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2.  Coding Geriatric syndromes: How good are we? 
High quality coding of hospital activity is important because the data is used for resource allocation and measuring performance. There is little information on the quality of coding of admissions of frail older people who have multiple diagnoses, co-morbidities and functional impairment. Presence or absence of four geriatric syndromes and eight medical conditions was noted on case note review (CNR). Discharge summaries (DS) and hospital coding (HC) were reviewed and compared with the CNR. Forty patients had at least one geriatric syndrome noted in the DS; 16 (40.0%) were captured by the HC. Of 57 patients with at least one medical condition noted in the DS, 52 (91.2%) were captured by the HC (p<0.0001 for difference in HC capture rates). We have demonstrated poor capture of information on geriatric syndromes compared to medical conditions in discharge summaries and hospital coding and propose a problem list bookmark approach to improve this.
PMCID: PMC3191527  PMID: 22003315
Coding; routine data; geriatric syndromes; frailty
3.  Nutrition and bone health projects funded by the UK Food Standards Agency: have they helped to inform public health policy? 
The British journal of nutrition  2008;99(1):198-205.
The UK Food Standards Agency convened an international group of expert scientists to review the Agency-funded projects on diet and bone health in the context of developments in the field as a whole. The potential benefits of fruit and vegetables, vitamin K, early-life nutrition and vitamin D on bone health were presented and reviewed. The workshop reached two conclusions which have public health implications. First, that promoting a diet rich in fruit and vegetable intakes might be beneficial to bone health and would be very unlikely to produce adverse consequences on bone health. The mechanism(s) for any effect of fruit and vegetables remains unknown, but the results from these projects did not support the postulated acid–base balance hypothesis. Secondly, increased dietary consumption of vitamin K may contribute to bone health, possibly through its ability to increase the γ-carboxylation status of bone proteins such as osteocalcin. A supplementation trial comparing vitamin K supplementation with Ca and vitamin D showed an additional effect of vitamin K against baseline levels of bone mineral density, but the benefit was only seen at one bone site. The major research gap identified was the need to investigate vitamin D status to define deficiency, insufficiency and depletion across age and ethnic groups in relation to bone health.
doi:10.1017/S0007114507771891
PMCID: PMC2755801  PMID: 18086331
Bone; Osteoporosis; Fracture; Calcium; Vitamin D; Vitamin K; Fruit and vegetables
4.  Evaluating the Role of LPIN1 Variation in Insulin Resistance, Body Weight, and Human Lipodystrophy in U.K. Populations 
Diabetes  2008;57(9):2527-2533.
OBJECTIVE— Loss of lipin 1 activity causes lipodystrophy and insulin resistance in the fld mouse, and LPIN1 expression and common genetic variation were recently suggested to influence adiposity and insulin sensitivity in humans. We aimed to conduct a comprehensive association study to clarify the influence of common LPIN1 variation on adiposity and insulin sensitivity in U.K. populations and to examine the role of LPIN1 mutations in insulin resistance syndromes.
RESEARCH DESIGN AND METHOD— Twenty-two single nucleotide polymorphisms tagging common LPIN1 variation were genotyped in Medical Research Council (MRC) Ely (n = 1,709) and Hertfordshire (n = 2,901) population-based cohorts. LPIN1 exons, exon/intron boundaries, and 3′ untranslated region were sequenced in 158 patients with idiopathic severe insulin resistance (including 23 lipodystrophic patients) and 48 control subjects.
RESULTS— We found no association between LPIN1 single nucleotide polymorphisms and fasting insulin but report a nominal association between rs13412852 and BMI (P = 0.042) in a meta-analysis of 8,504 samples from in-house and publicly available studies. Three rare nonsynonymous variants (A353T, R552K, and G582R) were detected in severely insulin-resistant patients. However, these did not cosegregate with disease in affected families, and Lipin1 protein expression and phosphorylation in patients with variants were indistinguishable from those in control subjects.
CONCLUSIONS— Our data do not support a major effect of common LPIN1 variation on metabolic traits and suggest that mutations in LPIN1 are not a common cause of lipodystrophy in humans. The nominal associations with BMI and other metabolic traits in U.K. cohorts require replication in larger cohorts.
doi:10.2337/db08-0422
PMCID: PMC2518506  PMID: 18591397
5.  Six new loci associated with body mass index highlight a neuronal influence on body weight regulation 
Willer, Cristen J | Speliotes, Elizabeth K | Loos, Ruth J F | Li, Shengxu | Lindgren, Cecilia M | Heid, Iris M | Berndt, Sonja I | Elliott, Amanda L | Jackson, Anne U | Lamina, Claudia | Lettre, Guillaume | Lim, Noha | Lyon, Helen N | McCarroll, Steven A | Papadakis, Konstantinos | Qi, Lu | Randall, Joshua C | Roccasecca, Rosa Maria | Sanna, Serena | Scheet, Paul | Weedon, Michael N | Wheeler, Eleanor | Zhao, Jing Hua | Jacobs, Leonie C | Prokopenko, Inga | Soranzo, Nicole | Tanaka, Toshiko | Timpson, Nicholas J | Almgren, Peter | Bennett, Amanda | Bergman, Richard N | Bingham, Sheila A | Bonnycastle, Lori L | Brown, Morris | Burtt, Noël P | Chines, Peter | Coin, Lachlan | Collins, Francis S | Connell, John M | Cooper, Cyrus | Smith, George Davey | Dennison, Elaine M | Deodhar, Parimal | Elliott, Paul | Erdos, Michael R | Estrada, Karol | Evans, David M | Gianniny, Lauren | Gieger, Christian | Gillson, Christopher J | Guiducci, Candace | Hackett, Rachel | Hadley, David | Hall, Alistair S | Havulinna, Aki S | Hebebrand, Johannes | Hofman, Albert | Isomaa, Bo | Jacobs, Kevin B | Johnson, Toby | Jousilahti, Pekka | Jovanovic, Zorica | Khaw, Kay-Tee | Kraft, Peter | Kuokkanen, Mikko | Kuusisto, Johanna | Laitinen, Jaana | Lakatta, Edward G | Luan, Jian'an | Luben, Robert N | Mangino, Massimo | McArdle, Wendy L | Meitinger, Thomas | Mulas, Antonella | Munroe, Patricia B | Narisu, Narisu | Ness, Andrew R | Northstone, Kate | O'Rahilly, Stephen | Purmann, Carolin | Rees, Matthew G | Ridderstråle, Martin | Ring, Susan M | Rivadeneira, Fernando | Ruokonen, Aimo | Sandhu, Manjinder S | Saramies, Jouko | Scott, Laura J | Scuteri, Angelo | Silander, Kaisa | Sims, Matthew A | Song, Kijoung | Stephens, Jonathan | Stevens, Suzanne | Stringham, Heather M | Tung, Y C Loraine | Valle, Timo T | Van Duijn, Cornelia M | Vimaleswaran, Karani S | Vollenweider, Peter | Waeber, Gerard | Wallace, Chris | Watanabe, Richard M | Waterworth, Dawn M | Watkins, Nicholas | Witteman, Jacqueline C M | Zeggini, Eleftheria | Zhai, Guangju | Zillikens, M Carola | Altshuler, David | Caulfield, Mark J | Chanock, Stephen J | Farooqi, I Sadaf | Ferrucci, Luigi | Guralnik, Jack M | Hattersley, Andrew T | Hu, Frank B | Jarvelin, Marjo-Riitta | Laakso, Markku | Mooser, Vincent | Ong, Ken K | Ouwehand, Willem H | Salomaa, Veikko | Samani, Nilesh J | Spector, Timothy D | Tuomi, Tiinamaija | Tuomilehto, Jaakko | Uda, Manuela | Uitterlinden, André G | Wareham, Nicholas J | Deloukas, Panagiotis | Frayling, Timothy M | Groop, Leif C | Hayes, Richard B | Hunter, David J | Mohlke, Karen L | Peltonen, Leena | Schlessinger, David | Strachan, David P | Wichmann, H-Erich | McCarthy, Mark I | Boehnke, Michael | Barroso, Inês | Abecasis, Gonçalo R | Hirschhorn, Joel N
Nature genetics  2008;41(1):25-34.
Common variants at only two loci, FTO and MC4R, have been reproducibly associated with body mass index (BMI) in humans. To identify additional loci, we conducted meta-analysis of 15 genome-wide association studies for BMI (n > 32,000) and followed up top signals in 14 additional cohorts (n > 59,000). We strongly confirm FTO and MC4R and identify six additional loci (P < 5 × 10−8): TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2 and NEGR1 (where a 45-kb deletion polymorphism is a candidate causal variant). Several of the likely causal genes are highly expressed or known to act in the central nervous system (CNS), emphasizing, as in rare monogenic forms of obesity, the role of the CNS in predisposition to obesity.
doi:10.1038/ng.287
PMCID: PMC2695662  PMID: 19079261
6.  Evaluating the role of LPIN1 variation on insulin resistance, body weight and human lipodystrophy in UK populations 
Diabetes  2008;57(9):2527-2533.
OBJECTIVE:
Loss of Lpin1 activity causes lipodystrophy and insulin resistance in the fld mouse, and LPIN1 expression and common genetic variation were recently suggested to influence adiposity and insulin sensitivity in humans. We aimed to conduct a comprehensive association study to clarify the influence of LPIN1 common variation on adiposity and insulin sensitivity in UK populations, and to examine the role of LPIN1 mutations in insulin resistance syndromes.
RESEARCH DESIGN AND METHOD:
Twenty-two SNPs tagging LPIN1 common variation were genotyped in MRC Ely (N = 1709) and Hertfordshire (N = 2901) population-based cohorts. LPIN1 exons, exon/intron boundaries and 3′UTR were sequenced in 158 patients with idiopathic severe insulin resistance (including 23 lipodystrophic patients), and 48 controls.
RESULTS:
We found no association between LPIN1 SNPs and fasting insulin, but report a nominal association between rs13412852 and BMI (P = 0.042) in a meta-analysis of 8504 samples from in-house and publicly available studies. Three rare nonsynonymous variants (A353T, R552K and G582R) were detected in severely insulin resistant patients. However, these did not co-segregate with disease in affected families and Lipin1 protein expression and phosphorylation in patients with variants was indistinguishable from controls.
CONCLUSIONS:
Our data do not support a major effect of LPIN1 common variation on metabolic traits and suggest that mutations in LPIN1 are not a common cause of lipodystrophy in humans. The nominal associations with BMI and other metabolic traits in UK cohorts require replication in larger cohorts.
doi:10.2337/db08-0422
PMCID: PMC2518506  PMID: 18591397
7.  Common variants near MC4R are associated with fat mass, weight and risk of obesity 
Loos, Ruth J F | Lindgren, Cecilia M | Li, Shengxu | Wheeler, Eleanor | Zhao, Jing Hua | Prokopenko, Inga | Inouye, Michael | Freathy, Rachel M | Attwood, Antony P | Beckmann, Jacques S | Berndt, Sonja I | Bergmann, Sven | Bennett, Amanda J | Bingham, Sheila A | Bochud, Murielle | Brown, Morris | Cauchi, Stéphane | Connell, John M | Cooper, Cyrus | Smith, George Davey | Day, Ian | Dina, Christian | De, Subhajyoti | Dermitzakis, Emmanouil T | Doney, Alex S F | Elliott, Katherine S | Elliott, Paul | Evans, David M | Farooqi, I Sadaf | Froguel, Philippe | Ghori, Jilur | Groves, Christopher J | Gwilliam, Rhian | Hadley, David | Hall, Alistair S | Hattersley, Andrew T | Hebebrand, Johannes | Heid, Iris M | Herrera, Blanca | Hinney, Anke | Hunt, Sarah E | Jarvelin, Marjo-Riitta | Johnson, Toby | Jolley, Jennifer D M | Karpe, Fredrik | Keniry, Andrew | Khaw, Kay-Tee | Luben, Robert N | Mangino, Massimo | Marchini, Jonathan | McArdle, Wendy L | McGinnis, Ralph | Meyre, David | Munroe, Patricia B | Morris, Andrew D | Ness, Andrew R | Neville, Matthew J | Nica, Alexandra C | Ong, Ken K | O'Rahilly, Stephen | Owen, Katharine R | Palmer, Colin N A | Papadakis, Konstantinos | Potter, Simon | Pouta, Anneli | Qi, Lu | Randall, Joshua C | Rayner, Nigel W | Ring, Susan M | Sandhu, Manjinder S | Scherag, André | Sims, Matthew A | Song, Kijoung | Soranzo, Nicole | Speliotes, Elizabeth K | Syddall, Holly E | Teichmann, Sarah A | Timpson, Nicholas J | Tobias, Jonathan H | Uda, Manuela | Vogel, Carla I Ganz | Wallace, Chris | Waterworth, Dawn M | Weedon, Michael N | Willer, Cristen J | Wraight, Vicki L | Yuan, Xin | Zeggini, Eleftheria | Hirschhorn, Joel N | Strachan, David P | Ouwehand, Willem H | Caulfield, Mark J | Samani, Nilesh J | Frayling, Timothy M | Vollenweider, Peter | Waeber, Gerard | Mooser, Vincent | Deloukas, Panos | McCarthy, Mark I | Wareham, Nicholas J | Barroso, Inês | Jacobs, Kevin B | Chanock, Stephen J | Hayes, Richard B | Lamina, Claudia | Gieger, Christian | Illig, Thomas | Meitinger, Thomas | Wichmann, H-Erich | Kraft, Peter | Hankinson, Susan E | Hunter, David J | Hu, Frank B | Lyon, Helen N | Voight, Benjamin F | Ridderstrale, Martin | Groop, Leif | Scheet, Paul | Sanna, Serena | Abecasis, Goncalo R | Albai, Giuseppe | Nagaraja, Ramaiah | Schlessinger, David | Jackson, Anne U | Tuomilehto, Jaakko | Collins, Francis S | Boehnke, Michael | Mohlke, Karen L
Nature genetics  2008;40(6):768-775.
To identify common variants influencing body mass index (BMI), we analyzed genome-wide association data from 16,876 individuals of European descent. After previously reported variants in FTO, the strongest association signal (rs17782313, P = 2.9 × 10−6) mapped 188 kb downstream of MC4R (melanocortin-4 receptor), mutations of which are the leading cause of monogenic severe childhood-onset obesity. We confirmed the BMI association in 60,352 adults (per-allele effect = 0.05 Z-score units; P = 2.8 × 10−15) and 5,988 children aged 7–11 (0.13 Z-score units; P = 1.5 × 10−8). In case-control analyses (n = 10,583), the odds for severe childhood obesity reached 1.30 (P = 8.0 × 10−11). Furthermore, we observed overtransmission of the risk allele to obese offspring in 660 families (P (pedigree disequilibrium test average; PDT-avg) = 2.4 × 10−4). The SNP location and patterns of phenotypic associations are consistent with effects mediated through altered MC4R function. Our findings establish that common variants near MC4R influence fat mass, weight and obesity risk at the population level and reinforce the need for large-scale data integration to identify variants influencing continuous biomedical traits.
doi:10.1038/ng.140
PMCID: PMC2669167  PMID: 18454148
9.  The developmental origins of sarcopenia: using peripheral quantitative computed tomography to assess muscle size in older people 
Background
A number of studies have shown strong graded positive relationships between size at birth and grip strength and estimates of muscle mass in older people. However no studies to date have included direct measures of muscle size.
Methods
We studied 313 men and 318 women born in Hertfordshire UK between 1931 and 1939 who were still resident there and had historical records of growth in early life. Information on lifestyle was collected and participants underwent peripheral quantitative computed tomography to directly measure forearm and calf muscle size.
Results
Birth weight was positively related to forearm muscle area in the men (r = 0.24 p < 0.0001) and women (r = 0.17 p =0.003). There were similar but weaker associations between birth weight and calf muscle area in the men (r=0.13, p=0.03) and in the women (r=0.17, p=0.004). These relationships were all attenuated by adjustment for adult size.
Conclusion
We present first evidence that directly measured muscle size in older men and women is associated with size at birth. This may reflect tracking of muscle size and is important because it suggests that benefit may be gained from taking a life course approach both to understanding the aetiology of sarcopenia and to developing effective interventions.
PMCID: PMC2652118  PMID: 18772471
10.  Does perceived financial strain predict depression among young women? Longitudinal findings from the Southampton Women's Survey 
Background Social and financial environment has an influence on the incidence of depression. We studied perceived financial strain as a risk factor for development of depression among a large cohort of young women in Southampton, UK.
Methods We recruited a large number of young women in Southampton in the Southampton Women's Survey, a longitudinal study looking at factors influencing the health of women and their offspring. Women were asked to complete a baseline questionnaire, which included the GHQ-12 (an assessment of mental health), as well as questions on perceived financial strain and past history of depression. They were followed up two years later through their general practitioner (GP) records for evidence of incident mental illness.
Results A total of 7020 women completed the baseline questionnaire including the GHQ-12. Of these, 5237 (74.6%) had records available for follow-up. Among those developing depression, there was a higher proportion receiving benefits, and a higher level of perceived financial strain. There were also modest elevations in perceived stress, and poorer levels of educational attainment. Among women not depressed at baseline, and with no previous history of depression, those in receipt of state benefits at baseline had a significantly elevated risk of developing the disorder – hazard ratio 1.61 (95% confidence interval (CI) 1.13–2.3). The risk associated with perceived financial strain was 2.16 (95% CI 1.14–4.11), but this did not remain statistically significant after adjustment was made for receipt of benefits, educational qualification, and perceived stress.
Conclusion Financial hardship as evidenced by receipt of benefits is a strong independent predictor for the development of depression. Although perception of financial strain is also a predictor for incident depression, the risk associated with this subjective characteristic does not remain significantly elevated after adjustment. Future studies of the aetiology of depression should incorporate ascertainment of actual financial status.
PMCID: PMC2777551  PMID: 22477842
depression; finance; women
11.  Evaluation of symptomatic slow-acting drugs in osteoarthritis using the GRADE system 
Background
Symptomatic slow-acting drugs (SYSADOA) have been largely studied over the last decade. The objective of this study is to prepare a document providing recommendations for the use of SYSADOA in osteoarthritis (OA).
Methods
The following interventions were taken into consideration: avocado/soybean unsaponifiables, chondroitin sulfate, diacereine, glucosamine sulfate, hyaluronic acid, oral calcitonin, risedronate, strontium ranelate. Recommendations were based on the GRADE (Grading of Recommendations Assessment, Development and Evaluation) system. The GRADE system is based on a sequential assessment of the quality of evidence, followed by assessment of the balance between benefits versus downsides and subsequent judgment about the strength of recommendations.
Results
Chondroitin sulfate, diacereine, glucosamine sulfate, avocado/soybean unsaponifiables and hyaluronic acid have demonstrated pain reduction and physical function improvement with very low toxicity, with moderate to high quality evidence. Even if pre-clinical data and some preliminary in vivo studies have suggested that oral calcitonin and strontium ranelate could be of potential interest in OA, additional well-designed studies are needed.
Conclusion
In the benefit/risk ratio, the use of chondroitin sulfate, diacereine, glucosamine sulfate, avocado/soybean unsaponifiables and hyaluronic acid could be of potential interest for the symptomatic management of OA.
doi:10.1186/1471-2474-9-165
PMCID: PMC2627841  PMID: 19087296

Results 1-11 (11)