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Background: Major sporting event catering is a significant undertaking for foodservice providers, particularly with an increasing focus on sustainability, global health, and nutrition demands of athletes. Yet, the inclusion of nutrition expertise in catering varies significantly between events. Foodservice systems models are commonly used to evaluate foodservice operations but to date have not been applied to catering and nutrition at major sporting events., Objective: The aim of this exploratory case study was to gain in-depth insights of key stakeholders (catering management, chefs, organizers, and dietitians) regarding the integration of nutrition into the catering operation of a major global sporting event, with a focus on future continuity, and map this to the foodservice systems model using a program logic model., Setting: Semistructured interviews were conducted with 12 stakeholders during and after the 2018 Commonwealth Games, Gold Coast, Australia., Results: The 8 themes that emerged were related to planning and preparation, refining processes, improvement of the menu, better technology, increase in food allergies/intolerances, organization controls, experience of the workforce, and increased client knowledge of nutrition. The logic model demonstrated that the system is driven by policy and budget at the level of control prior to and during the planning phase but modified by the environment during operation., Conclusions: Despite recognition by stakeholders on the importance of change, there are barriers to the provision of suitable food. Integration of nutrition expertise into tender documents and budgets in major event catering will help ensure nutritionally adequate, culturally suitable, and safe menus for future events., (Copyright © 2021 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved.)

Background: Pneumothorax is a feared complication of cystic fibrosis. With improved survival into adult life the incidence of pneumothorax is expected to increase. The optimal management of these patients is unclear., Methods: Case review of patients from the three Scottish adult CF centres., Results: A total of 22 episodes of pneumothorax occurred in 20 patients over a 12year period. 2 patients died as a result of the pneumothorax. 16 pneumothoraces were treated by insertion of an intercostal drain and 8 by observation. 8 patients suffered a prolonged air leak. 5 patients were treated with pleurodesis. Pneumothorax was associated with a small decline in lung function which persisted for at least 1year., Conclusion: Pneumothorax can present a challenge to treat in adult CF. However successful outcomes can be achieved even in cases of prolonged air leaks. Current national guidelines help in selecting optimal pleural interventions., (Copyright 2010 Elsevier B.V. All rights reserved.)

The crystal structure of a site-specific mutant of the N-terminal half-molecule of human lactoferrin, Lf(N), in which the iron ligand Asp60 has been mutated to Ser, has been determined at 2.05 A resolution in order to determine the effects of the mutation on iron binding and domain closure. Yellow monoclinic crystals of the D60S mutant, in its iron-bound form, were prepared, and have unit cell dimensions a = 110.2 A, b = 57.0 A, c = 55.2 A, beta = 97.6 degrees, space group C2, with one molecule of 333 residues in the asymmetric unit. The structure was determined by molecular replacement, using the wild-type Lf(N) as search model, and was refined by restrained least-squares methods. The final model, comprising 2451 protein atoms (from residues 2 to 315) one Fe3+ and one CO2-(3), and 107 water molecules, gives an R-factor of 0.175 for all data in the resolution range 20.0 to 2.05 A. The model conforms well with standard geometry, having root-mean-square deviations of 0.014 A and 1.2 degrees from standard bond lengths and angles. The structure of the D60S mutant deviates in two important respects from the parent Lf(N) molecule. At the mutation site the Ser side-chain neither binds to the iron atom nor makes any interdomain contact as the substituted Asp does; instead a water molecule fills the iron coordination site and participates in interdomain hydrogen bonding. The domain closure is also changed, with the D60S mutant having a more closed conformation. Consideration of crystal packing suggests that the altered domain closure is a genuine molecular property but both the iron coordination and interdomain contacts are consistent with weakened iron binding in the mutant. The implications for iron binding in transferrins generally are discussed.

The three-dimensional structure of the N-terminal half-molecule of human lactoferrin, LfN, prepared by recombinant DNA methods, has been determined by X-ray crystallography at 2.0 A resolution. The protein is in its iron-bound form and is deglycosylated. X-ray diffraction data were obtained by diffractometry to 3.2 A resolution and synchrotron data collection, using Weissenberg photography with imaging plates, to 1.8 A resolution. The structure was solved by molecular replacement, using the N-lobe of native diferric human lactoferrin (Lf) as search model. Restrained least squares refinement (program TNT) has resulted in a model structure with an R-factor of 0.184 for all data 34,180 (reflections) in the resolution range 8.0 to 2.0 A. The model comprises 2490 protein atoms (residues 4 to 327), 1 Fe3+, 1 CO3(2-) and 180 solvent molecules, all regarded as water. The structure of LfN is essentially the same as that of the N-lobe of intact Lf, being folded into two similar alpha/beta domains, with the Fe3+ and CO3(2-) bound in a specific site in the interdomain cleft. These details are not affected by either deglycosylation or expression in a non-native system. At the C terminus, however, the conformation of residues 321 to 333 is changed. Whereas in Lf residues 321 to 332 form a helix crossing between the domains at the back of the iron site, in LfN residues 321 to 326 have an extended conformation, forming a third interdomain beta-strand, and residues 328 to 333 appear disordered. The conformational change is attributed to the loss of stabilizing interactions from the C-lobe and is mediated by two Gly residues, at positions 321 and 323. It is further proposed that the conformational change is responsible for the more facile iron release properties of LfN, by its effect on the hinge mechanism and increased solvent exposure of residues near the back of the iron site. Other details of the polypeptide chain conformation and the binding site have also been analysed. Two cis-proline residues are found at positions 71 and 142. The bidentate binding of the CO3(2-) to the metal ion is unambiguous, and a network of hydrogen bonds in and around the binding site links the two domains. Clearly-defined amino-aromatic hydrogen bonds are found for Arg210, near the metal site, and some 31 internal water molecules have been identified, 15 of them in essentially discrete sites, and 16 in a cluster filling a cavity in the interdomain cleft.

The amino terminal half of human lactoferrin (LfN) produced from transfected baby hamster kidney cells has been crystallized in its iron-saturated and iron-free forms. The crystals of glycosylated LfN and deglycosylated LfN are monoclinic, space group C2, with cell dimensions a = 133.0 A, b = 58.3 A, c = 58.3 A, alpha = 90.0 degrees, beta = 114.7 degrees, gamma = 90.0 degrees, and one molecule per asymmetric unit. Crystals of apo LfN have also been prepared using deglycosylated protein. These crystals are tetragonal, space group P4(1)2(1)2 (or P4(3)2(1)2), with cell dimensions of a = b = 58.4 A and c = 217.2 A and one molecule per asymmetric unit. Both the iron-saturated and the iron-free crystals are suitable for high resolution X-ray analysis.

Pancreatic secretion is abnormal in at least 90% of patients with pancreatic cancer. Any of the standard tests of pancreatic function that employ an exogenous secretin or CCK-like stimulus effectively reveal those abnormalities. However, despite a high sensitivity, the tests lack the specificity necessary to distinguish reliably between pancreatic cancer and chronic pancreatitis. With the current practice of testing pancreatic function in symptomatic patients and in the absence of an identifiable high-risk group within the population, it is unlikely that the established pancreatic function tests will provide a means for the earlier detection of pancreatic cancer.