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Differences in the NMR detectability of 39K in various excised rat tissues (liver, brain, kidney, muscle, and testes) have been observed. The lowest NMR detectability occurs for liver (61 ± 3% of potassium as measured by flame photometry) and highest for erythrocytes (100 ± 7%). These differences in detectability correlate with differences in the measured 39K NMR relaxation constants in the same tissues. 39K detectabilities were also found to correlate inversely with the mitochondrial content of the tissues. Mitochondria prepared from liver showed greatly reduced 39K NMR detectability when compared with the tissue from which it was derived, 31.6 ± 9% of potassium measured by flame photometry compared to 61 ± 3%. The detectability of potassium in mitochondria was too low to enable the measurement of relaxation constants. This study indicates that differences in tissue structure, particularly mitochondrial content are important in determining 39K detectability and measured relaxation rates.

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Endocrinopathic laminitis is frequently associated with hyperinsulinaemia but the role of glucose in the pathogenesis of the disease has not been fully investigated. This study aimed to determine the endogenous insulin response to a quantity of glucose equivalent to that administered during a laminitis-inducing, euglycaemic, hyperinsulinaemic clamp, over 48. h in insulin-sensitive Standardbred racehorses. In addition, the study investigated whether glucose infusion, in the absence of exogenous insulin administration, would result in the development of clinical and histopathological evidence of laminitis. Glucose (50% dextrose) was infused intravenously at a rate of 0.68 mL/kg/h for 48. h in treated horses (n = 4) and control horses (n = 3) received a balanced electrolyte solution (0.68 mL/kg/h). Lamellar histology was examined at the conclusion of the experiment. Horses in the treatment group were insulin sensitive (M value 0.039 ± 0.0012. mmol/kg/min and M-to-I ratio (100×) 0.014 ± 0.002) as determined by an approximated hyperglycaemic clamp. Treated horses developed glycosuria, hyperglycaemia (10.7 ± 0.78. mmol/L) and hyperinsulinaemia (208 ± 26.1. μIU/mL), whereas control horses did not. None of the horses became lame as a consequence of the experiment but all of the treated horses developed histopathological evidence of laminitis in at least one foot. Combined with earlier studies, the results showed that laminitis may be induced by either insulin alone or a combination of insulin and glucose, but that it is unlikely to be due to a glucose overload mechanism. Based on the histopathological data, the potential threshold for insulin toxicity (i.e. laminitis) in horses may be at or below a serum concentration of ∼200. μIU/mL.

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We present a formalism for the analysis of sensitivity of nuclear magnetic resonance pulse sequences to variations of pulse sequence parameters, such as radiofrequency pulses, gradient pulses or evolution delays. The formalism enables the calculation of compact, analytic expressions for the derivatives of the density matrix and the observed signal with respect to the parameters varied. The analysis is based on two constructs computed in the course of modified density-matrix simulations: the error interrogation operators and error commutators. The approach presented is consequently named the Error Commutator Formalism (ECF). It is used to evaluate the sensitivity of the density matrix to parameter variation based on the simulations carried out for the ideal parameters, obviating the need for finite-difference calculations of signal errors. The ECF analysis therefore carries a computational cost comparable to a single density-matrix or product-operator simulation. Its application is illustrated using a number of examples from basic NMR spectroscopy. We show that the strength of the ECF is its ability to provide analytic insights into the propagation of errors through pulse sequences and the behaviour of signal errors under phase cycling. Furthermore, the approach is algorithmic and easily amenable to implementation in the form of a programming code. It is envisaged that it could be incorporated into standard NMR product-operator simulation packages.

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Background The adverse consequences of lymphedema following breast cancer in relation to physical function and quality of life are clear; however, its potential relationship with survival has not been investigated. Our purpose was to determine the prevalence of lymphedema and associated upper-body symptoms at 6 years following breast cancer and to examine the prognostic significance of lymphedema with respect to overall 6-year survival (OS). Methods and Results A population-based sample of Australian women (n=287) diagnosed with invasive, unilateral breast cancer was followed for a median of 6.6 years and prospectively assessed for lymphedema (using bioimpedance spectroscopy [BIS], sum of arm circumferences [SOAC], and self-reported arm swelling), a range of upper-body symptoms, and vital status. OS was measured from date of diagnosis to date of death or last follow-up. Kaplan-Meier methods were used to calculate OS and Cox proportional hazards models quantified the risk associated with lymphedema. Approximately 45% of women had reported at least one moderate to extreme symptom at 6.6 years postdiagnosis, while 34% had shown clinical evidence of lymphedema, and 48% reported arm swelling at least once since baseline assessment. A total of 27 (9.4%) women died during the follow-up period, and lymphedema, diagnosed by BIS or SOAC between 6–18 months postdiagnosis, predicted mortality (BIS: HR=2.5; 95% CI: 0.9, 6.8, p=0.08; SOAC: 3.0; 95% CI: 1.1, 8.7, p=0.04). There was no association (HR=1.2; 95% CI: 0.5, 2.6, p=0.68) between self-reported arm swelling and OS. Conclusions These findings suggest that lymphedema may influence survival following breast cancer treatment and warrant further investigation in other cancer cohorts and explication of a potential underlying biology.

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Overweight and obesity are strongly associated with endometrial cancer. Several independent genome-wide association studies recently identified two common polymorphisms, FTO rs9939609 and MC4R rs17782313, that are linked to increased body weight and obesity. We examined the association of FTO rs9939609 and MC4R rs17782313 with endometrial cancer risk in a pooled analysis of nine case-control studies within the Epidemiology of Endometrial Cancer Consortium (E2C2). This analysis included 3601 non-Hispanic white women with histologically-confirmed endometrial carcinoma and 5275 frequency-matched controls. Unconditional logistic regression models were used to assess the relation of FTO rs9939609 and MC4R rs17782313 genotypes to the risk of endometrial cancer. Among control women, both the FTO rs9939609 A and MC4R rs17782313 C alleles were associated with a 16% increased risk of being overweight (p = 0.001 and p = 0.004, respectively). In case-control analyses, carriers of the FTO rs9939609 AA genotype were at increased risk of endometrial carcinoma compared to women with the TT genotype [odds ratio (OR) = 1.17; 95% confidence interval (CI): 1.03–1.32, p = 0.01]. However, this association was no longer apparent after adjusting for body mass index (BMI), suggesting mediation of the gene-disease effect through body weight. The MC4R rs17782313 polymorphism was not related to endometrial cancer risk (per allele OR = 0.98; 95% CI: 0.91–1.06; p = 0.68). FTO rs9939609 is a susceptibility marker for white non-Hispanic women at higher risk of endometrial cancer. Although FTO rs9939609 alone might have limited clinical or public health significance for identifying women at high risk for endometrial cancer beyond that of excess body weight, further investigation of obesity-related genetic markers might help to identify the pathways that influence endometrial carcinogenesis.

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Objectives: Malnutrition is common in older hospitalised patients, and barriers to adequate intake in hospital limit the effectiveness of hospital-based nutrition interventions. This pilot study was undertaken to determine whether nutrition-focussed care at discharge and in the early post-hospital period is feasible and acceptable to patients and carers, and improves nutritional status. Design: Prospective cohort study Setting: Internal medicine wards of a tertiary teaching hospital in Brisbane, Australia Participants: Patients aged 65 and older admitted for at least 3 days, identified as malnourished or at risk of malnutrition using Mini Nutritional Assessment (MNA). Interventions: An interdisciplinary discharge team (specialist discharge planning nurse and accredited practicing dietitian) provided nutrition-focussed education, advice, service coordination and follow-up (home visits and telephone) for 6 weeks following hospitalisation Measurements: Nutritional intake, weight, functional status and MNA were recorded 6 and 12 weeks after discharge. Service intensity and changes to care were noted, and hospital readmissions recorded. Service feedback from patients and carers was sought using a brief questionnaire. Results: 12 participants were enrolled during the 6 week pilot (mean age 82 years, 50% male). All received 1-2 home visits, and 3-8 telephone calls. Four participants had new community services arranged, 4 were commenced on oral nutritional supplements, and 7 were referred to community dietetics services for follow-up. Two participants had a decline in MNA score of more than 10% at 12 week follow-up, while the remainder improved by at least 10%. Individualised care including community service coordination was valued by participants. Conclusion: The proposed model of care for older adults was feasible, acceptable to patients and carers, and associated with improved nutritional status at 12 weeks for most participants. The pilot data will be useful for design of intervention trials.

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Aim: Up to 60% of older medical patients are malnourished with further decline during hospital stay. There is limited evidence for effective nutrition intervention. Staff focus groups were conducted to improve understanding of potential contextual and cultural barriers to feeding older adults in hospital. Methods: Three focus groups involved 22 staff working on the acute medical wards of a large tertiary teaching hospital. Staff disciplines were nursing, dietetics, speech pathology, occupational therapy, physiotherapy, pharmacy. A semistructured topic guide was used by the same facilitator to prompt discussions on hospital nutrition care including barriers. Focus groups were tape-recorded, transcribed and analysed thematically. Results: All staff recognised malnutrition to be an important problem in older patients during hospital stay and identified patient-level barriers to nutrition care such as non-compliance to feeding plans and hospital-level barriers including nursing staff shortages. Differences between disciplines revealed a lack of a coordinated approach, including poor knowledge of nutrition care processes, poor interdisciplinary communication, and a lack of a sense of shared responsibility/coordinated approach to nutrition care. All staff talked about competing activities at meal times and felt disempowered to prioritise nutrition in the acute medical setting. Staff agreed education and ‘extra hands’ would address most barriers but did not consider organisational change. Conclusions: Redesigning the model of care to reprioritise meal-time activities and redefine multidisciplinary roles and responsibilities would support coordinated nutrition care. However, effectiveness may also depend on hospitalwide leadership and support to empower staff and increase accountability within a team-led approach.

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In the structure of the title compound C14H9Cl3I2, which is the p-iodophenyl analogue of the insecticide DDT [1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane], isomorphism between the two compounds has been confirmed. In the molecule the dihedral angle between the planes of the two phenyl rings is 65.8(4)deg. which compares with 64.7(7)deg. in DDT.

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In the structure of the title compound C22H27Cl302, which is the p-butoxyphenyl analogue of the insecticidally active p-methoxyphenyl compound methoxychlor, the dihedral angle between the two phenyl rings is 79.61(11)deg. Present also in the structure is an intramolecular aromatic C-H...Cl interaction [3.361(2)Ang].

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The structures of the open chain amide carboxylic acid rac-cis-[2-(2-methoxyphenyl)carbamoyl]cyclohexane-1-carboxylic acid, C15H19NO4, (I) and the cyclic imides rac-cis-2-(4-methoxyphenyl)-3a,4,5,6,7,7-hexahydroisoindole-1,3-dione,C15H17NO3, (II), chiral cis-2-(3-carboxyphenyl)-3a,4,5,6,7,7a-hexahydroisoindole-1,3-dione, C15H15NO4,(III) and rac-cis-2-(4-carboxyphenyl)- 3a,4,5,6,7,7a-hexahydroisoindole-1,3-dione monohydrate, C15H15NO4. H2O) (IV), are reported. In the amide acid (I), the phenylcarbamoyl group is essentially planar [maximum deviation from the least-squares plane = 0.060(1)Ang. for the amide O atom], the molecules form discrete centrosymmetric dimers through intermolecular cyclic carboxy-carboxy O-H...O hydrogen-bonding interactions [graph set notation R2/2(8)]. The cyclic imides (II)--(IV) are conformationally similar, with comparable phenyl ring rotations about the imide N-C(aromatic) bond [dihedral angles between the benzene and isoindole rings = 51.55(7)deg. in (II), 59.22(12)deg. in (III) and 51.99(14)deg. in (IV). Unlike (II) in which only weak intermolecular C-H...O(imide) hydrogen bonding is present, the crystal packing of imides (III) and (IV) shows strong intermolecular carboxylic acid O-H...O hydrogen-bonding associations. With (III), these involve imide O-atom acceptors, giving one-dimensional zigzag chains [graph set C(9)], while with the monohydrate (IV), the hydrogen bond involves the partially disordered water molecule which also bridges molecules through both imide and carboxyl O-atom acceptors in a cyclic R4/4(12) association, giving a two-dimensional sheet structure. The structures reported here expand the structural data base for compounds of this series formed from the facile reaction of cis-cyclohexane-1,2-dicarboxylic anhydride with substituted anilines, in which there is a much larger incidence of cyclic imides compared to amide carboxylic acids.

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Purpose To compare self-reported driving ability with objective measures of on-road driving performance in a large cohort of older drivers. Methods 270 community-living adults aged 70 – 88 years recruited via the electoral roll completed a standardized assessment of on-road driving performance and questionnaires determining perceptions of their own driving ability, confidence and driving difficulties. Retrospective self-reported crash data over the previous five years were recorded. Results Participants reported difficulty with only selected driving situations, including driving into the sun, in unfamiliar areas, in wet conditions, and at night or dusk. The majority of participants rated their own driving as good to excellent. Of the 47 (17%) of drivers who were rated as potentially unsafe to drive, 66% rated their own driving as good to excellent. Drivers who made critical errors, where the driving instructor had to take control of the vehicle, had no lower self-rating of driving ability then the rest of the group. The discrepancy in self-perceptions of driving and participants’ safety rating on the on-road assessment was significantly associated with self-reported retrospective crash rates, where those drivers who displayed greater overconfidence in their own driving were significantly more likely to report a crash. Conclusions This study demonstrates that older drivers with the greatest mismatch between actual and self-rated driving ability pose the greatest risk to road safety. Therefore licensing authorities should not assume that when older individuals’ driving abilities begin to decline they will necessarily be aware of these changes and adopt appropriate compensatory driving behaviours; rather, it is essential that evidence-based assessments are adopted.