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Articles by L Jones
Total Records ( 9 ) for L Jones
  C. M Lewis , M. Y Ng , A. W Butler , S Cohen Woods , R Uher , K Pirlo , M. E Weale , A Schosser , U. M Paredes , M Rivera , N Craddock , M. J Owen , L Jones , I Jones , A Korszun , K. J Aitchison , J Shi , J. P Quinn , A MacKenzie , P Vollenweider , G Waeber , S Heath , M Lathrop , P Muglia , M. R Barnes , J. C Whittaker , F Tozzi , F Holsboer , M Preisig , A. E Farmer , G Breen , I. W Craig and P. McGuffin
  Objective

Studies of major depression in twins and families have shown moderate to high heritability, but extensive molecular studies have failed to identify susceptibility genes convincingly. To detect genetic variants contributing to major depression, the authors performed a genome-wide association study using 1,636 cases of depression ascertained in the U.K. and 1,594 comparison subjects screened negative for psychiatric disorders.

Method

Cases were collected from 1) a case-control study of recurrent depression (the Depression Case Control [DeCC] study; N=1346), 2) an affected sibling pair linkage study of recurrent depression (probands from the Depression Network [DeNT] study; N=332), and 3) a pharmacogenetic study (the Genome-Based Therapeutic Drugs for Depression [GENDEP] study; N=88). Depression cases and comparison subjects were genotyped at Centre National de Génotypage on the Illumina Human610-Quad BeadChip. After applying stringent quality control criteria for missing genotypes, departure from Hardy-Weinberg equilibrium, and low minor allele frequency, the authors tested for association to depression using logistic regression, correcting for population ancestry.

Results

Single nucleotide polymorphisms (SNPs) in BICC1 achieved suggestive evidence for association, which strengthened after imputation of ungenotyped markers, and in analysis of female depression cases. A meta-analysis of U.K. data with previously published results from studies in Munich and Lausanne showed some evidence for association near neuroligin 1 (NLGN1) on chromosome 3, but did not support findings at BICC1.

Conclusions

This study identifies several signals for association worthy of further investigation but, as in previous genome-wide studies, suggests that individual gene contributions to depression are likely to have only minor effects, and very large pooled analyses will be required to identify them.

  D Grozeva , G Kirov , D Ivanov , I. R Jones , L Jones , E. K Green , D. M St Clair , A. H Young , N Ferrier , A. E Farmer , P McGuffin , P. A Holmans , M. J Owen , M. C O'Donovan , N Craddock and for the Wellcome Trust Case Control Consortium
 

Context  Recent studies suggest that copy number variation in the human genome is extensive and may play an important role in susceptibility to disease, including neuropsychiatric disorders such as schizophrenia and autism. The possible involvement of copy number variants (CNVs) in bipolar disorder has received little attention to date.

Objectives  To determine whether large (>100 000 base pairs) and rare (found in <1% of the population) CNVs are associated with susceptibility to bipolar disorder and to compare with findings in schizophrenia.

Design  A genome-wide survey of large, rare CNVs in a case-control sample using a high-density microarray.

Setting  The Wellcome Trust Case Control Consortium.

Participants  There were 1697 cases of bipolar disorder and 2806 nonpsychiatric controls. All participants were white UK residents.

Main Outcome Measures  Overall load of CNVs and presence of rare CNVs.

Results  The burden of CNVs in bipolar disorder was not increased compared with controls and was significantly less than in schizophrenia cases. The CNVs previously implicated in the etiology of schizophrenia were not more common in cases with bipolar disorder.

Conclusions  Schizophrenia and bipolar disorder differ with respect to CNV burden in general and association with specific CNVs in particular. Our data are consistent with the possibility that possession of large, rare deletions may modify the phenotype in those at risk of psychosis: those possessing such events are more likely to be diagnosed as having schizophrenia, and those without them are more likely to be diagnosed as having bipolar disorder.

  M Chopra , L Jones , C Boulanger , J Benger , I Higginson , D Williamson , P Younge and G. Lloyd
  Background

Tracheal mucosal blood flow is impaired when tracheal tube cuff pressure is above 30 cm of water, with the potential for tracheal mucosal necrosis. Previous studies have found excessive cuff pressures in simulated patients intubated by North American emergency physicians as well as patients intubated in the prehospital setting and emergency department (ED). This study assessed whether patients intubated in a UK prehospital setting or ED had excessive cuff pressures.

Method

Prospective observational study in five ED in southwest England over a 2-month period. All patients over 18 years and intubated in the prehospital setting or in the ED were included. Clinical staff independent of the patients' care recorded the following: age, sex, presenting complaint and indication for intubation, tube size and cuff pressure. Neither the paramedics nor the participating ED staff were aware of the study purpose. Cuff pressure measurements were recorded using a standardised cuff inflator pressure gauge.

Result

61 patients were recruited. The median and mean cuff pressures were 58 and 62 cm of water, respectively. 75% of patients had a cuff pressure greater than 30 cm of water. The median cuff pressures in those patients intubated by senior emergency physicians, junior emergency physicians and paramedics were 70, 46 and 79 cm of water, respectively.

Conclusion

Excessive tracheal tube cuff pressures were demonstrated in the majority of patients intubated both in the prehospital setting and ED. This is in keeping with existing evidence. Early measurement and adjustment of cuff pressures is recommended for those patients who require ongoing care.

  L Jones , J. S Thomsen , J Barlach , L Mosekilde and B. Melsen
 

Zinc has been demonstrated to play an important role in bone metabolism and is required for normal growth. However, no studies have investigated the influence of zinc on calvarial bone healing in aged or adult rats. The aim of the study was to evaluate whether alimentary zinc supplementation and depletion affect bone healing of calvarial defects implanted with osteopromotive substances in adult rats. Two 5 mm full thickness critical size bone defects were trephined in the central part of each parietal bone of 60 six-month-old male Wistar rats. The bone defects were filled with demineralized bone matrix (DBM), autogenous bone chips, or were left as unfilled controls. The rats were divided into three groups of 20 rats each and received a semi-synthetic diet containing 20, 60, or 120 mg zinc/kg. After 4 months, the biomechanical integrity of the healing defects was evaluated by a punch out test and the healed defects were examined with histomorphometry. Statistical analysis of the data was carried out by two-way analysis of variance and Wilcoxon's non-parametric signed rank test.

Biomechanical testing revealed that the maximum load was significantly higher in DBM-filled defects than in those filled with autogenous bone, and that the defects filled with autogenous bone were stronger than the unfilled controls. The biomechanical findings indicated that the alimentary zinc content did not influence the healing of calvarial defects. No significant difference in maximum load could be established between the three diet groups for any of the filling materials, whereas the highest zinc supplement resulted in an increase in the relative extension on mineralizing surfaces in the control group. Thus, healing of adult rat calvarial defects is not influenced by alimentary zinc supplementation or depletion. Defects filled with DBM were significantly stronger and exhibited significantly more new bone formation than defects filled with autogenous bone or unfilled controls.

  L. D Gomez , C. G Steele King , L Jones , J. M Foster , S Vuttipongchaikij and S. J. McQueen Mason
 

Arabinans are found in the pectic network of many cell walls, where, along with galactan, they are present as side chains of Rhamnogalacturonan l. Whilst arabinans have been reported to be abundant polymers in the cell walls of seeds from a range of plant species, their proposed role as a storage reserve has not been thoroughly investigated. In the cell walls of Arabidopsis seeds, arabinose accounts for approximately 40% of the monosaccharide composition of non-cellulosic polysaccharides of embryos. Arabinose levels decline to ~15% during seedling establishment, indicating that cell wall arabinans may be mobilized during germination. Immunolocalization of arabinan in embryos, seeds, and seedlings reveals that arabinans accumulate in developing and mature embryos, but disappear during germination and seedling establishment. Experiments using 14C-arabinose show that it is readily incorporated and metabolized in growing seedlings, indicating an active catabolic pathway for this sugar. We found that depleting arabinans in seeds using a fungal arabinanase causes delayed seedling growth, lending support to the hypothesis that these polymers may help fuel early seedling growth.

  M. L Hamshere , E. K Green , I. R Jones , L Jones , V Moskvina , G Kirov , D Grozeva , I Nikolov , D Vukcevic , S Caesar , K Gordon Smith , C Fraser , E Russell , G Breen , D St Clair , D. A Collier , A. H Young , I. N Ferrier , A Farmer , P McGuffin , Holmans Wellcome Trust Case Control Consortium , M. J Owen , M. C O'Donovan and N. Craddock
 

Background

Psychiatric phenotypes are currently defined according to sets of descriptive criteria. Although many of these phenotypes are heritable, it would be useful to know whether any of the various diagnostic categories in current use identify cases that are particularly helpful for biological–genetic research.

Aims

To use genome-wide genetic association data to explore the relative genetic utility of seven different descriptive operational diagnostic categories relevant to bipolar illness within a large UK case–control bipolar disorder sample.

Method

We analysed our previously published Wellcome Trust Case Control Consortium (WTCCC) bipolar disorder genome-wide association data-set, comprising 1868 individuals with bipolar disorder and 2938 controls genotyped for 276 122 single nucleotide polymorphisms (SNPs) that met stringent criteria for genotype quality. For each SNP we performed a test of association (bipolar disorder group v. control group) and used the number of associated independent SNPs statistically significant at P<0.00001 as a metric for the overall genetic signal in the sample. We next compared this metric with that obtained using each of seven diagnostic subsets of the group with bipolar disorder: Research Diagnostic Criteria (RDC): bipolar I disorder; manic disorder; bipolar II disorder; schizoaffective disorder, bipolar type; DSM–IV: bipolar I disorder; bipolar II disorder; schizoaffective disorder, bipolar type.

Results

The RDC schizoaffective disorder, bipolar type (v. controls) stood out from the other diagnostic subsets as having a significant excess of independent association signals (P<0.003) compared with that expected in samples of the same size selected randomly from the total bipolar disorder group data-set. The strongest association in this subset of participants with bipolar disorder was at rs4818065 (P = 2.42x10–7). Biological systems implicated included gamma amniobutyric acid (GABA)A receptors. Genes having at least one associated polymorphism at P<10–4 included B3GALTS, A2BP1, GABRB1, AUTS2, BSN, PTPRG, GIRK2 and CDH12.

Conclusions

Our findings show that individuals with broadly defined bipolar schizoaffective features have either a particularly strong genetic contribution or that, as a group, are genetically more homogeneous than the other phenotypes tested. The results point to the importance of using diagnostic approaches that recognise this group of individuals. Our approach can be applied to similar data-sets for other psychiatric and non-psychiatric phenotypes.

  E. L Sampson , M. R Blanchard , L Jones , A Tookman and M. King
 

Background

Increasing numbers of people will die with dementia, many in the acute hospital. It is often not perceived to be a life-limiting illness.

Aims

To investigate the prevalence of dementia in older people undergoing emergency medical admission and its effect on outcomes.

Method

Longitudinal cohort study of 617 people (aged over 70). The main outcome was mortality risk during admission.

Results

Of the cohort, 42.4% had dementia (only half diagnosed prior to admission). In men aged 70–79, dementia prevalence was 16.4%, rising to 48.8% of those over 90. In women, 29.6% aged 70–79 had dementia, rising to 75.0% aged over 90. Urinary tract infection or pneumonia was the principal cause of admission in 41.3% of the people with dementia. These individuals had markedly higher mortality; 24.0% of those with severe cognitive impairment died during admission (adjusted mortality risk 4.02, 95% CI 2.24–7.36).

Conclusions

The rising prevalence of dementia will have an impact on acute hospitals. Extra resources will be required for intermediate and palliative care and mental health liaison services.

  L Jones , J Scott , C Cooper , L Forty , K. G Smith , P Sham , A Farmer , P McGuffin , N Craddock and I. Jones
 

Background

Only some women with recurrent major depressive disorder experience postnatal episodes. Personality and/or cognitive styles might increase the likelihood of experiencing postnatal depression.

Aims

To establish whether personality and cognitive style predicts vulnerability to postnatal episodes over and above their known relationship to depression in general.

Method

We compared personality and cognitive style in women with recurrent major depressive disorder who had experienced one or more postnatal episodes (postnatal depression (PND) group, n=143) with healthy female controls (control group, n=173). We also examined parous women with recurrent major depressive disorder who experienced no perinatal episodes (non-postnatal depression (NPND) group, n=131).

Results

The PND group had higher levels of neuroticism and dysfunctional beliefs, and lower self-esteem than the control group. However, there were no significant differences between the PND and NPND groups.

Conclusions

Established personality and cognitive vulnerabilities for depression were reported by women with a history of postnatal depression, but there was no evidence that any of these traits or styles confer a specific risk for the postnatal onset of episodes.

  L Jones , G Wei , S Sevcikova , V Phan , S Jain , A Shieh , J. C. Y Wong , M Li , J Dubansky , M. L Maunakea , R Ochoa , G Zhu , T. R Tennant , K. M Shannon , S. W Lowe , M. M Le Beau and S. C. Kogan
 

Gain of chromosome 8 is the most common chromosomal gain in human acute myeloid leukemia (AML). It has been hypothesized that gain of the MYC protooncogene is of central importance in trisomy 8, but the experimental data to support this are limited and controversial. In a mouse model of promyelocytic leukemia in which the MRP8 promoter drives expression of the PML-RARA fusion gene in myeloid cells, a Myc allele is gained in approximately two-thirds of cases as a result of trisomy for mouse chromosome 15. We used this model to test the idea that MYC underlies acquisition of trisomy in AML. We used a retroviral vector to drive expression of wild-type, hypermorphic, or hypomorphic MYC in bone marrow that expressed the PML-RARA transgene. MYC retroviruses cooperated in myeloid leukemogenesis and suppressed gain of chromosome 15. When the PML-RARA transgene was expressed in a Myc haploinsufficient background, we observed selection for increased copies of the wild-type Myc allele concomitant with leukemic transformation. In addition, we found that human myeloid leukemias with trisomy 8 have increased MYC. These data show that gain of MYC can contribute to the pathogenic effect of the most common trisomy of human AML.

 
 
 
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