but this may not lead to acceptance of these personnel by local health care providers as sources of referrals for specialized health services such as genetics. Cultural competence training of genetic service providers is enthusiastically accepted and utilized in the provision of locally accessible genetics clinics.

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Residents in six specialty training programs completed a 126-item questionnaire designed to assess their skill or confidence to manage adolescent health issues. The residency programs studied were family practice, internal medicine, pediatrics, emergency medicine, obstetrics/gynecology, and combined medicine/pediatrics. Although almost three-fourths of the residents were at least moderately interested in adolescent health care and 90% expected to care for adolescents, only 26% believed an adolescent rotation should be required during training. Residents generally considered themselves unskilled to manage adolescents in the areas of sexuality, handicapping conditions, and psychosocial problems. Significant differences in perceived skills were found among the specialty programs on 45% of the items presented. Resident training appears to be needed in the areas of adolescent growth and development, counseling, and sexuality.

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Light responses of Hermissenda type-B photoreceptors evoked by flashes of light were enhanced and prolonged by bath application of serotonin (5-HT). 5-HT appears to act directly on the B photoreceptors and not indirectly through 5-HT-sensitive interneurons since similar effects were observed in the presence of tetrodotoxin and in axotomized preparations which eliminated synaptic input to the B photoreceptors. We also examined the effect of 5-HT on light-evoked membrane currents with voltage-clamp techniques. The increase in the duration of the light response in 5-HT can be explained by the prolonged decay of the light-activated current evoked by constant-intensity test flashes. 5-HT appears to prolong the light response by slowing a late process in the decay of light-activated membrane current. In contrast to the effects of 5-HT an alpha 2-agonist, clonidine, enhanced the peak photoresponse but did not prolong the light response. Serotoninergic modulation of light-dependent processes in the B photoreceptors may contribute to the development of long-term changes produced by conditioning.

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A new fluorescent lipid analogue, bimanephosphatidylcholine, has been synthesized for use in lipid bilayers. This probe is well suited as an energy-transfer donor with N-(7-nitro-2,1,3-benzoxadiazol-4-yl)phosphatidylethanolamine as the acceptor. Dimyristoylphosphatidylethanolamine vesicles are prepared by sonication at pH 9 and characterized by electron microscopy and other methods. Resonance energy transfer between separately labeled donor and acceptor vesicles is monitored during HCl-induced aggregation to determine the kinetics of lipid randomization. Light scattering is also monitored to measure the kinetics of aggregation. The light scattering shows a marked reversal with NaOH while the energy transfer does not, indicating lipid exchange during a reversibly aggregated state; the extent of energy transfer suggests that only lipids in the outer monolayers exchange. The gel to liquid-crystalline phase transition temperature in HCl-treated vesicles is found to be 47 degrees C with diphenylhexatriene. The initial sonicated dispersion does not show a sharp phase transition. In vesicles labeled with both donor and acceptor probes, a small, irreversible increase in energy transfer is obtained upon lowering and then restoring the pH. These results suggest a metastable phase in the sonicated vesicles containing a randomized distribution of lipid and probes within the bilayers; the thermodynamically favored phase, whose formation is triggered by the pH shock, contains domains within which the probe lipids are more highly concentrated.

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A valinomycin-mediated K+ diffusion potential across the membrane of multilamellar liposomes is stable for longer than 30 min and can be collapsed by a nonselective channel such as gramicidin. The kinetics of the potential collapse are complex but can be qualitatively broken down into a series of processes involving (1) binding of the gramicidin to the outer membrane, (2) dimerization to form a functional channel, (3) the flow of ions through the channel, (4) the establishment of a new diffusion potential on the next bilayer within the multilamellar liposome, and (5) the dissociation of gramicidin from the outer bilayer into the adjacent internal aqueous space. These processes are then repeated, in turn, for all the internal bilayers until the K+ concentration gradient (and membrane potential) is completely dissipated. Process 5 appears to be rate limiting at high gramicidin concentrations, but ion flux, process 3, becomes slower at low gramicidin concentrations where the collapse of the K+ gradient displays voltage dependence. Of course the rates of these processes can also be manipulated by changing the composition or size of the liposome and by varying the ion concentrations. Since the diffusion potential can be conveniently monitored with a voltage-sensitive fluorescent dye, 3,3'-diethylthiodicarbocyanine iodide [diS-C2-(5)], a simple method for the detection and partial characterization of membrane pores emerges from this investigation.

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The authors report the unique case of a patient with the Peutz-Jeghers (P-J) syndrome who had multiple small bowel hamartomatous polyps, some of which also showed adenomatous and carcinomatous changes. Over the course of 30 years, over 100 small bowel and colonic polyps were resected; all histologically demonstrated the typical features seen in hamartomatous polyps. Several jejunoileal polyps excised during the last few months of the patient's life showed not only hamartomatous features but also adenomatous epithelium. As far as the authors can determine, this is the first documented case of adenomatous changes found within a small bowel hamartomatous polyp. In addition, at least one duodenal polyp demonstrated areas of hamartoma, adenoma, and in situ carcinoma. The literature on the occurrence of gastrointestinal adenomas and carcinomas in patients with the P-J syndrome is reviewed, and the relationship of hamartomas, adenomas, and carcinomas of the gastrointestinal tract is discussed.

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The authors studied 51 patients who had small bowel tumors that contained adenomatous epithelium. These rare lesions were identified among 392,000 surgical pathology cases seen during a 62-year period. Grossly and histologically, adenomas arising in the mucosa of the small intestine are similar to the adenomas found in the colon. Of the 51 patients, 18 had adenomas, and 33 had tumors that contained both adenoma and carcinoma in the same lesion, including five intramucosal and 28 invasive carcinomas. The location of the tumor usually determined which clinical problems were produced. The data indicate that adenomas originating in the small bowel mucosa probably are premalignant lesions and that many primary adenocarcinomas of the small intestine arise in adenomas. Of the authors' 130 apparently primary small bowel carcinomas (including the papilla of Vater), 33 (25%) histologically demonstrated adenomatous epithelium in the same lesion. Factors associated with an increased chance of finding carcinoma in an adenoma include adenoma type, size of lesion, location, and multicentricity. Carcinomas appear to develop more frequently in papillary (villous) adenomas than in ordinary adenomas. The larger the lesion is, the more likely carcinoma will be identified. Adenomas involving the ampulla contain carcinoma more often than do lesions found elsewhere in the duodenum and small intestine. Three patients had multiple adenomatous polyps of the small bowel; two of these individuals also had duodenal carcinomas. Various problems in pathologic diagnosis and clinical management are discussed.

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Over the past ten years clinicians have been stampeded by the introduction of newer non-steroidal anti-inflammatory drugs. These drugs share analgesic, antipyretic and, most importantly, clinical anti-inflammatory activity and are therefore useful in treating rheumatic diseases. These medications often have less frequent adverse reactions than aspirin and offer alternatives to patients who are intolerant to the more conventional NSAID. The authors review some of the principles which determine choice of the non-steroidal anti-inflammatory drugs, list some specifics on each of the currently available medications, and recommend drugs of choice in a number of specific rheumatic processes.

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The clinical and pathologic features of 43 primary adenacarcinomas of the small intestine (32 jejunal and 11 ileal) are reported. Seventy-four percent of the patients presented with partial or complete small bowel obstruction, 56% complained of abdominal pain, 37% had symptoms of anemia (weakness, easy fatigability), and 35% had lost weight. Anemic hemoglobin levels occurred in 69%, and a palpable abdominal mass in 25%. Treatment consisted of a "curative" or "palliative" resection, or a bypass procedure. Seventy-nine percent of the tumors showed an annular, constricting pattern, while the remaining 21% had a predominantly fungating or polypoid appearance. Three individuals currently free of clinical recurrence have been followed less than 5 years. Of the remaining 40 patients, a 5-year cure was achieved in 11 (28%), including 6 (15%) who at present have no recurrence and 5 (13%) who subsequently died of other causes. Within 5 years, 28 of these 40 patients (70%) were known or presumed dead tumor, and 1 had succumbed to other causes (2%). Various pathologic features were correlated with the clinical course. Documented lymph node metastasis proved to be the most valuable prognostic finding, 88% of these individuals dying of tumor, as contrasted to 45% of those with tumor-free nodes. A few cases of superficially invasive carcinoma found in an otherwise benign adenomatous lesion had a good prognosis when symptoms were produced mainly by the adenoma, the carcinoma being a relatively minor component.

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